>c-»o-

is“.

 

 

 

 

I'HEBIS

NIEV ERS lTY LIBRARI

Illllllll‘lll llllllllIlllllll

3 1293 015725

 

 

 

 

 

This is to certify that the

thesis entitled

TRENDS IN UTILIZATION OF SELECTED TREATMENTS

FOR ACUTE MYOCARDIAL INFARCTION
ACROSS RACE, GENDER, AGE AND PAYER GROUP

IN A COMMUNITY H ITAL, 1990-1994
presen eS by

VALERIE ROSE LINT

has been accepted towards fulfillment
of the requirements for

. MASIELdegree in EEIDEMLOLOGY

 

 

Major professor

7////7/

0-7639 MS U is an Affirmative Action/Equal Opportunity Institution

 

 

LIBRARY

Michigan State
University

 

 

 

PLACE N RETURN BOX to remove thle checkout tron your record.
TO AVOID FINES return on or before date due.

DATE DUE DATE DUE DATE DUE

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

EL;
l—l—T

MSU to An Nflrmetlve ActionEquel Opportunlty InethIon
m

 

 

 

 

 

 

 

 

 

 

 

 

I'M-9.1

TRENDS IN UTILIZATION OF SELECTED TREATMENTS
FOR ACUTE MYOCARDIAL INFARCTION
ACROSS RACE, GENDER, AGE AND PAYER GROUP
IN A COMMUNITY HOSPITAL, 1990-1994

By

Valerie Rose Lint

A THESIS
Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

MASTER OF SCIENCE

Program in Epidemiology

1996

ABSTRACT
TRENDS IN UTILIZATION OF SELECTED TREATMENTS
FOR ACUTE MYOCARDIAL INFARCTION
ACROSS RACE, GENDER, AGE, AND PAYER GROUP
IN A COMMUNITY HOSPITAL, 19904994
By

Valerie Rose Lint

The main purpose of my thesis project was to describe the provision of care for
acute myocardial infarction over a five year period among patients admitted at a
community hospital. I was interested in assessing whether my data provided evidence
that differential provision of thrombolytic therapy, cardiac catheterization, coronary
artery bypass grafting, or percutaneous transluminal coronary angioplasty existed
among the different patient subpopulation groups of my study population.

I found for time trends, there was no effect modification or confounding by any
of the other variables of age, race, gender, insurance, and comorbidity. However, for
the different procedures, some of the above mentioned variables were independent
predictors of utilization, either as main effects only, or as interactions between
themselves. Nevertheless, the inclusion of these significant independent predictors and
their interactions did not change my conclusion about the time trends in the utilization

of a given procedure.

Dedicated to my wonderful family and friends for their unconditional love, support,
and guidance.

iii

ACKNOWLEDGMENTS

This one page acknowledgment is in no way a direct reflection of the amount of
appreciation that I have for my family and friends for their encouragement and
guidance. The last two years have been a time of reflection, as well as an adjustment
period. I am grateful for their unconditional love and support especially during this
confusing time. They each continuously reminded me to believe in myself and not to
settle for less. Personal goals and dreams that seemed impossible, were again aspired
with the strength that they each gave because they never stopped believing. In
addition, I wish to acknowledge Dr. Srinivas Bhadriraju and the medical records staff
at McLaren Regional Medical Center. With their cooperation and help, this thesis was
made possible.

There is one special person that I am especially grateful for, and that is my
mother. She has devoted her life to my happiness. This happiness has not always been
easy to find; however, my mother gave me the faith to believe in myself and God.
Through the many tears and long nights, I could always rely on my mother to provide
me with the inspiration and strength to continue, even when the impossible was staring
back at me. I could never thank her enough, but can only hope that one day I, too,
will be able to provide my children with the comfort and love that she has showed with

me.

iv

TABLE OF CONTENTS

LIST OF TABLES
LIST OF FIGURES
INTRODUCTION

CHAPTER 1
CORONARY HEART DISEASE
General Anatomy
Clinical presentation of acute myocardial infarction

CHAPTER 2

EPIDEMIOLOGY OF CORONARY HEART DISEASE
Coronary heart disease mortality
Hospitalization for acute myocardial infarction
Acute myocardial hospital case fatality rates
Medical care

CHAPTER 3

THROMBOLYTIC THERAPY
Streptokinase
Recombinant tissue-type plasminogen activator
Anistreplase
Contraindications to thrombolytic therapy
Thrombolytic therapy in older patients
Distribution by demographics

CHAPTER 4
CARDIAC CATHETERIZATION
History
Procedures
Purposes
Distribution by demographics

CHAPTER 5
CORONARY ARTERY BYPASS GRAFTING
History
Procedure
Outcome Events
Guidelines
Distribution by demographics

vii

#030.)

OOxooooo

y—sp—s

13
15
19
20
21
22

25
25
26
27
29

32
32
33
34
35
36

CHAPTER 6
PERCUTANEOUS TRANSLUMINAL CORONARY AN GIOPLASTY
History
Procedure
Limitations
Restenosis
Abrupt reclosure
National Heart, Lung, and Blood Institute Registry
Guidelines
Distribution by demographics

CHAPTER 7
CORONARY ANGIOPLASTY Vs. BYPASS SURGERY

CHAPTER 8

METHODS
Data Base
Patient Population
Definition of Variables
Procedure Use
Statistical Analysis

CHAPTER 9

RESULTS
Patient Population
Procedure Use
Statistical Analysis

CHAPTER 10
DISCUSSION

vi

4O
40
42
46
46
47
48
49
5 1

54

59
59
59
61
62
63

65
65
68
70

76

LIST OF TABLES
(See Appendix H)

Table 1 - Characteristics of patients admitted to community hospital with acute
myocardial infarction diagnosis: 1990-1994

Table 2 - Age distribution by gender, race, insurance, and comorbidity; 1990-1994
Table 3 - Gender distribution by age, race, insurance, and comorbidity; 1990-1994

Table 4 - No. of AMI’s by insurance, distributed across age, race, gender, and
comorbidity; 1990- 1994

Table 5 - No. of AMI’s by race, distributed across age, gender, comorbidity, and
insurance; 1990—1994

Table 6 - No. of AMI’s by comorbidity, distributed across age, gender, race, and
insurance; 1990-1994

Table 7 - Unadjusted odds ratios on thrombolytic therapy utilization for patients up to
64 years of age, and individually adjusted by age, gender, race, comorbidity,
and insurance for other effects of admission year on utilization

Table 8 - Unadjusted odds ratios on thrombolytic therapy utilization for patients
65 years and older, and individually adjusted by age, gender, race, comorbidity,
and insurance for other effects of admission year on utilization

Table 9 - Unadjusted odds ratios on cardiac catheterization utilization for patients up to
64 years of age, and individually adjusted by age, gender, race, comorbidity,
and insurance for other effects of admission year on utilization

Table 10 - Unadjusted odds ratios on cardiac catheterization utilization for patients 65
years and older, and individually adjusted by age, gender, race, comorbidity,
and insurance for other effects of admission year on utilization

Table 11 - Unadjusted odds ratios on coronary artery bypass grafting utilization for
patients up to 64 years of age, and individually adjusted by age, gender, race,
comorbidity, and insurance for other effects of admission year on utilization

Table 12 - Unadjusted odds ratios on coronary artery bypass grafting utilization for

patients 65 years and older, and individually adjusted by age, gender, race,
comorbidity, and insurance for other effects of admission year on utilization

vii

Table 13 - Unadjusted odds ratios on percutaneous transluminal coronary angioplasty
utilization for patients up to 64 years of age, and individually adjusted by age,
gender, race, comorbidity, and insurance for other effects of admission year on
utilization

Table 14 - Unadjusted odds ratios on percutaneous transluminal coronary angioplasty
utilization for patients 65 years and older, and individually adjusted by age,
gender, race, comorbidity, and insurance for other effects of admission year on
utilization

Table 15 - Unadjusted odds ratios on thrombolytic therapy utilization and adjusted by
statistically significant predictors for other effects of admission year on
utilization as the final models

Table 16 - Unadjusted odds ratios on cardiac catheterization utilization and adjusted by
statistically significant predictors for other effects of admission year on
utilization as the final models

Table 17 - Unadjusted odds ratios on coronary artery bypass grafting utilization and
adjusted by statistically significant predictors for other effects of admission year
on utilization as the final models

Table 18 - Unadjusted odds ratios on percutaneous transluminal coronary angioplasty
utilization and adjusted by statistically significant predictors for other effects
of admission year on utilization as the final models

Table 19 - Utilization of Thrombolytic Therapy; Change in Chi-Square for patients up
to 64 years of age

Table 20 - Utilization of Thrombolytic Therapy; Change in Chi-Square for patients
more than 65 years of age

Table 21 - Utilization of Cardiac Catheterization; Change in Chi-Square for patients up
to 64 years of age

Table 22 - Utilization of Cardiac Catheterization; Change in Chi-Square for patients
more than 65 years of age

Table 23 - Utilization of Coronary Artery Bypass Grafting; Change in Chi-Square for
patients up to 64 years of age

Table 24 - Utilization of Coronary Artery Bypass Grafting; Change in Chi-Square for
patients more than 65 years of age

viii

Table 25 - Utilization of Percutaneous Transluminal Coronary Angioplasty; Change in
Chi-Square for patients up to 64 years of age

Table 26 - Utilization of Percutaneous Transluminal Coronary Angioplasty; Change in
Chi-Square for patients more than 65 years of age

Table 27 - Unadjusted odds ratios on thrombolytic therapy utilization across all ages,
and individually adjusted by age, gender, race, and comorbidity for other
effects of admission year on utilization

Table 28 — Unadjusted odds ratios on cardiac catheterization utilization across all ages,
and individually adjusted by age, gender, race, and comorbidity for other
effects of admission year on utilization

Table 29 - Unadjusted odds ratios on coronary artery bypass grafting utilization across
all ages, and individually adjusted by age, gender, race, and comorbidity for
other effects of admission year on utilization

Table 30 - Unadjusted odds ratios on percutaneous transluminal coronary angioplasty
utilization across all ages, and individually adjusted by age, gender, race, and
comorbidity for other effects of admission year on utilization

Table 31 - Unadjusted and fully-adjusted odds ratios on thrombolytic therapy utilization
across all ages

Table 32 - Unadjusted and fully-adj usted odds ratios on cardiac catheterization
utilization across all ages

Table 33 - Unadjusted and fully-adjusted odds ratios on coronary artery bypass grafting
utilization across all ages

Table 34 - Unadjusted and fully-adjusted odds ratios on percutaneous transluminal
coronary angioplasty utilization across all ages

Table 35 - Utilization of Thrombolytic Therapy; Change in Chi-Square across all ages
Table 36 - Utilization of Cardiac Catheterization; Change in Chi-Square across all ages

Table 37 - Utilization of Percutaneous Transluminal Coronary Angioplasty; Change in
Chi-Square across all ages

Table 38 - Utilization of Coronary Artery Bypass Grafting; Change in Chi-Square
across all ages

ix

Figure 1 -

Figure 2 -

Figure 3 -

Figure 4 -

Figure 5 -
Figure 6 -
Figure 7 -
Figure 8 -

Figure 9 -

Figure 10 -
Figure 11 -
Figure 12 -
Figure 13 -
Figure 14 -
Figure 15 -
Figure 16 -

Figure 17 -

LIST OF FIGURES
(See Appendix I)

Age-adjusted death rates per 100,000 for ischemic heart disease by gender
and race: United States
Trends in Mortality Due to Coronary Heart Disease from 1970 to 1990,
According to the Location of Death, among Residents of the Twin Cities
Area Who Were 30 to 74 Years of Age
Number of coronary artery bypass graft (ICD-9-CM 36.1) and coronary
angioplasty procedures (removal of coronary obstruction, ICD-9-CM 36.0);
United States
Trends in Acute Medical Care for Residents of the Twin Cities Area, 30 to
74 Years of Age, Who Were Hospitalized for Definite Acute Myocardial
Infarction in 1985 and 1990
AMI Admission by Age 1990-1994

AMI Admission by Gender 1990-1994

% 65 Years of Age & Older, AMI Admission by Insurance, 1990-1994

% Less Than 65 Years of Age, AMI Admission by Insurance, 1990-1994
AMI Admission by Insurance, 1990-1994

AMI Admission by Race, 1990-1994

AMI Admission by Comorbidity, 1990—1994

% Receiving Thrombolytic Therapy, AMI Admission, 1990-1994

% Receiving Cardiac Cath, AMI Admission, 1990-1994

% Receiving CABG, AMI Admission, 1990-1994

% Receiving PTCA, AMI Admission, 1990-1994

% Receiving Thrombolytic Therapy, AMI Admission by Age, 1990-1994

% Receiving Thrombolytic Therapy, AMI Admission by Gender, 1990-
1994

Figure 18 - % Receiving Thrombolytic Therapy, AMI Admission by Race, 1990-1994

Figure 19 - % Receiving Thrombolytic Therapy, AMI Admission by Insurance,
1990-1994

Figure 20 - % Receiving Cardiac Cath, AMI Admission by Comorbidity, 1990-1994
Figure 21 - % Receiving Cardiac Cath, AMI Admission by Age, 1990-1994

Figure 22 - % Receiving Cardiac Cath, AMI Admission by Gender, 1990-1994
Figure 23 - % Receiving Cardiac Cath, AMI Admission by Race, 1990-1994

Figure 24 - % Receiving Cardiac Cath, AMI Admission by Insurance, 1990-1994
Figure 25 - % Receiving Cardiac Cath, AMI Admission by Comorbidity, 1990-1994
Figure 26 - % Receiving CABG, AMI Admission by Age, 1990-1994

Figure 27 — % Receiving CABG, AMI Admission by Gender, 1990-1994

Figure 28 - % Receiving CABG, AMI Admission by Race, 1990-1994

Figure 29 - % Receiving CABG, AMI Admission by Insurance, 1990-1994

Figure 30 - % Receiving CABG, AMI Admission by Comorbidity, 1990-1994
Figure 31 - % Receiving PTCA, AMI Admission by Age, 1990-1994

Figure 32 - % Receiving PTCA, AMI Admission by Gender, 1990—1994

Figure 33 -% Receiving PTCA, AMI Admission by Race, 1990—1994

Figure 34 - % Receiving PTCA, AMI Admission by Insurance, 1990-1994

Figure 35 - % Receiving PTCA, AMI Admission by Comorbidity, 1990-1994

xi

INTRODUCTION

Sufferers from coronary heart disease are in need of medical attention. The
type of medical procedure administered continues to be a topic of controversy.

Because of recent technological advances, the once accepted treatment regimen for
acute myocardial infarction patients has been under scrutiny. The treatment regimen
included receiving thrombolytic therapy, particularly the thrombolytic agent
streptokinase, and then surgery. The type of surgery depended upon whether the
patient was suffering from single or multiple vessel disease. Percutaneous transluminal
coronary angioplasty was a cardiovascular procedure that was an option only for single
vessel disease patients. However, with the introduction of the balloon catheter,
angioplasty is now commonly used for multiple vessel disease patients as an alternative
to bypass surgery. The severity of the patient’s condition, comorbidity states, and the
patient’s demographics are also potential predictors of the utilization of cardiovascular
procedures.

These predictors in the utilization of cardiovascular procedures have been
suspicioned as the cause of disparity in their provision among certain patient subgroups.
Even though the mortality rate of coronary heart disease is declining, the decline is not
consistent among all patient subpopulation groups. Many studies suggest a disturbing
disparity in the utilization of procedures in myocardial infarction management across
different patient subgroups (110,111,112,113,1 14). However, whether the unequal

distribution of treatment is as a result of demographics, is not clearly defined.

The purpose of my analysis is to determine whether a discrepancy exists in the
provision of cardiovascular treatment among certain subgroups, in the community
teaching hospital to which the patients in my database were admitted. By providing
you first with a description of the provision of care for acute myocardial infarction over
a five year period (1990-1994) among patients admitted at the hospital, I will examine
the provision of the four cardiovascular procedures: cardiac catheterization (CATH),
coronary artery bypass grafting (CABG), percutaneous transluminal coronary
angioplasty (PTCA), and thrombolytic therapy across age, gender, race, insurance, and
comorbidity. I will provide information to answer the following two research
questions:

1. Do age, gender, race, insurance, and comorbidity individually or jointly
predict the utilization of each of the four cardiovascular procedures (CATH, CABG,
PTCA, and thrombolytic therapy)?

2. Is admission year (time) alone or jointly with each or all the variables a

predictor of each of the four cardiovascular procedures?

Chapter 1

CORONARY HEART DISEASE

To understand the implications of procedure utilization, one needs to have a
general knowledge of the problem at hand, coronary heart disease (CI-ID). In
addition, one needs to have a basic knowledge of the vascular system. This brief
summary will be helpful when later discussing the medical procedures of interest.
General Anatomy

The coronary artery and its branches provide nourishment to the coronary
muscles of the heart, with oxygen and nutrients. The coronary artery is the branching
vessel from the aorta that is the main vessel that routes oxygenated blood out of the left
ventricle of the heart. The left ventricle is one of four chambers of the heart. When
the left ventricle contracts, it forces the blood out of the chamber. Once circulated
through the body, the deoxygenated blood returns to the right side of the heart, where
the right atrium accepts the venous blood from the body and the right ventricle forces
the blood out to the lungs. Once reoxygenated, the blood returns to the left side of the
heart, where the left atrium accepts the oxygenated blood and the left ventricle by way
of the aorta, pushes the blood out the heart and through the body.

The normal coronary circulation is able to provide oxygen to the heart under a
range of conditions by increasing its blood flow through dilation. Coronary arteries
that are diseased with atherosclerosis may fail to do so by lacking the ability to

normally dilate under conditions of increased need. Impairment of coronary blood

flow results from narrowing of the coronary arterial lumen by atheromatous plaques.
Atheromatous plaques are usually present in the epicardial portions of the coronary
arteries. The general pathological sequence of atherosclerosis is intimal smooth muscle
proliferation, lipid deposition, and aggregation of platelets in the final development of a
complex atheromatous plaque. Thrombosis formation on a coronary artery
atheromatous plaque results in a myocardial infarction. Acute myocardial infarction,
hence-forth known as AMI, is the clinical manifestation of focus in this paper.
However, additional manifestations of CHD include angina, arrhythmias, ischemic
cardiomyopathy, and sudden death. Myocardial infarction refers to necrosis of heart
muscle caused by inadequate blood supply as a result of severe atheroslerotic narrowing
of one or more of the coronary arteries.
Clinical presentation of acute myocardial infarction

The textbook presentation of myocardial infarction (MI) describes a patient with
the onset of substemal chest pain lasting longer than 30 minutes. The pain is often
described as having a heavy object sitting on one's chest. The pain may radiate to the
arms (usually left), the neck, or the jaw. High epigastric discomfort may be a
manifestation of myocardial ischemia and dismissed as “indigestion.” Thus, those
“indigestion” cases that occur for an unusual or prolonged time deserve special
attention. Accompanying symptoms may include diaphoresis, restlessness and
anxiousness, shortness of breath, nausea, and vomiting. Also to note, is the range of

pain that myocardial infarction may present. Cases exist with, or without slight chest

discomfort. This is due to the differences in the neural sensory networks of
individuals.

To complicate matters, painless myocardial infarctions are common, occurring
in up to one-third of the cases (1). The incidence of silent myocardial infarction is
greater in women and patients with diabetes mellitus, and it increases with age. A
multicenter study showed that symptoms and signs that were predictive of AMI in
younger patients (i.e. , pain quality) were less helpfirl in the evaluation of the elderly
(2). The study enrolled patients that were evaluated for acute chest pain in the
emergency departments of 7 hospitals. The relative risks of pressure-like quality of
pain, substemal location, typical pattern of pain radiation and electrocardiographic
evidence of ischerrria or AMI were consistently closer to 1.0 for the male gender.
Meaning, these classic features for the endpoint acute ischemic heart disease (i.e. AMI)
among the elderly, were less likely to be predictive of an AMI. This study’s data
supports the hypothesis that diagnosis of an AMI is especially difficult in elderly
patients.

Pathologically, an acute myocardial infarction classification involves two
separate categories: transmural myocardial infarction and nontransmural myocardial
infarction. The difference is the thickness of affected ventricular wall in the infarct. A
transmural myocardial infarction involves more than 50% of the ventricular wall,
whereas, a nontransmural myocardial infarction affects less than 50% . However, a
clinician would distinguish an AMI as either a Q wave or a non-Q wave myocardial

infarction, as opposed to transmural and nontransmural myocardial infarction. A Q-

wave, detected during an electrocardiogram (ECG), is a negative deflection caused by
an abnormal ECG if an infarction has occurred. The interpretation of an ECG for a
patient who has suffered a nontransmural infarction (non-Q wave infarct) is more
difficult.

Besides pathological and clinical classifications, classes of indications for
diagnostic procedures and therapeutic interventions have been defined by a Task Force
on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures that was
developed in 1980 by the American College of Cardiology and the American Heart
Association. The following defined three classes will be referred to throughout this
report (67):

Class I : Usually indicated, always acceptable, and considered useful/effective

Class II: Acceptable, of uncertain efficacy, and may be controversial

a. Weight of evidence in favor of usefulness/efficacy

b. Not well established by evidence, can be helpful, and probably not
harmful

Class III: Not indicated, may be harmful

Looking more closely at the definitions of the individual classes, one would
rightfully assume that Class II is the classification group where the procedural
controversy originates. The established Task Force has only provided categories to be
used as guidelines for which the physicians will then appropriately modify on an
individual basis. These classes provide a foundation for which I will later fit CABG,

PTCA, and tPA. However, as long as procedures are classified under Class II ,

inappropriate and unequal distribution of the treatments available for acute myocardial

infarction is possible with the uncertainty factor involved.

Chapter 2

EPIDEMIOLOGY OF CORONARY HEART DISEASE

Coronary heart disease mortality

Coronary heart disease (CHD) remains the number one cause of death in the
United States among both men and women. The age-adjusted mortality rates of
coronary heart disease increased steadily each year from early in the century to the
mid-1960’s. Since then, it has been declining. The age-adjusted mortality rate
declined 42% between the peak year of 1963 and that of 1985 (4). Despite this
decline, in 1990 there were 489,171 deaths attributed to CHD [ICD-9 codes 410-414]
in the United States (236,574 women and 252,597 men) (5,6).

Reports indicate on the national level, that there is disparity in the decreasing
mortality rates among subpopulation groups. As Figure 1 shows, the US coronary
heart disease death rates decreased faster for white men than white women and blacks
between 1976 and 1985 (7,8,9). The average annual decrease for 1980 to I988 by race
and gender in greater than or equal to 35 year olds was 3.7% for white men, 3.1% for
black men, 2.9% for white women and 2.2% for black women (4). This finding on the
national level is consistent on a smaller scale. A study, conducted with the residents of
Worcester, Massachusetts as the study population (8), showed that the incidence of
acute myocardial infarction decreased less in women than in men from 1975 to 1988,

especially among the 25 to 54 and the 65 to 74 year olds.

A more recent study that examined the trends of mortality and morbidity due to
CHD was the Minnesota Heart Study (10). It took a closer look at the trends in the
second-half of the 1980’s. The study population focused on 30 to 74 year olds
consisting of 550,719 men and 576,690 women. The target population was from the
Twin Cities metropolitan area that is predominantly white. Between 1985 and 1990,
the age-adj usted rate of mortality due to CHD declined approximately 25 % in both
sexes. They measured both in-hospital and out—of-hospital deaths. As Figure 2 shows,
the downward trend was seen in both in-hospital and out-of-hospital deaths for both
sexes. However, in men, in-hospital mortality declined much more rapidly than out-of—
hospital mortality, (9.9% as compared with 3.6% per year; p<0.001). Women had a
consistent decline in mortality in both in-hospital and out-of-hospital mortality,
(between 5 and 6%).
Hospitalization for acute myocardial infarction

The national discharge rates for patients with acute myocardial infarction
decreased between 1988 and 1990. The rates per 100,000 in 1988 were 524 for 45 to
64 year olds and 1,416 for greater than or equal to 65 year olds as compared with
respective rates in 1990; 497 and 1,270. The Minnesota Heart Study reported a 12 %
increase among the men discharged with acute CHD between 1985 and 1990.
Whereas, the women remained about the same during this same time period. Two
reasons have been postulated for the increased rate of CHD hospital discharges among
men, when other measures of CHD show declines. The first explanation involves the

coding expansion in the late 1980’s of the ICD-9-CM code to describe previous care

for myocardial infarctions and the second explanation may be the effects of
reimbursement (11). With the mortality rate declining, it is certainly possible to
assume that the Minnesota’s report of increasing discharge rates could be exaggerated
with the help of new implemented coding and reimbursement effects.
Acute myocardial hospital case fatafity rates

Nationally, the case fatality rates of acute myocardial infarction continue to
decline for both sexes. However, reports have indicated that women, especially > 70
year olds, have a higher hospital acute myocardial infarction case fatality rate (12,13)
than men. In the Minnesota Heart Study, they measured survival after hospitalization
for acute myocardial infarction. Overall, the results indicated a lower risk of death
both at 28 days and within 3 years in 1990, as compared to 1985. For US hospitals
during the 1988 to 1990 period, the in-hospital acute myocardial infarction case fatality
rate was 10.1% in women and 8.4% in men aged 55 to 64 years and 14.9% in women
and 12.9% in men aged 65 to 74 years.
Medical care

As medical advancements are made in upgrading the treatments and procedures
for AMI, it is important to evaluate the trends in the utilization of medical care to
assess whether the distribution is biased. Data from the National Hospital Discharge
Survey for 1980, 1985, and 1988 to 1990 show a marked increase in the rate of cardiac
catheterization and CABG at ages 45 to 64 and > 65 years (14,15). However, before
1985 , reports indicate that men aged 45 to 64 years underwent both procedures at equal

or higher rates than men aged greater than or equal to 65 years. This increase in

10

utilization among the elderly indicates the greater tendency to diagnose and perform the
procedures, ( 12) or the greater reassurance of the benefits of the procedures due to
increased technological advances. Figure 3 shows how the estimated number of
coronary angioplasty procedures steadily increased from 1985 to 1990. The recent
national data indicate a disproportionate distribution of cardiac procedures among the
females and blacks. In 1990, age-adjusted rates per 100,000 were as follows: for
coronary angioplasty- men 165.7, women 66.2; for coronary bypass graft surgery-men
155.6, women 57.8; and for cardiac catheterization-men 512.4, women 292.6. And in
1990, the reported rates per 100,000 for blacks as compared to whites: for coronary
angioplasty-whites 99.9, blacks 17.6; for coronary bypass graft surgery-whites 98.5,
blacks 19.6; and for cardiac catheterization-whites 350.1, blacks 209.7. This disparity
in utilization among subpopulation groups is yet to be fully explained. However, these
discrepancies raise questions about differential benefits and availability among the
groups.

The Minnesota Heart Study reported the utilization of the cardiac treatments and
procedures between the two years; 1985 and 1990 (Figure 4). The frequency of
administration of the various cardiac therapies largely increased, (as reported in the
proportions of patients receiving them) in the following; thrombolytic therapy, (more
than doubled; 13 to 30%); coronary angioplasty (5 to 21%); aspirin (27 to 81%); and
heparin (5 3 to 75 %). Whereas, only moderate declines were documented among
patients given warfarin (20 to 14%) and beta-blockers (56 to 50%). And little change

was documented in the use of bypass surgery (8 to 10%).

11

As previously indicated, the trends in the use of therapy for AMI are reflective
of the decreasing mortality due to CHD. The next few chapters will describe in greater
detail the kind of impact each cardiovascular procedure has made which is reflective of
their increasing use. Each chapter will describe the development of each of the
procedures and the recent technological advances that have been made that assure a

more effective treatment with less contraindications.

12

Chapter 3

Thrombolytic Therapy

Thrombolytic therapy is a clot dissolving therapy. Intravenously injected,
streptokinase (SK [Streptase/KabikinaseD, recombinant tissue-type plasminogen
activator (rt-PA [Activase]) or anisoylated plasminogen streptokinase activator complex
(APSAC [AnistreplaseD can dissolve the clot and restore blood flow, interrupt the
infarction, reduce myocardial necrosis, and improve the survival rate if administered
within six hours of onset of an acute myocardial infarction. Approximately 66% of
heart attack victims at hospital entry are prime candidates for thrombolytic therapy,
given that an occlusive coronary clot caused the attack (verified with ST segment
elevation) (3).

Streptokinase

Streptokinase (SK) was first described in 1933 when it was used in the canine
model. It was not investigated in humans until 1949, and was FDA (Food and Drug
Administration) approved for use in myocardial infarction patients in 1987. It
systematically works in catalyzing the conversion of plasminogen to plasmin, which
then stimulates the conversion of fibrin to fibrin degradation products (FDPs). These
FDPs are responsible for dissolving the thrombus. These FDPs act as an anticoagulant,
thus preventing subacute vessel reclosure.

Reductions in mortality of acute myocardial infarction patients, with the use of

SK, has been observed in randomized control trials. One of these trials that studied the

13

use of SK, was the GISSI trial (Gruppo Italiano per 10 Studio della Streptochinasi nell’
Infarto Miocardico) (30,31). The study enrolled 11,712 patients who were randomly
assigned to the treatment group, (treatment with a l-hour intravenous infusion of 1.5
million units of SK), or to the control group. All the patients enrolled in the GISSI
study were within 12 hours of the onset of acute myocardial infarction and free of
contraindications to thrombolytic therapy. The study results proved that the earlier the
treatment was started, the more effective it was. For those treated within the first hour
of symptom onset, reduction in mortality was 47% , as compared to patients treated
within 3 to 6 hours where there was a 17% reduction. In the O to 3 hours treatment
group, there was a 23 % reduction. However, there was no benefit for those patients
treated after 6 hours. The 21-day mortality rate, as compared to the control group was
reduced by 18%, (10.7% as compared to 13.0%; p=0.0002). Additionally, the l-year
mortality rate paralleled that of the 21-day mortality, indicating long-term benefits
(30,31).

Another large randomized trial, which confirmed the results of the GISSI study,
is the ISIS-2 (the Second International Study of Infarct Survival) (32). A total of
17,187 patients, of no age limit, who were within 24 hours of onset of acute
myocardial infarction were enrolled in the study. They were randomly assigned to one
of four groups: intravenous streptokinase (1.5 mU over 60 minutes), oral aspirin (160
mg/day for 1 month), to both, or to neither. The 5-year mortality rate experienced by
the SK group versus the placebo group was a 23 % reduction. This was similar to that

seen in the GISSI study; a 18% reduction. In addition, the ISIS-2 results also

14

concluded that the earlier the treatment, the more effective it was. The observed 5-
week mortality at the various times of administration confirmed that the greater
reduction was seen during the earlier times. A 32 % reduction was observed in those
treated within 4 hours, a 13% reduction in those treated between 4 and 12 hours, and a
19% reduction in those treated between 12 and 24 hours. In patients treated within 1
hour, the 5-week mortality rate was reduced by 42% in the SK group. This was
similarly observed in the GISSI study, who observed a 47% reduction at 3-weeks.
Thus, these two trials, GISSI and ISIS-2, were consistent in their observations and
conclusions that show the earlier the administration of the therapy, the more beneficial.

In addition to confirming the results of the GISSI study, the ISIS-2 study
provided strong evidence for the additive effect of aspirin on mortality in patients with
infarction. There was a reported 21% reduction in mortality by 5 weeks for those who
received aspirin as compared to those who received the placebo (p< 0.00001). A
comparison was made between those patients who received both the SK and aspirin and
those who received the placebo, and a 39 % reduction in mortality was observed at 5
weeks (p < 0.00001) for those in the SK/aspirin treatment group.
Recombinant tissue-type plasminogen activator

Tissue plasminogen activator (t—PA) was first described in 1947, and in 1981 it
was synthesized by recombinant DNA technology and administered to nonhumans as
recombinant tissue-type plasminogen activator (rt-PA) (107). It was not until 1987 that
rt-PA became FDA approved for use in acute myocardial patients. As a second

generation agent, rt-PA is considered to have clot specific action which has potential

15

advantages over the functional capabilities of SK. Because of this, rt—PA’s local action
activates plasminogen, attached to fibrin, and bypasses the systematic action of SK.

Reductions in mortality of acute myocardial infarction patients have also been
demonstrated with the use of rt-PA. The major survival trial for rt-PA is the Anglo-
Scandinavian Study of Early Thrombolysis (ASSET) (33). The study population was
made up of 5,011 patients, excluding > 75 year olds, who were within 5 hours of onset
of suspected myocardial infarction. The enrollees of the study were randomized to
either the treatment group or the control group. The treatment group received 100 mg
of rt—PA, (10 mg bolus injection, 50 mg in the first hour, 20 mg in the second and third
hours) and the control group received a placebo. The overall mortality rate showed a
26% reduction (p=0.0011) at 1 month; the rt-PA assigned group had a 7.2% mortality
rated as compared to the 9. 8 % for the placebo group. This led investigators to believe
that the superiority of rt-PA over SK was not reflective in mortality rates.

The European Cooperative Study (35) randomly assigned 129 patients to either
the rt—PA or the SK group. Both groups received the treatment intravenously after
about 3 hours of symptom onset. The study demonstrated that at approximately 90
minutes, the patency rate for the rt-PA group was greater than that for the SK group;
70% for the rt—PA group and 55% for the SK group (p=0.058). A second trial
conducted to compare the two thrombolytic agents was performed by the investigators
in the National Heart, Lung, and Blood Institute Thrombolysis in Myocardial Infarction
(TIMI) study (36). They observed a patency rate of 70% for the rt-PA group and a

43 % rate for the SK group after 90 minutes of symptom onset. Both studies

16

demonstrated the same patency rate for those that received rt-PA, and a slight
difference in patency rates for the SK group; 55 % in the European Cooperative Study
and 43 % in the TIMI study. In addition, both studies demonstrated that the dissolving
of elements of the clotting system was less marked with rt-PA as compared with SK.
However, both rt-PA and SK had similar hemorrhagic complications, which were
largely due to hematoma formation at the arterial catheterization site.

A second trial conducted by the European Cooperative Group (108), compared
the rt-PA with a placebo. It was a randomized, double-blinded controlled trial that
enrolled 721 patients, with chest pain and ST segment elevation, that were within 5
hours of symptom onset. The treatment group was given 100 mg of rt-PA over 3 hours
and the control groups received a placebo. Both randomized groups received aspirin
and heparin. The assigned primary endpoint of the study was detectable differences in
left ventricular function. Mortality at 14 days and 3 months were secondary
endpoints. At 14—days, patients randomized to rt-PA showed a 51% mortality
reduction (NS, p=0.06) as compared to the placebo group. The ejection fraction was
higher in the rt-PA group, (2.2 ejection points higher) as compared to the placebo
group. In addition, the study demonstrated a 20% reduction of infarct size in the
treatment group as compared to the placebo group (p =0.0018).

Both of these trials did not report statistically significant reductions in the
mortality of rt-PA treated patients; however, it was suggested that the size of their

study population could be the contributing factor (34). Thus, to determine without any

17

speculation which agent, SK or rt-PA, is the more beneficial thrombolytic agent,
several trials have been conducted.

One of the largest studies to make a comparison between SK and rt-PA is the
Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded
Coronary Arteries (GUSTO) trial. GUSTO was first presented in May, 1993 and then
published (37) with a subsequent substudy (38). The GUSTO trial randomized a total
of 41,021 patients from 1,081 hospitals. All patients were within 6 hours of chest pain
onset and all had electrocardiographic evidence of infarction. This 26-month study
reported on the 30-day mortality (the indicated primary endpoint), 24 hour and 1 year
mortality, in-hospital clinical events, and 30 day net clinical benefit (% of patients who
were alive at 30 days and free of an in-hospital stroke). All patients received 160 mg
of oral aspirin on the day of the myocardial infarction and were given 160-325 mg
daily thereafter. The patients were randomly assigned to one of four treatment groups:
(1) accelerated t-PA with intravenous IV heparin; (2) IV t-PA plus simultaneous SK
with IV heparin; (3) SK plus IV heparin; (4) SK plus subcutaneous heparin. The
results from the GUSTO trial strongly indicate that enhanced thrombolysis with
accelerated dosing of rt-PA + IV heparin is directly associated with superior early
angiographic patency, improved left ventricular function, and reduced 30-day mortality
compared to SK with subcutaneous or IV heparin, or the combination of rt-PA plus SK
with IV heparin.

One factor probably related to the mortality that was observed in the GUSTO

trial was the speed in which the therapy was administered (37). The 30-day mortality

18

increased as the administration time of the accelerated t-PA increased from symptom
onset. The mortality was 4.3 % who received the treatment within 2 hours after chest
pain, 5.5% for those within 2 to 4 hours, and 8.9% for those between 4 and 6 hours.
The elderly patients (>/ = 75 years) had a 30-day mortality rate of 20.6% in SK
groups as compared to 19.3% in the accelerated t-PA group (37). The GUSTO
investigators concluded that the accelerated t-PA will save 10 more lives than SK for
every 1,000 patients receiving thrombolytic therapy. The GUSTO investigators believe
the mortality difference between the two thrombolytic agents is related to earlier infarct
vessel patency in the t-PA group.

The angiographic substudy of 2,400 patients examined patency rates at 90
minutes, 180 minutes, 24 hours, and 7 days after thrombolytic administration (38).
There was a significant difference in patency rates at 90 minutes between the four
treatment groups. The accelerated t-PA group had a patency rate of 81% , as
compared to the t-PA with SK group (73%), the SK with IV heparin group (60%), and
the SK with subcutaneous heparin group (54 %). However, there was no significant
difference in patency rates between groups at 180 minutes, 24 hours, and 5 to 7 days.
Anistreplase

Anistreplase (APSAC) is one of the new thrombolytic agents, also classified as
a second generation agent like rt-PA. APSAC functionally works in the same way as
rt-PA, by activating plasminogen preferentially on the surface of the clot rather than in

the general circulation as SK works. APSAC was FDA approved in 1990.

19

Many studies have been conducted to assess the patency rate of APSAC, and
have found similar rates as that of SK. Bonnier et a1. (39) found a patency rate of
64%, which is similar to that found with SK (68%). Bassand et a1. (34) demonstrated
a 77 % patency rate and a 31% reduction in myocardial infarction size with salvage of
left ventricular systolic function.

A group from the United Kingdom, the AIMS Trial Study Group, conducted a
multicenter, double-blinded controlled trial to study the efficacy of APSAC ( 109). The
1,004 patients were randomly assigned to the treatment group (30 units of APSAC
intravenously over 5 minutes) or to the placebo group. The patients enrolled in the
study were < 70 years of age and between 30 rrrinutes and 6 hours of symptom onset.
They reported a 30—day mortality reduction of 47% of those enrolled within 4 to 6
hours of symptom onset. They reported that there was a greater mortality reduction
among those patients entered < 4 hours. The 1-year mortality reduction was 44 %
(p=0.0006); 19.4% in the treatment group as compared to 10.8% in the placebo
group. APSAC has presently proven to be a viable thrombolytic agent. It joins SK
and rt—PA as a useful therapeutic alternative.

Contraindications to thrombolytic therapy

The major side effect to thrombolytic therapy is hemorrhage. Additionally, the
Task force has provided a list of absolute contraindications to thrombolytic therapy (3).
The task force also provides relative contraindications that should be considered on a

case by case analysis of risk versus benefit. (See ACC/AHA Task Force on the

20

Management of Acute Myocardial Infarction for those) (3). The relative
contraindications include:

Active internal bleeding.

Suspected aortic dissection.

Prolonged or traumatic cardiopulmonary resuscitation.

Recent head trauma or known intracranial neoplasm.

Diabetic hemorrhagic retinopathy or other hemorrhagic ophthalmic
condition.

Pregnancy.

Previous allergic reaction to the thrombolytic agent (SK or APSAC).
Recorded blood pressure >200/120 mm Hg.

History of cerebrovascular accident known to be hemorrhagic.

E‘PPPI‘

Pmsa

Thrombolytic therapy in older patients

I have provided evidence of a steep increase in case fatality rate with age.
Nearly 50% of all deaths in patients hospitalized for acute infarction occur in those
>75 years of age (13). Because of the fear of hemorrhaging, most trials, with the
exception of ISIS-2 and GISSI have excluded patients either > 70 or > 75 years of age.
The ISIS-2 study reported a greater mortality reduction at 5-weeks in the younger
cohorts; however, a mortality reduction was still observed among the treatment group
in the eldest cohort. The results were as follows: a 16% reduction (18.2% versus
21.6%) in the SK group >70 years of age; a 26% reduction (10.6% versus 14.4%) in
the SK group 60 to 69 years of age; and a 28% reduction (4.2% versus 5.8%) in the
SK group < 60 years of age.

The GISSI study observed the same decreasing trend in mortality reduction as
the patient population age increased. The GISSI trial noted a 13 % reduction in
mortality at 3 weeks in those >75 years of age, an 8% reduction in those 65-75 years,

and a 26% reduction in those < / = 65 years. However, the results in the oldest two

21

patient population cohorts were not statistically significant than that of the reference
group for mortality . These studies demonstrated that the weakened affect of SK with
increasing age needs to be carefully evaluated when recommending thrombolytic
therapy for the elderly population. Recommendations have been provided by the Task
Force for administration of thrombolytic therapy to patients with myocardial infarction
and without contraindications to the therapy. (See Appendix E).

Distribution by demographies

Thrombolytic therapy is currently used in the United States for only a rrrinority
of AMI patients. Abiding by strict inclusion and exclusion criteria, as defined by the
current recommendations, have resulted in the underuse of this medical therapy. This
is reflective of current estimates that show only 10% of AMI patients in the United
States actually receive thrombolytic therapy (115). There are four major medical
reasons that AMI patients are not treated with thrombolytic therapy (116): advanced
age, nondiagnostic electrocardiogram (ECG), specific contraindications, and excessive
delay to treatment.

Advanced age is of particular interest in this study. AMI is the leading cause of
mortality in the elderly, and more importantly, the number of elderly patients is
projected to increase in the future (116-119). Yet these patients have not been
consistently included in the pool of patients that receive thrombolytic therapy, because
of fear of the increased risk of hemorrhage from this medical treatment. The increased
hemorrhagic risk has not been in all the thrombolytic trials among the elderly. For

example, the ISIS-2 study included over 400 patients that were over the age of 80

22

years, and still there was no significant bleeding complications reported as a result of
thrombolytic therapy administration (32). Nevertheless, the efficacy of thrombolytic
therapy in the elderly remains unproven, however pooled data suggest possible benefits
(115,120-123). For example, the absolute number of lives saves is greater among the
elderly group of patients, because of their elevated mortality without thrombolytic
therapy (32,115,123).

Demographic, procedural, and outcome data were collected from 1,073 US
hospitals on AMI patients during 1990 and 1993 (124). This data comprises the
National Registry of Myocardial Infarction (MITI) Registry. Registry hospitals
composed 14.4% of all US hospitals. Among the 240,989 AMI patients enrolled in the
study, 84,477 (35.1%) of them received thrombolytic therapy. Overall, the patients to
receive the therapy were younger, more likely to be male, presented sooner after onset
of symptoms, and were more likely to have localizing ECG changes. A trend analysis
from 1990 through 1993, shows that the time from hospital evaluation to administration
time of thrombolytic therapy is shortening. The national registry confirms on a large
scale what the smaller studies conclude, that thrombolytic therapy is underused among
the elderly patients, as well as the late presenters.

In summary, thrombolytic therapy is the medical treatment for AMI patients
that is underused among certain subgroup populations. We know that approximately
66% of heart attack victims at hospital entry are prime candidates for thrombolytic
therapy, however, only approximately 10% of AMI patients in US hospitals actually

receive thrombolytic therapy. Despite the strict inclusion and exclusion criteria as

23

recommended for administration of thrombolytic therapy, the benefits especially that

for the elderly, outweigh that of hemorrhagic risks.

24

Chapter 4

Cardiac Catheterization

Of the patients surviving to hospital admission, approximately 30% admitted
with myocardial infarction will require revascularization within the first 30 days
(16,17). With the introduction of thrombolytic agents to treat acute myocardial
infarction, the post-infarction evaluation and management have become increasingly
complex. Cardiac catheterization is the means used to determine if a patient has
responded to thrombolytic therapy. Should the infarct-related artery still be occluded
after therapy, the use of catheterization will be important in deciding whether additional
cardiovascular procedures should be performed. However, controversy has been raised
as to the routine use of cardiac catheterization. An additional important use of
catheterization is for diagnostic purposes. Both purposes will be discussed in more
detail, but I will first review the development of cardiac catheterization.

History

In 1929, Werner Forssmann was the first to establish cardiac catheterization
(18). His interest was in injecting drugs directly into the right atrium. He performed
the first cardiac catheterization on himself. Forssmann’s motivation spread, and his
technique was soon adopted by others. Klein, Coumarrd, Richards, and others used his
technique for studying the physiology of the human circulation (18). The most famous
example of this, is the work of Swan and Ganz, who used a catheter to obtain useful
physiological measurements. The cardiac catheterization was first used for diagnostic

purposes by James Warren, Emmett Brannon, and Heinz Weens. They used the

25

catheter to diagnose the atrial septal defect, for which the description was published in
1945 ('19).

After the creation of cardiac angiography, the right side of the heart was an easy
target, while the left side remained a difficult one. Zimmerman, Scott, and Becker
were responsible for initiating the development of a technique that allowed for the
visualization of the left side. In the late 1940’s, Zimmerman, Scott, and Becker
performed the first catheterization in which the cardiac catheter passed from the aorta
into the left ventricle (20). It was not until Mason Sones in 1958 introduced selective
coronary arteriography using the brachial approach (21), that diagnostic and therapeutic
work on coronary disease would be possible. Melvin Judkin and others modified his
approach, which lead to firrther developments, such as percutaneous transluminal
coronary angioplasty, which will be discussed later in this report.

Procedures

As indicated with the history of the cardiac catheterization, there are two
techniques of coronary arteriography; the Sones technique and the percutaneous
femoral technique. The Sones technique introduces the catheter by way of the brachial
artery, whereas the percutaneous femoral technique uses the femoral artery. The latter
approach was introduced in the 1960’ s and gained popularity. However, the Sones
technique has the following advantages over the percutaneous femoral technique (22):
(1) only one catheter is necessary to visualize both coronary arteries, the left ventricle,
and aortacoronary bypass grafts; (2) this method can be used in patients with severe

obstructive disease of the iliofemoral system; (3) the procedure can be done on an

26

outpatient basis; (4) the depth of insertion of the catheter tip into the left coronary
artery can be better controlled; and (5) the catheter tip can be rapidly shifted from one
coronary artery to the other. Specifically using the Sones technique, the mortality risk
is no more than 0.1 percent (22).
Purposes

Cardiac catheterization has a dual purpose. It is a powerful diagnostic tool and
additionally is important in assessing whether a patient has responded to thrombolytic
therapy (23). The majority of physicians will agree that cardiac catheterization and
coronary arteriography should be performed on patients who survive an acute
myocardial infarction (24); however, indications remain controversial (25). Thus,
guidelines have been recommended by the American College of Cardiology/ American
Heart Association Task Force on Assessment of Diagnostic and Therapeutic
Cardiovascular Procedures (67). These guidelines are divided into three separate
categories, depending on the time after a myocardial infarction has occurred that
cardiac catheterization is to be performed: (1) during the initial 6 hours of myocardial
infarction; (2) after the initial 6 hours up to but not including predischarge evaluation;
and (3) from immediate predischarge up to 8 weeks after discharge. (See Appendix
G). It has been agreed that the following are definite clinical indications for cardiac
catheterization and coronary arteriography in the early post infarction period: recurrent
ischerrria, persistent moderate to severe left ventricular dysfunction, and uncontrollable

ventricular tachyarrhythmias (24,25,3,26,27).

27

The most important use of cardiac catheterization is for diagnostic purposes.
Used as a diagnostic tool, cardiac catheterization provides valuable information of
anatomic and physiologic change in many cardiovascular diseases. The following are
the measurements that can be made using a cardiac catheter (28): (1) pressures in
various cardiac chambers and blood vessels; (2) pressure gradients across stenotic
cardiac valves; (3) cardiac output; (4) systemic and pulmonary vascular resistances; (5)
hemodynarrrics during stress (cg, supine exercise); and (6) shunts between systemic and
pulmonary circulations.

The important role for cardiac catheterization is providing precise anatomic and
physiologic details of the cardiac abnormality in patients who are being evaluated for
cardiac surgery. During catheterization, contrast material is selectively injected to
assist in diagnosis. This material is helpful for defining the anatomy of coronary
arteries and various congenital heart diseases, quantifying valvular regurgitation, and
calculating the chamber volume, particularly the left ventricular end—diastolic and end-
systolic volumes, and the ejection fraction (28). Additionally, for patients who suffer
with multi-vessel disease, cardiac catheterization will be helpful in revealing
unsuspected abnormalities or nrisj udged severity of the disease.

Routine use of cardiac catheterization remains to be a t0pic of controversy.
Since they are currently are no noninvasive techniques that allow visualization of the
complete coronary artery circulation, it is recommended that each patient after an acute
myocardial infarction should have selective coronary arteriography (29). However, on

the other hand, this recommendation extends to warn that it is not practical to perform

28

a routine cardiac catheterization on every patient (29). Routine cardiac catheterization
and coronary arteriography may be performed unnecessarily in some cases. These
cases include patients who may have no evidence of myocardial ischemia and who are
at low risk of recurrent cardiac events (29). This is an important reason to promote
identification of high-risk patient subsets before any cardiovascular procedure is
performed. Many recent technological advances have been made since the
development of cardiac catheterization. However, coronary arteriography continues to
set the standard for diagnostic measurements and acts as the guide for further
cardiovascular care.
Distribution by demographics

Cardiac catheterization is a low-risk procedure performed for the purposes of
gaining information on coronary artery anatomy and physiologic abnormalities in order
to assess for possible surgical intervention. Not all patients with cardiac symptoms
need this procedure, nevertheless, it is most often used on a routine basis. Clinical
judgment is key when patients do not clearly meet the strict criteria as recommended by
the ACC/ AHA guidelines. This judgment in some cases has been shown to result in
unequal distribution of cardiac catheterization among certain subpopulation groups.

Men seem to have cardiac catheterization ordered at a rate disproportionately
higher than women. A study conducted in 1987 (125), enrolled 390 patients all of
which had abnormal exercise radionuclide scans. The results of administering cardiac
catheterization between the sexes was alarmingly disproportionate; 40% of the males as

compared to 4% of the females were referred for cardiac catheterization. Additionally,

29

once the researchers controlled for variables of abnormal test results, age, types of
angina, presence of symptoms, and confirmed previous myocardial infarction, men
were still 6.5 time more likely to be referred for cardiac catheterization than women.

Racial differences in the use of invasive cardiovascular procedures have also
been explored. One study in particular, analyzed the used of cardiovascular procedures
among black and white male veterans discharged from Veterans Affairs hospitals with
primary diagnosis of cardiovascular disease or chest pain during 1987 through 1991
( 126). The study concluded that even when financial incentives were absent, whites
were more likely than blacks to undergo invasive cardiac procedures. After they
adjusted for all the potential confounders, they found that white veterans were more
likely than black veterans to undergo cardiac catheterization (odds ratio, 1.38; 95 % CI,
1. 38 to 1.64).

However, this racial difference for administering cardiac catheterization was not
confirmed on the national level. As results from the MITI registry, admitted to 19
hospitals in metropolitan Seattle were a total of 641 blacks and 11,892 white patients
with chest pain of presumed cardiac origin since 1988 (127). Black men and women
were younger (58 vs. 66 years; p < .0001), more often admitted to central city hospitals
(p< .0001), and developed evidence of AMI less often (19 vs 23%; p< .01). During
hospitalization, whites had higher rates of coronary angioplasty and coronary artery
bypass grafting, although thrombolytic therapy and cardiac catheterization were used

equally among the two groups.

30

Additionally, age-related differences in the utilization of therapies post AMI
have been investigated. In particular, a retrospective chart review was performed on
all cases with a primary or secondary discharge diagnosis of AMI (110). The total of
771 charts that were reviewed came from two large community hospitals in Milwaukee,
Wisconsin from July 1, 1990 to June 30, 1991. They concluded that a very high
percentage of those older than 65 years of age received invasive tests and interventions.
There was a high cardiac catheterization rate, approximately 77 % of all patients, and
did not decline until after the age of 75 years, after which it fell steeply.

In summary, according to the recommendation for performing cardiac
catheterization, no specifically relate to demographics. These guidelines do suggest to
be cautious when performing cardiac catheterization on patients with uncomplicated
complete myocardial infarction in whom no acute mechanical or surgical intervention is
contemplated. Nevertheless, cardiac catheterization is most often used on a routine

basis.

31

Chapter 5

Coronary Artery Bypass Grafting

Assessing the comparative role and efficacy of coronary artery bypass grafting
(CABG) and percutaneous transluminal coronary angioplasty (PTCA) continues to be
an issue. Several randomized studies concerning the comparability of these two
procedures will be evaluated. Furthermore, addressing the impact that patient
demographics have on the utilization of CABG will be of importance. Before
examining these critical areas, lets begin with the development of the procedure,
coronary artery bypass grafting.

History

The early 1970’s marked the beginning of surgical revascularization methods for
patients suffering from a thrombus (blood clot) in a coronary artery. This new method
was an efficient means to promote normal blood flow to the heart muscle with low
morbidity and mortality. Results of studies during this time, confirmed and supported
the surgical method of revascularization. One study performed during this period
reported that mortality was < 10% and 50% of the infarctions were eliminated in 11
patients from the Brigham Hospital (76).

It was not until the late 1970’s that aggressive action was taken to perform
surgery for acute evolving myocardial infarction. In fact, in the early 1970’s, if the
patient had had an uncomplicated transmural myocardial infarction, most clinicians felt

that coronary bypass surgery was inappropriate for at least 6 weeks, unless there was

32

some complicating mechanical effect (77,78). The early results (77,78) were
suggestive that speed of reperfusion was critical to decrease long-term mortality and to
increase salvage of heart muscle. The results of the long-term investigation conducted
in Spokane, Washington confirmed the critical time factor (79,80). This 13—year
retrospective study consisted of 387 acute myocardial infarction patients, managed
medically or surgically. The surgical (CABG) and medical groups had a statistically
significant different rate of sudden cardiac death (7.4% & 17.5%; p<0.01). In
addition, the patients who underwent surgery during the late phase of an acute
myocardial infarction had a mortality rate similar to that in the medically managed
group. Those patients that did undergo the surgery within 2 hours of the onset of the
acute myocardial infarction, the mortality rate was only 2 % . This confirmed earlier
studies that stressed the importance of performing the surgical procedure promptly.
Procedure

During a coronary artery bypass operation, a large vein or artery is removed
and used during the procedure. Most commonly removed are short segments of the
saphenous vein (in the leg), or alternatively removed are other large veins or arteries in
the body, such as the internal mammary artery (in the chest). The removed segment of
the vein is used to create an alternate passage for the blood flow to avoid the
obstruction. One end of the vein is implanted in the aorta while the other end is
connected to the coronary vessel beyond the place of obstruction. This new route,
hence the name, ‘bypass surgery, ’ will allow enough blood flow to reach the heart

muscles to prevent chest pain, at exertion or at rest.

33

Outcome Events

CABG is not a curative procedure, rather it has proven effective in reducing the
conditions associated with an acute myocardial infarction, particularly angina.

The Coronary Angioplasty versus Bypass Revascularization Investigation (CABRI) is a
multinational, multicenter randomized trial comparing the two surgical procedures,
PTCA versus CABG (88). This is one of many randomized trials which will be later
explored, all of which confirm the results that patients in the PTCA group are more
likely to have clinically significant angina after the procedure. In the CABRI study, the
PTCA randomized group had a statistically higher risk of angina after one year
(RR=1.54 [1.09-2.16], p=0.012) than the CABG randomized group. This effect was
present in both sexes, but statistically significant only among the females. The return
of angina is most prevalent of the postoperative ischerrric events. The return of angina
very early after surgery is primarily due to incomplete revascularization or early
closure of grafts. And the return of angina occurring later is usually due to narrowing
or closure of one or more grafts and/or the development of native vessel disease.

The surgery is complex and can vary drastically between patients, thus it is
important to explore the possible outcomes. Survival after the coronary artery bypass
graft operation has been the outcome variable from several reported studies.
Specifically looking at the data from the CASS (Coronary Artery Surgery Study)
Randomized Trial, Alderman, et a1. conducted a ten-year follow-up study on survival
(81). About 98.5 % of patients survived at least 1 month after the operation, and

98.1%, 94.7%, and 82%, survived 1, 5, and 10 years respectively, following the

34

operation. Studies using cardiac death as the outcome variable after the coronary artery
bypass grafting operation have suggested that cardiac death depends on: the year in
which the operation was performed given recent medical advances in recent years, the
severity of the coronary disease, and the severity of the left ventricular dysfunction
(82).

Patency rates for coronary artery bypass grafts are dependent on the grafted
vessel. The highest patency rates are associated with the use of the left internal
mammary (thoracic) artery to bypass proximal stenoses of the left anterior descending
coronary artery. Loop et al. reported, after a 10-year survival of patients having the
internal mammary bypass, patency rates were approximately 95 % (83). However, the
use of saphenous veins for the bypass develops disease, contributed to stenoses and
occlusions. Reports have indicated variable patency rates for vein grafts in coronary
artery bypass grafting. In some reports (84,85), only 50% to 60% overall remain
freely open after the 10—year follow-up. While other studies suggest that the patency
rate of vein grafts is dependent on the location of its anastomosed artery. It is
important to note that the analysis done in this report does not take into account the
specific artery used in the coronary artery bypass grafting.

Guidelines

In an era when options are available, The American College of Cardiology and

the American Heart Association have designated a Task Force on Assessment of

Diagnostic and Therapeutic Cardiovascular Procedures, who then appointed a

35

Subcommittee to develop guidelines and indications for the coronary artery bypass
operation (86). Defined are three classes for CABG indications:

Recommendations for Surgery in the Early Management of Myocardial Infarction
Recommendations for Emergency or Urgent Coronary Bypass Surgery

Class I
1. Failed angioplasty with persistent pain or hemodynamic instability.
2. Postinfarct angina with left main or three-vessel disease or where coronary
angioplasty is not indicated, with two-vessel disease involving the proximal left anterior
descending coronary artery or two-vessel disease and poor left ventricular function.
Class II
1. At the time of surgical repair of ventricular septal defect or acute mitral
insufficiency.
2. Cardiogenic shock not suitable for angioplasty.
Class HI
1. Where the available surgical mortality rate exceeds the mortality rate associated
with appropriate medical therapy.
Distribution by demographics

The data from the National Hospital Discharge Survey for 1980, 1985 and 1988
to 1990 show a marked increase in the rate of coronary artery bypass grafting at ages
45 to 64 and >65 years of age (5,15). During 1988 to 1990, rates for CABG were
higher in men at age 65 years or older, than what was seen before 1985, with an equal
rate between the two age groups. This indicates a greater tendency to treat the elderly
with more aggression as compared to the younger patients. Additionally, as earlier
indicated in Chapter 2, recent US rates for cardiac procedures were lower in women
than men.

Despite the national rates of CABG disproportionately distributed among the

genders, there are no apparent differences in 5 and 10 year survival rates between

36

males and females after successful CABG (128-132). Nevertheless, several studies
have shown that operative mortality has been consistently higher in women than men
(128,129,133,134), with a relative risk of death in women after CABG ranging from
1.46 to 4. 84. Studies have tried to adjust for preoperative baseline differences between
men and women. In conclusion, CASS investigators found that mortality differences
between the sexes were as a result of differences in coronary artery size (135).
However, artery size is not a factor that is reason for gender differences in outcome in
all studies. Another reason for the increased mortality in women found in some of the
studies is possibly referral bias (106). In summary, the studies suggest that CABG
outcome may depend more on patient size or coronary size and preoperative risk
factors than on gender itself. The women’s’ longterm survival is similar to that of
men, however, studies have shown that women do have a higher surgical mortality rate
and less angina relief after CABG than men.

Additionally, studies suggest that there are substantial interracial differences in
cardiac procedure rates. One study in particular that suggested just that was a study
that obtained discharge data from the Massachusetts Health Data Consortium on all
patients discharged from hospitals in Massachusetts during the 1985 fiscal year (114) .
Despite that age and sex adjusted admission rates for white and blacks were similar,
whites underwent more than twice as many coronary artery bypass grafts than blacks.
More specifically, 3,131 coronary bypasses were performed on white patients as
compared to only 35 coronary bypasses being performed for blacks. The white-black

bypass rate was 2.27 (p< .05).

37

This disproportionate distribution among the races is reflective of the national
data. Results from the MITI registry shows that black patients admitted to coronary
care units in metropolitan Seattle were less likely to receive coronary bypass surgery as
compared to the white patients admitted to the same care units. During the patients’
hospitalization, whites had higher rates of coronary artery bypass graft surgery (10 vs
4%; p=.04) as compared to the blacks (127).

The Society of Thoracic Surgeons’ National Cardiac Database was used in part
to determine the changes in preoperative characteristics of patients undergoing CABG
during the lO-year period of 1984 to 1993 (136). Data show that an increase of 2.5
years in age and decreases of 3 % both in incidence of male patients and in incidence of
first operation occurred during this decade. This means that CABG is being utilized
more among the elderly patients and less among the male patients and first time
patients.

The benefits of performing CABG on the elderly patients are not consistent
among the several trials conducted. Additionally, the long-term benefits of CABG
outweigh taking a less invasive route with less risks, such as medical therapy.
Advancing age was a significant independent predictor of operative mortality in several
studies (137-141). However, a study reporting only elective CABG in patients greater
than 65 years of age had an operative mortality rate of only 1.6% (142). Additionally,
the extent of coronary disease did not affect survival of elderly patients at 5 years in the
CASS study (137) (p=.08) or at 10 years in the data from the Cleveland Clinic (139).

In summary, a decreased risk of sudden death and a better prognosis for 10-year

38

survival than the normal population, adjusted for age and sex are jointly beneficial
(143). There are significantly higher risks among the elderly patients, however, patient
selection is currently individualized according to severity of symptoms, coexisting
illnesses, and angiographic findings (143). Advanced age is considered an additional
risk factor, but does not contraindicate operation.

In summary, CABG is becoming more widely disseminated among the patient
population. Studies have proven that their is disproportionate distribution of CABG
among certain subgroups, however, as national data indicate, these trends are becoming
less as the years progress. Additionally, there is no need for concern that gender or
race are factors in differential outcome when having had CABG. The long-term
outlook are similar, in particular between males and females. And as indicated earlier,

the benefits of surgery outweigh the risks among the elderly patients.

39

Chapter 6

Percutaneous Transluminal Coronary Angioplasty

Percutaneous transluminal coronary angioplasty (PTCA) has been rapidly
growing in popularity, from performance on only a few cases in the 1977-1980 period
to 133,000 performed in 1986 (40). PTCA is a surgical procedure commonly used for
patients with single-vessel disease; however its use has been extended to treat patients
suffering from multi—vessel disease. The United States experienced over the past
decade a more than tenfold increase, with approximately 300,000 angioplasty
procedures performed in 1990 (41). Despite the popularity of the procedure, studies
have suggested that the utilization is not uniform across certain subpopulation groups,
such as Kern et al.. (144), Holmes et al.. (145), and Harman et al.. (146). To begin, a
brief summary of the development and the procedure itself will be described.

History

After success with cadaver studies, Dotter found that dilation of localized
stenoses without dislodging atheromatous plaques was possible. On January 16, 1964,
Dotter performed the first translurrrinal dilation on a patient, an 82-year old woman.
This woman had a 0.5 cm stenosis of the adductor hiatus (in the leg). Her only option
was for leg amputation because she was not a candidate for reconstructive vascular
surgery. Immediately following Dotter’s dilation procedure, he felt distal pulses that
were previously undetected in her lower leg. The woman was able to walk for the first

time in 6 months; however she later died of congestive heart failure.

40

After Dotter’s initial dilation procedure proved successful, he teamed with
J udkin, and by November 1964, they performed 15 dilations on nine patients (42).
The initial results were encouraging; the elimination of four amputations and six of the
nine patients improved. They concluded that the best results were for those patients
with small area stenoses, in contrast to poor results on blockages of long segments.
The technique of transluminal angioplasty grew in popularity in Europe during the next
decade, while clinicians in the United States remained skeptical. It was not until the
invention of balloon catheters that the United States showed interest in transluminal
angioplasty.

In 1964, Dotter and J udkin (42) saw a need to have a catheter that featured the
ability to produce maximal dilation of a stenotic lesion especially for large vessels.
Latex balloons were first tried, but proved ineffective (43). Revisions of angioplasty
balloon catheters were underway. In 1973, Porstmann (44) developed a caged or
“Korsett” balloon catheter, revised in 1974 by Dotter et al... (43). Neither balloon
catheter, the caged nor the “Korsett” balloon catheter, were recommended because of
the potential for excessive damage to the intima or the vessel wall. Finally in 1974,
Gruentzig introduced a balloon catheter that proved successfirl. The new type of
balloon catheter was capable of producing a rigid balloon that inflated to a preset
diameter (4 to 8 mm) and produced a large radial force (3 to 5 atmospheres of
pressure) (45,46). In 1977, he had performed the angioplasty using his balloon

catheter on 200 patients; 136 with femoropopliteal disease (diseased vessels found in

41

the posterior region of the knee) and 41 patients with iliac disease (47). These 200
patients were recorded to have a 2-year patency rate of 70 percent (48).

The fear of acute coronary artery occlusion and infarction justifies the
apprehension of implementing balloon angioplasty. Gruentzig et al. . . (48) first tried
coronary angioplasty on animals and then dilated coronary arteries of human cadavers.
Both attempts were successful using the new balloon catheter of a smaller size. Then
on September 16, 1977, Gruentzig performed the first successful percutaneous
translurrrinal coronary angioplasty (PTCA) on a human (49). The patient was a 38-year
old man with 85 percent narrowing of the left anterior descending coronary artery.
Procedure

As indicated with the history of the development of coronary angioplasty, the
procedure is an extension of diagnostic angiography. The procedure begins when a
catheter is guided into the coronary artery from either the arteries in the leg, or less
commonly, in the arm. Inserted into the guiding catheter, is a separate catheter; the
dilating balloon catheter. This balloon catheter is a double lumen catheter used for the
dilation; hence, the name ‘double lumen catheter. ’ This catheter is used to inflate the
balloon at the distal end and simultaneously used to inject solutions or measure pressure
at the opposite end. Unique qualities such as the elongated and cylindrical structure of
the catheter make it possible to travel the lumen of the coronary arteries. In addition,
the flexibility of the catheter allows for the mobility through the branching of the
coronary arteries by way of a wire. This flexible wire can travel the route of the

vascular tree, making way for the balloon system to maneuver through the guiding

42

catheter into the stenotic coronary artery. The balloon is dilated when the surgeon
centers the catheter in the stenosis. Dilation happens once the balloon is inflated in the
atherosclerotic plaque (50,51). Dilation was originally believed to result in the
compaction and redistribution of translunrinal atherosclerotic plaque substance.
However, more recent studies have shown that dilation occurs once intimal disruption
and stretching of vascular media and adventitia happens (52).

PTCA use as the primary treatment for AM] entails the need to always have a
cardiac surgical team available. For this reason, intravenous tlrromobolysis has become
established as the first-line therapy when appropriate. However, thrombolytic therapy
has also been administered to patients as an adjunct to PTCA. Thrombolytic therapy
administered early to patients with acute myocardial infarction has been shown to
decrease mortality. However, this decline in mortality is accompanied by instability of
the recanalized vessel that feeds the area of the infarct. This instability probably results
from the considerable residual stenosis in the majority of patients after successful
thrombolysis (53,54,55). Additionally, after administration of one of the thrombolytic
agents (tissue plasminogen activator), thrombolysis is incomplete 1.5 to 3 hours after
infusion. And because some thrombolytic agents (tPA included) have been shown to
cause platelet activation, it is possible to have an increase risk of hemorrhagic
infarction when PTCA is performed immediately after thrombolysis. With the
immediate use of PTCA, it may further predispose to platelet deposition (56,57).

Reports have indicated that the delayed use of PTCA following successful

thrombolysis has proven beneficial in the following ways: by reducing the narrowing

43

of the luminal diameter in the underlying plaque, decreasing reocclusion, lessening the
residual stenosis, improving coronary blood flow, and by promoting the recovery of
myocardial function (5 8). However, the role and proper timing of PTCA after
thrombolysis are still controversial topics.

Two main trials that have been able to provide specifics on the role and most
beneficial time of PTCA administration following thrombolysis are the Thrombolysis in
Myocardial Infarction (TIMI) Study (59) and the Thrombolysis and Angioplasty in
Myocardial Infarction (TAMI) Study (5 8). Both of these studies investigated the role
of recombinant tissue plasrrrinogen activator (rt-PA) prior to a PTCA. The TIMI study
indicated that immediate performance of PTCA, compared with delaying the
procedures for 18 to 48 hours, provides no advantage and may be harmful. These
harmful events include emergency coronary artery bypass surgery, reinfarction, and
required transfusions due to immediate bleeding.

The TIMI-II A Study was carried out at seven of the 50 TIMI hospitals. From
April 1986 through September 1987, a total of 389 patients were randomly assigned to
one of three treatment strategies after r-tPA treatment. The three treatment groups
were: (1) immediate coronary arteriography followed by PTCA; (2) 18 to 48 hour
arteriography with PTCA; (3) no PTCA unless required by evidence of spontaneous or
provokable ischemia. The primary end point for TIMI II A was ventricular function at
the time of hospital discharge. Of the 195 patients assigned to the immediate PTCA
group, 84 % of the attempts were judged to have shown improvement. Of another 194

patients that were assigned to the 18 to 48 hour PTCA group, 93 % of the attempts

44

showed improvement. It was concluded from this trial that immediate PTCA is not
required after administration of rt-PA to patients with acute myocardial infarction for
beneficial results.

The TAMI study results confirmed results of the TIMI study. The TAMI study
group concluded that in patients with initial successful thrombolysis, immediate
angioplasty offers no clear advantage over delayed elective angioplasty. This
multicenter randomized trial was performed to compare the efficacy of immediate
coronary angioplasty after AM, with that of elective angioplasty (7-10 days) in patients
initially treated with intravenous tPA. The incidence of reocclusion was similar in the
two randomized groups: 11% in the immediate PTCA group, and 13% in the elective
PTCA group. This comparative study resulted in similar improvements in the two
defined end points of the study: global left ventricular function and regional wall
motion in the infarct zone. In view of the data, a conservative approach after
thrombolysis seem indicated. The Task Force has classified the recommendations for
angioplasty after intravenous thrombolysis (60) (See Appendix F).

The National Heart, Lung, and Blood Institute (NHLBI) defines a successful
angioplasty as one in which a greater than or equal to 20% change in luminal diameter
is achieved, with the final-diameter stenosis < 50% and without the occurrence of
death, acute myocardial infarction, or the need for emergency bypass operation during
hospitalization. There are patient-related factors that influence the success rate of a

PTCA procedure. Some factors that are associated with increased failure rate are

45

female gender, age > 65 years, unstable angina, congestive heart failure, chronic renal
failure, left main coronary disease, and three-vessel disease (67).
Limitations

Restenosis

Despite the initial success of PTCA, restenosis is of concern, occurring in an
average of 20% to 30% of cases within the first 6 months of the procedure
(61 ,62,63,64). Possible contributions to the occurrence of restenosis are platelet
adhesion and thrombus formation at the dilation site. These events can occur within
one hour after arterial injury (65). If the initial PTCA is unsuccessful, successful
revascularization during a second angioplasty, occurs approximately 97 % of the time
(66). The National Heart, Lung, and Blood Institute Registry identified several factors
associated with increased incidence of restenosis: male gender, Canadian Heart
Classification 11] or IV angina (see Appendix D for definitions), and dilation of bypass
graft (67). Additional factors associated with risk of restenosis include: proximal left
anterior descending coronary artery stenosis, diabetes, smoking after PTCA, and
multiple lesions in a single-vessel (68,69,63,70). Factors that have not been correlated
with an increased incidence of restenosis include age, functional class, history of
previous myocardial infarction, hypertension, serum cholesterol, presence of
calcification at the site of dilation, morphological features of the lesion, inflation

pressure, and medications taken at the time of discharge (60).

46

Abrupt reclosure

Another limitation of coronary angioplasty is the possibility of incomplete
restoration of blood flow upon deflation. At present, 2 % to 5 % of patients undergoing
PTCA will require emergency surgery due to damage done to the coronary arteries
(60). As a result, the immediate assistance of a cardiac surgical team is always
required. Studies associate a 6% operative mortality and a greater than 50%
perioperative myocardial infarction rate following emergency bypass used to treat
abrupt reclosure (71,72). With the technological advances and improvements with the
balloon catheter, repeat balloon dilation is advantageous in treating abrupt reclosure.

At a hospital in Boston, 1,160 patients who underwent PTCA between
December 1981 and December 1986 were enrolled in a study to assess factors that
relate to the occurrence and management of abrupt reclosure (73). Abrupt reclosure,
experienced by 54 patients (4.7 %), developed during the dilation procedure in 43
patients (80%) and 9 to 13 hours following the PTCA in 11 patients (20%). Of the 43
patients that experienced abrupt reclosure during the procedure, 22 (51%) had
successful redilation.

Despite the successful redilation, the patients’ long-term conditions were not
favorable. The health status of the 96% of patients that were discharged alive was
obtained between 6 and 60 months. Patients with successful redilated arteries and
patients whose reclosure was treated medically were 3 times more likely to have

ongoing or recurrent angina than patients who underwent emergency bypass surgery.

47

However, with the exception of 1 patient who died suddenly, there were no late
myocardial infarctions in the redilated group.
National Heart, Lung, and Blood Institute Registry

The National Heart, Lung, and Blood Institute (NHLBI) identified PTCA to be
a worthwhile procedure (60). As a result, they sponsored workshops on the procedure,
along with establishing an early registry to study the safety and efficacy of the
technique. The initial PTCA Registry enrolled patients from September 1977 until
September 1982. The registry provided a way to monitor the procedure during the
beginning years of utilization. The registry defined strict inclusion criteria:

(1) single-vessel disease; (2) concentric, proximal, noncalcified coronary lesions;
(3) recent onset of angina; (4) good left ventricular function; (5) failed medical
management; and (6) candidacy for coronary artery bypass graft surgery (CABG).
Despite the strict inclusion criteria, more than 3000 patients were entered into the
voluntary registry (74).

The results from the PTCA Registry were first tabulated in the beginning year
of setup. The initial success rate was only 68%; failure defined by the inability to
cross and/ or dilate the lesion. Nearly 30% of the successful cases experienced
restenosis of the PTCA site within 6 months of the procedure. In addition, 6.1% had
an emergency CABG, 4.9% had a nonfatal myocardial infarction, and 1.3 % patients
with single-vessel disease died (68).

As a result of improved technique and technology (steerable catheter and revised

balloon designs), PTCA has continued to be successful. Meier and Gruentzig (75)

48

reported that from 1978 to 1982, the success rate increased from 63 percent to 91
percent. In 1985, the NHLBI Registry continued monitoring PTCA among fourteen of
the original NHLBI Registry centers after closure of the Early NHLBI Registry in
1982. From the Early Registry to the Late Registry, patient indications for PTCA
extended to include patients with unstable angina and multivessel disease. As a result,
the late registry had a higher prevalence of older aged patients than that of the early
registry. The increase in the number of complex angioplasty in the late registry is
reflective of an increasing number of patients with multiple lesions, total occlusions,
bifurcation lesions, and prior bypass surgery. This cohort of complex angioplasty
patients accounts for nearly 60% of the current PTCA population (67). Reports indicate
that success rate increased from the Early to the Late Registry (68% to 91%) as the
rate of complications declined. The occurrence of nonfatal myocardial infarction in the
late registry was 4.3 % , the need for an emergency coronary artery bypass graft surgery
was 3.4%, and mortality was 1.0% (69).
Guidelines

In 1980, a task force was formed to provide recommendations on appropriate
technology to use for diagnosis and treatment of patients suffering from cardiovascular
disease. This task force is referred to as the American College of
Cardiology/ American Heart Association Task Force on Assessment of Diagnostic and
Therapeutic Cardiovascular Procedures. One technique of particular interest is that of

coronary angioplasty. Guidelines were determined for percutaneous translurrrinal

49

coronary angioplasty (PTCA) in 1988 (3). Currently, the committee classifies
indications for the application of angioplasty into three classes:
Recommendations for Primary Angioplasty of Infarct-Related Artery Only

Class I:

1. Patients presenting within 6 hours of onset of pain and who meet the criteria for
thrombolysis but in whom thrombolytic therapy is clearly contraindicated and only if
facilities and personnel are immediately available. This recommendation is operative
only when data indicate a large amount of myocardium is at risk.

Class 11a:

1. Intermittent continuous pain indicating the possibility of “stuttering” infarction,
especially if there are ECG changes, but without clear indication for thrombolytic
therapy.

2. Within 18 hours of acute infarction in patients developing cardiogenic shock or
pump failure.

3. Patients who have had previous coronary artery bypass graft surgery in whom
recent occlusion of a vein graft is suspected.

Class 11b:

1. Patients who known coronary anatomy in whom thrombolytic therapy is not
contraindicated, but who develop symptoms and ECG evidence of acute infarction in
hospital at a time when rapid access to a catheterization laboratory with personnel
experienced in performing expeditious angioplasty for acute myocardial infarction is
available (completion within 1 hour).

» 2. Patients in whom thrombolytic therapy is not contraindicated who present within 4
hours of onset of symptoms of acute infarction at a facility where rapid access to a
catheterization laboratory with personnel experienced in performing expeditious
angioplasty for acute myocardial infarction is available (completion within 1 hour).

Class III:
This category applies to patients with acute myocardial infarction who do not fulfill the
Class I or 11 criteria:

1. Patients with severe left main coronary artery disease with instrumentation of a

more distal occluded artery may be hazardous.

2. Patients in whom only a small area of myocardium is involved, as evidenced by
clinical data or previously known coronary anatomy.

3. Dilation of vessels other than the infarct-related artery within the early hours of
infarction. (This may not apply to the patient in shock or pump failure.)

50

The committee also provides indications for angioplasty according to single-
vessel coronary artery disease, symptomatic patients with angina pectoris with medical
therapy and single-vessel disease, multivessel coronary artery disease, symptomatic
patients with angina pectoris with medical therapy and multivessel disease, direct
immediate coronary angioplasty for evolving acute myocardial infarction, and after
acute myocardial infarction (see ACC/ AHA Task Force Report on coronary
angiOPIasty) (60).

Distribution by demographics

As earlier indicated, the use of PTCA has increased steadily over time. The
United States use of PTCA has increased over ten-fold in the past decade, resulting in
over 300,000 PTCA procedures performed in 1990. Despite the procedure’s
popularity, studies suggest that this increase may not be equal among certain
subpopulation groups. For example, US rates for cardiac procedures were lower in
women than in men. In 1990, for example, rates per 100,000 were 165.7 for men and
66.2 for women ( 147). Additionally, similar disproportionately low rates were
previously reported for blacks as compared with white. In 1990, rates per 100,000
were 99.9 for whites and 17.6 for blacks (147).

The National Heart, Lung and Blood Institute (NHLBI) developed a registry to
examine gender-related differences in PTCA. The first registry (1977- 1982) showed
that PTCA risk was higher and efficacy was lower in women. A second registry was
developed from 1985 to 1986 to determine if women still had a worse effect after a

PTCA than men. The registry collected 2, 136 patients (546 women). They concluded

51

that women undergoing PTCA have a higher procedural mortality rate (2.6% vs. 0.3%;
p< .001), in addition to having higher initial complications (29% vs. 20%; p< .001) as
compared to men (148). However, this is explained in part due to women having a
worse cardiovascular risk profile, such as more severe angina than men. Otherwise,
the success rate (79 %) and long-term prognosis after PTCA were similar between men
and women. In summary, the female gender was an independent predictor of reduced
success with angioplasty (148). In contrast, data from the Medical College of Virginia
comparing results from before and after 1985 found no significant gender differences
after 1985 (152).

It has been suggested that women have also been at higher risk of complications
related to their older age and greater degree of concurrent illness, although few studies
actually have adjusted for these discrepancies. As a result of this, data suggests that
PTCA carry higher procedure morbidity in women with coronary disease.
Nevertheless, long-term outcome suggests that PTCA is a beneficial intervention for
women. However, with the increased complications at the time of PTCA performed
among women, the procedure needs to be performed with great caution.

Interracial access to selected cardiac procedures for patients hospitalized with
coronary artery disease have been evaluated, such as data from national registries.
From the NHLBI Percutaneous Transluminal Coronary Angioplasty Registry, the
clinical characteristics, in-hospital event rates, and 5-year follow-up results were
examined with respect to race for 1985-1986 (153). A total of 2,015 patients (90.8%

white, 3.6% black) were enrolled into the registry. Among the black patients, more

52

were women (50% vs 24%; p < .001) and the black patients were more likely to have
multivessel disease (72% vs 48%; p< .001), hypertension (73% vs 45%; p< .001), and
diabetes (23% vs 13%; p< .05). Additionally, clinical success rates were similar

(76.3 % for blacks and 79.3 % for whites). However, because blacks had more vessels
with disease, complete revascularization was achieved in only 26% of the black patients
as compared to 44% among the white patients. After PTCA, there was no significant
difference in major complications (death, myocardial infarction, or emergency bypass
surgery) between the races. Finally, five-year follow-up indicated that the races did
not differ in their outcome. The was no significant difference in mortality, myocardial
infarction, coronary bypass surgery, or repeat PTCA.

PTCA has proven to be a feasible cardiovascular procedure among the elderly,
with angiographic success rates at least 78% (144,149,150). Although, major
complications were more frequent in the elderly patients undergoing PTCA. Hartzler
et al.. (151) reported a 5 to 7 fold increase in mortality in older patients,'Kem et al..
(144) reported a 19% mortality in elderly patients and Holt et a1. . (149) noted a 20%
incidence of emergency or elective coronary artery bypass grafting in his series.

In summary, in assessing the benefits of PTCA among certain population
subgroups, it is important to evaluate the short-term and the long-term outcomes. As

indicated, the long-term outcome among the demographics are similar.

53

Chapter 7

Coronary Angioplasty Vs. Bypass Surgery

Patients suffering from severe angina now have two options for surgical
treatment; coronary angioplasty (PTCA) and coronary bypass (CABG). As discussed
in former chapters, guidelines will include recommendations to guide clinicians in
using the most appropriate procedure for their patient. However, controversy still
exists whether one procedure is more beneficial under certain circumstances, as
opposed to another.

A meta-analysis conducted by Pocock, et a1. (87) compared coronary
angioplasty with bypass surgery by combining eight sizeable randomized trials. The
trials include: Coronary Angioplasty versus Bypass Revascularization Investigation
(88) (CABRI), Randomized Intervention Treatment of Angina trial (89) (RITA),
Emory Angioplasty versus Surgery Trial (90) (EAST), German Angioplasty Bypass
Surgery Investigation (91) (GABI), The Toulouse trial (92) (Toulouse), Medicine
Angioplasty or Surgery study (93) (MASS), The Lausanne trial (94) (Lausanne), and
Argentine Trial of PTCA versus CABG (95) (ERACI). Pocock and his colleagues
combined the data comparing initial revascularization, of PTCA and CABG, in patients
suffering from coronary artery disease. There were a total of 3,371 patients enrolled in
the studies that were eligible for either treatment strategy, PTCA or CABG. The mean
follow-up was 2.7 years. The trials differed in design, inclusion criteria, and exclusion

criteria, (which may be reason for possible heterogeneity between the trials). Reported

54

results include mortality, cardiac death and myocardial infarction, additional non-
randorrrized procedures, angina, and single versus multi-vessel disease.

The mortality results between the PTCA and CABG recipients gave no
indication of a treatment difference (RR for PTCA:CABG 1.08 [C10.79-1.50]). Given
the various follow-up lengths between trials, Pocock and colleagues calculated a
mortality risk (per 100 patient-years of follow-up) beyond the first year of 1.22 for
CABG and 1.04 for PTCA. Specifically looking at endpoints, cardiac death and non-
fatal myocardial infarction, there was again no indication of a treatment difference for
the first year in each study. Though reported during the initial hospital admission, the
PTCA group had fewer infarcts. The total number of infarcts in the first year of
follow-up in both groups was similar (135 in the PTCA group and 127 in the CABG
group). Both CABG and PTCA groups reported having a much lower risk of cardiac
death and myocardial infarction in the first follow-up year as compared to during
subsequent follow-up years.

The need for additional interventions, once received the randomized procedure,
was much greater in the assigned PTCA group, both at one year follow-up and
subsequent years, compared to the group initially randorrrized to CABG. From the
combined trials, 17.8% [95% CI 16.0-19.6%] of the PTCA group required CABG
within a year following the initial PTCA and 33.7% [95% CI 31.3-35.7%] required at
least one additional PTCA and/or CABG. In contrast, only 3.3% of those randomized

to CABG required additional interventions during the first year. Again from the

55

combination of all trials, the reintervention rates were 1.8 (CABG) and 4.5 (PTCA) per
100 patient-years of follow-up.

In conclusion, those randomized to the PTCA groups were more at risk for
reinterventions as compared to those randomized for CABG. However, the less severe
reintervention risk rate between the two groups in subsequent years suggests that longer
follow-up years could explain more. The longest follow-up time among the eight trials
was 4.7 years. Thus, it is important to conduct a trial with a lengthy follow-up time to
confirm or refute the findings that suggest the possibility that CABG patients could
have a similar reintervention risk rate, as that of the PTCA patients several years after
the initial procedure.

The studies differ in their prevalence rates of angina. At one-year follow-up,
all trials had a higher prevalence rate among the randomized PTCA group as compared

to the randomized CABG group (RR 1.56 [CI 1.30-1.88]). Statistics indicate that there

is evidence of heterogeneity (X2 = 14.5; p=0.054 at one year). The author assumes
this because one of the trials, GABI, had similar angina rates for PTCA and CABG
patients, along with recruiting patients with more severe baseline angina (Class 2 or
greater) as compared to the other studies. (See Appendix D for angina classifications).
Comparing the six trials that had 3-year data, their angina prevalence rates for the
randornized‘PTCA group went from 1.93 [CI 1.50-2.48] at 1 year to 1.23 [€10.99-
1.54] at 3 years as compared to those patients randomized to the control group.

In assessing the different outcomes for those suffering from single versus multi-

vessel disease, the eight trials were combined. Of the eight trials, five strictly enrolled

56

multi-vessel disease patients, two trials strictly enrolled single-vessel disease patients,
and one study included both. The mortality rate for both the PTCA and CABG groups
at the first-year was lower in single-vessel disease (p < 0.01). Additionally, the
endpoints, cardiac death and myocardial infarction, single-vessel disease patients had a
lower risk if they were in the randomized CABG groups. Among the multi-vessel
disease patients, there was no treatment difference for risk of cardiac death and
myocardial infarction. The need for additional intervention (CABG and/or PTCA)
once the patient received the initial randomized procedure, was slightly higher among
the multi-vessel disease, however not significant (34.5% vs. 30.5%; p=0.2). In
addition, the single-vessel disease also had a slightly lower need for an additional
CABG once received a PTCA (16.0% vs. 18.3% within one year). The last outcome
assessed was prevalence rates of angina. Both at one and three years, the single-vessel
disease had a lower rate of angina for both CABG and PTCA procedure groups
(p<0.01 for one year and p=0.2 at three years).

Many conclusions can be drawn concerning the two surgical procedures, as
indicated from the results of the meta-analysis. There was a low risk of death and
myocardial infarction over three years, and neither method (CABG nor PTCA) proved
more beneficial. The authors explain the low mortality rates were a reflection of the
exclusion of the more severe cases because of their ineligibility for PTCA. The
prevalence of angina was higher in the PTCA patients than in the CABG patients. The
long-term comparisons (beyond 3 years) of the two procedures were unable to be made

with this analysis and are left unknown. What is known is that among CABG patients,

57

over a 5-10 year period, saphenous vein graft occlusion may lead to a requirement for
additional revascularization procedures (96,97). To avoid the higher risk of mortality
and morbidity that accompanies a second bypass operation, PTCA is the initial
revascularization procedure recommended. The analysis concludes that mortality,
cardiac event, and angina prevalence rates were slightly lower for single-vessel disease
patients as compared to multi-vessel disease patients. However, there is little evidence
to justify a difference in treatment between the single and multi-vessel disease. This
analysis only includes two trials that specifically enrolled single-vessel disease patients,
so the authors wam not to put much merit on the fact that the single-vessel patients in
the CABG group had a lower risk of cardiac death or nonfatal myocardial infarction

than that of the PTCA group.

58

Chapter 8

Methods

Data Base

I performed a retrospective analysis for all patients discharged from a
community hospital in Michigan with a diagnosis of acute myocardial infarction (AMI)
during the years 1990 through 1994. I used abstracted discharge data supplied by the
Medical Records and Coding staff at McLaren Hospital in Flint. The collection of
patient-specific data, routinely performed by the Medical Records and Coding staff, is
completed for all patients admitted to the community hospital. Fully trained staff
members review the accuracy of the medical file of each patient as dictated by the
attending physician. The data base, from which I conducted my analysis, included all
diagnoses, major procedures, age, gender, race, insurer, marital status, date of birth,
admission date, discharge date, discharge status, and the hospital identification chart
number.
Patient Population

Using the coded discharge data, I identified a total of 2,685 abstracted charts
and included them in the data set. Given readnrissions, I performed analysis on the
population universe of 2,659 patients; the first discharge of each patient was takes as
the index admission. To assure confidentiality, I used coded identifiers for each
patient. The original charts were not available; thus, the ability to match chart number
with the patient was not possible. Using the clinically modified ninth revision of the

International Classification of Diseases (ICD-9-CM) (98), I strictly included patients

59

with the principal diagnosis of acute myocardial infarction (ICD—9—CM codes 410
through 410.9). (See Appendix A & B).

Each patient in my data set was discharged from the teaching hospital with the
primary diagnosis of AMI. In addition, the initial data set also included 1,072 other
diagnoses. These diagnoses were abstracted from the patients’ charts, as made by the
physician. The following is a complete list of the possible ways that an AMI was
coded: AMI, anterolateral, initial; AMI, inferolateral, initial; AMI, inferoposterior,
initial; AMI, other anterior, initial; AMI, other anterior, subsequent; AMI, other
inferior, initial; AMI, other inferior, subsequent; AMI, other lateral, initial; AMI,
other lateral, subsequent; AMI, other site, initial; AMI, unspecified site, initial; AMI,
unspecified site, subsequent; AMI, subendoinfarction, initial; AMI, subendoinfarction,
subsequent; and AMI, true posterior wall, initial. (See Appendix A).

My data base did not include information on the patients’ past hospitalizations
for myocardial infarctions (fifth-digit classification), nor were the locations of the
infarction consistently coded. As a result, I condensed the location and the fifth-digit
classifications. After consulting with a cardiologist, I felt it was more beneficial to
merge the individually coded AMI diagnoses into one to enhance the power, in addition
to simplifying the analysis. I did not want to chance the possibility of not reaching
statistical significance due to a small sample size as a result of individually grouping

patient’s infarct location.

Definition of Variables

The variables I considered as possible predictors of treatment included
admission year, age, gender, race, insurance, and comorbidity. I classified race as
either white or black and I eliminated the groups Asian, Pacific Islander, and Other. I
excluded these groups based on their limited sample size; they only account for 0.4 %
of the total patient population. I merged age into five groups; 1 through 44 years, 45
through 54 years, 55 through 64 years, 65 through 74 years and 75 through 101 years.
I originally classified insurance as private, medicare, medicaid, commercial (including
Blue Cross, Blue Net and PPOM), HMO (Health Plus), and all other (worker
compensation). However, because insurance is predetermined by age (medicare
eligibility is 65 years of age), I merged insurance groups based on age. I combined the
seven insurance categories and recoded accordingly for the 65 years and older
population: all insurance and medicare. I again combined the seven insurance
categories and recoded accordingly for the younger than 65 years old population: all
other insurance, HMO, medicare/ medicaid, and commercial.

I assessed for comorbidity by creating an index variable that totals certain
diagnoses that were weighted according to the seriousness of the condition. I used the
diagnoses that were abstracted from the patients’ charts and condensed certain
diagnoses into weighted assigned groups. These certain diagnoses were chosen as
suggested in the Charlson, et al. article (100) on prognostic comorbidity in longitudinal
studies. They assigned a value (weighted index) for each condition that a patient was

diagnosed with during their hospital stay. The following are those weights and

61

conditions: 1 for myocardial infarct, congestive heart failure, peripheral vascular
disease, cerebrovascular disease, dementia, chronic pulmonary disease, connective
tissue disease, ulcer disease, mild liver disease, and diabetes; 2 for hemiplegia,
moderate or severe renal disease, diabetes with end organ damage, any tumor,
leukemia, and lymphoma; 3 for moderate or severe liver disease; and 6 for metastatic
solid tumor and AIDS. I was able to locate the conditions as coded in my data set for
the above conditions, except for diabetes with endstage organ damage and AIDS.
Diabetes with endstage organ damage was not separately coded in my data set,
however, I am confident that it was accounted for within the diabetes category; and
none of the patients in my study population had, AIDS.

After coding each of the conditions with their assigned weighted index, I
created a variable (index) that totaled the weighted index for each patient. I then
condensed the individual index values into three to have comparable cells. The three
index values were coded accordingly: 0 for having a total weighted index of zero, 1 for
having a total weighted index of one, and 2 for having a total weighted index of two or
more. Meaning that patients were assigned a 0 for having no additional illnesses
besides an AMI, a 1 for having an additional illness besides an AMI, and a 2 for
having multiple and/or more severe illnesses in addition to an AMI.

Procedure Use
The original data base included 1,063 procedures (See Appendix B). The

treatments of interest included cardiac catheterization (CATH), coronary arterial bypass

62

surgery (CABG), percutaneous transluminal coronary angioplasty (PTCA), and tissue
plasminogen activator (tPA). Thus, I examined the use of cardiac catheterization
(ICD-9-CM codes 37.21, 37.22, and 37.23), CABG (ICD-9-CM codes
36.11 through 36.16), PTCA (ICD-9-CM codes 36.01, 36.02, and 36.05), and
thrombolytic therapy (ICD-9-CM code 99.29), while disregarding all other procedures
that were performed on the patient during their hospital stay. (See Appendix C).
Statistical Analysis

In the primary analysis, I examined the utilization of the four cardiac procedures
over the five-year study period (1990 through 1994), the distribution of the study
population across age, gender, race, insurance, comorbidity, and admission year, in
addition to the distribution of the four procedures across the study population. I
performed identical age-stratified analyses for each of the four procedures; CATH,
CABG, PTCA, and thrombolytic therapy. I constructed separate logistic regression
models to determine the effect of race, gender, age, insurance, comorbidity, and
admission year on the use of cardiac catheterization, percutaneous coronary
angioplasty, coronary arterial bypass grafting, and thrombolytic therapy (101). Each of
these regression models adjusted for the possibility of confounding by the variables
previously listed. I also analyzed two-way interactions between variables. I reported
odds ratios as the results of the models.

I chose to use the backward hierarchical elimination method when I

performed my logistic regressions. I began with four saturated models with CATH,

CABG, PTCA, and thrombolytic therapy as the dependent variables and admission

63

year, age, gender, race, insurance, and comorbidity as the independent variables.
Given insurance is predetermined by age, I chose to evaluate the role of insurance
within two age-strata, (younger than 65 years and 65 years and older). This way, I was
able to look at the relationship between insurance and the procedures without possible
confounding due to age. For each procedure, I repeated the backward hierarchical
elimination method within each age-stratum. For each age-stratified analysis ( less than
65 years of age and 65 years and older), I determined what variables to keep in a model
based on a 0.05 p—value. To assess effect modification, I created two-way interactions
between each of these variables with the remaining independent variables that were not
statistically significant. I ran each of these two-way interactions in a model with
admission year, the main effect variables, and the interactions. In calculating the
difference in the chi-square between the interaction term and a model without the
interaction term, I was able to report on effect modification (based on a 0.05 p—value).
To determine confounding in my models, I assessed a 20% difference between the
unadjusted odds ratio and the adjusted odds ratio for admission year. After assessing
potential confounding, I determined whether the univariates were important predictors
based on the statistical significance when they were adjusted for with admission year in
the models. I chose to include those good predictors that added precision to the final
model. Personal judgments were made on individual cases of the inclusion of
variables, despite statistical significance. The final models are presented for each age-

stratum of the four procedures as odds ratios.

Chapter 9

Results

Patient Population

I identified 2,659 admissions with a primary diagnosis of acute
myocardial infarction (AMI) at a community hospital during the study period. Table 1
displays the characteristics of the study population. The overall distribution of
admissions during the study period remains relatively constant, increasing slightly over
the five-years. Accounting for the greatest percentage of admissions is the age group
65 years and older; they accounted for more than half of the discharged each year
(Figure 5). Male account for the majority of AMI admissions, between 58% and 67%
of the total admission population (Figure 6). Figures 7 and 8 show the age-stratified
distribution of adrrrissions across select insurance groups. Figure 7 shows that the
majority of my study population aged 65 years and older are receiving medicare.
While Figure 8 shows just the opposite. The study population aged less than 65 years
are largely distributed over private, commercial, and HMO insurance groups, not
medicare. Figure 9 shows that across the entire study population, medicare makes up
the greatest proportion of AMI admissions; between 5 3 % and 60% of the total study
population. However, this is because Figure 9 shows the distribution across all ages
and as seen in Figures 7 and'8, insurance is highly correlated with age. The white race
makes up the majority of the AMI admissions, between 93% and 96% (Figure 10).
And accounting for the greatest percentage of admissions across the comorbidity

indices, is the comorbidity index 0. Between 62 % and 69 % of the patients did not

65

receive another diagnosis that was weighted in the comorbidity index scale, besides
their primary diagnosis of AMI (Figure 11).

Table 2 shows the age distribution of these patients by gender, race, insurance,
and comorbidity. The 75-101 year cohort is the age group that accounts for the
greatest percentage of admissions for the females; with the 65-74 year cohort
accounting for almost as many female admissions. Whereas, the 65-74 year cohort
accounts for the greatest percentage of admissions for males; with the 55-64 year
cohort accounting for almost as many male adnrissions. The age distribution by the
black race fluctuates unevenly throughout the study period for each age group. For
example, the 55-64 age group accounts for 0% in 1990, 8.7% in 1991, 30.4% in 1992,
39.1% in 1993, and 21.7% in 1994. However, this is understandable given that the
black race only accounts between 4% and 6% of the total study population. The
youngest age group (1-44 years) accounts between 5 % and 7% of the total admissions
for the white population during the study period. And, as compared to the youngest
cohort of the white population, the percentage of the total admissions quadruples for
the oldest age cohort (75-101) of the white population. This reflects data indicating the
increasing prevalence of AMI with increasing age. The majority of patients covered by
commercial, private, and all other insurances are aged < 65 years. The majority of
patients covered by medicare and medicaid are > 64 years of age. Those covered by
HMO’s are unevenly distributed between the two age cohorts (1-64 and 65-101)

throughout the study period. Each of the weighted comorbidity indices are largely

66

distributed among the older cohorts and it increases with age because comorbidity and
age are related.

Table 3 shows the gender distribution of these patients by age, race, insurance,
and comorbidity. Accounting for the majority of admissions in all the age groups, with
the exception of the 75-101 year cohort, is the male gender. Additionally, the male
gender also accounts for the majority of admissions among both the white and the black
race. Those covered by HMO’s, medicare, and medicaid are almost equally distributed
between the males and females, slightly favoring the male gender. Whereas, the males
account for the larger proportion covered by private, commercial, and all other
insurances. Additionally, the males account for the larger proportion in each of the
weighted comorbidity indices, although it is more variable in comorbidity 2.

Table 4 shows the insurance distribution of these patients by age, race, gender,
and comorbidity. Accounting for the greatest percentage of all admissions aged 1-64
years, is commercial insurance. Accounting for the greatest proportion of patients
older than 64 years, black (except for the 1990 & 1993 admission years), white,
female, male, and that have a comorbidity index 1 and 2 are medicare and medicaid.
Whereas, accounting for the majority of admissions with a comorbidity index of 0 is
almost equally distributed between medicare & medicaid and commercial insurance.

Table 5 shows the race distribution of these patients by age, gender, insurance,
and comorbidity. Accounting for the greatest proportion of patients in all age, gender,
insurance, and comorbidity groups throughout the study period is the white race. This

is reflective of the fact that my study population is almost 95 % white.

67

Table 6 shows the comorbidity distribution of these patients across age, gender,
race, and insurance. The distribution of comorbidity across age is the following:
accounting for the greatest percentage of adrrrissions with a comorbidity index of 0 is
the 1-44 year cohort and the 45-54 year cohort and accounting for the greatest
proportion in the remaining age groups (55-64, 65-74, & 75-101) is the comorbidity
index 1. The distribution of comorbidity across select demographics shows that the
comorbidity index 0 accounts for the greatest proportion among males, females, blacks,
whites, and all insurances except for HMO’s. Also to note, is that the greatest
percentage of admissions with a comorbidity index 2 are the older (75-101), black,
female, and who have medicare & medicaid coverage.

Procedure Use

Thrombolytic therapy was performed during the days of the index admission in
509 patients. Figure 12 displays the distribution of the patient population that received
thrombolytic therapy over the study period. The rate jumped from 8.8% in 1990 to
20.7% in 1991, where it remained constant during the remainder of the study period
(odds ratios of undergoing thrombolytic therapy for a patient during 1990, 1991, 1992 ,
and 1993 as compared with 1994, respectively, .3632 (p<0.01), .9799 (p<0.01),
1.1037 (p=.4941), and .9897 (p=.9439).

For cardiac catheterization, the corresponding number is 1,541 patients. Figure
13 displays the distribution of the patient population that received a cardiac
catheterization over the study period. The rate is 50.2% in 1990, 50.5% in 1991,

51.4% in 1992, 66.9% in 1993, and 68.8% in 1994 (odds ratios of undergoing cardiac

68

catheterization for a patient during 1990, 1991, 1992, and 1993 as compared with
1994, respectively, .4552 (p<0.01), .4622 (p <0.01), .4788 (p <0.01), and .9164
(p < 0.01).

Similarly, 534 patients received a CABG over the study period. Figure 14
displays the distribution of the patient population that received a CABG over the study
period. The rate is 12.8% in 1990, 20.8% in 1991, 19.0% in 1992, 23.3% in 1993,
and 23.7% in 1994 (odds ratios of undergoing CABG for a patient during 1990, 1991,
1992, and 1993 as compared with 1994, respectively, .4751 (p<0.01), .8429
(p< 0.2443), .7527 (p=0.0527), and .9769 (p=.8679).

For PTCA, the corresponding number is 692 patients. Figure 15 displays the
distribution of the patient population that received a PTCA over the study period. The
rate increased during the study period; 19.6% in 1990, 19.8% in 1991, 26.0% in 1992,
28.5% in 1993 and 34.5% in 1994 (odds ratios over the five years, respectively, .4623
(p< 0.01), .4678 (p<0.01), .6689 (p=0.0021, and .7586 (p=0.0322). Many
independent variables other than admission year, were associated with the use of the
four cardiovascular procedures. These variables include age, gender, race, insurance,
and comorbidity. Figures 16 through 35 display the distribution of the patient
population grouped by age, race, gender, insurance, and comorbidity, that received
each of the four procedures (cardiac catheterization, CABG, PTCA, and thrombolytic
therapy). Figures 16 through 20 show the distribution of thrombolytic therapy across
age, gender, race, insurance, and comorbidity. Additionally, Figures 16 through 20

show that the utilization rate of therapy jumped from the low in 1990 to a maintained

69

level for the remaining years across each group. The oldest cohort (75 - 101) was the
age group that received thrombolytic therapy the least throughout the study period.
Males received thrombolytic therapy more frequently than females in each of the years.

Figures 21 through 25 show the distribution of cardiac catheterization across
age, gender, race, insurance, and comorbidity. Overall, the use of cardiac
catheterization remained at a constant level for the first three years of the study, where
it increased for the remaining two years. It is clear that males and whites received
cardiac catheterization more often as compared to their counterparts.

Figures 26 through 30 show the distribution of CABG across age, gender, race,
insurance, and comorbidity. With the exception of the distribution across the black
race, the figures show a slight increase throughout the study period. Again, the males
and the whites (except for the 1990 and 1991 admission years for the race distribution),
received a CABG more frequently as compared to their counterparts.

Figures 31 through 35 show the distribution of PTCA across age, gender, race,
insurance, and comorbidity. Overall, the procedure was used more frequently as the
study years progressed. Again males and whites received a PTCA more frequently as
compared to females and blacks. Also, the admissions in the medicare insurance
group, received a PTCA less frequently as compared to all other insurance groups.
Statistical Analysis

I used a multiple logistic-regression model to examine the independent
contribution of admission year, race, age, gender, insurance, and comorbidity for the

use of each of the four cardiovascular procedures. Tables 7 through 14 present the

70

results of the logistic regression analyses that predict the performance of select
cardiovascular procedures across each of the two age-strata (less than 65 years and 65
years and older). The tables provide the unadjusted and the age-adj usted, gender-
adjusted, race-adjusted, comorbidity-adjusted and insurance-adj usted odds ratios for
each age-strata. While independently controlling for race, age, gender, insurance, and
comorbidity, admission year was a statistically significant predictor (p < 0.01) for the
use of each of the four procedures across both age-strata. The tables provide the
unadjusted and respective adjusted odds ratios across both age-strata. More importantly
these tables confirm that there is no confounding of the use of any of the four
procedures for either age-strata. Tables 15 through 18 provide the unadjusted odds
ratios on utilization for each of the four procedures and adjusted by statistically
significant predictors for other effects of admission year on utilization as the final
model. For example, the odds ratios for undergoing each of the four cardiovascular
procedures in 1990 through 1993 as compared to 1994 for both age-strata are reported.
For assessing potential effect modification, two-way interactions were created.
Tables 19 through 26 provide the change in chi-square, degrees of freedom, and p-
values from which 1 evaluated the interactions for inclusion into my final models. In
some cases, the interactions proved to be statistically significant effect modifiers;
however, the interactions did not remain statistically significant in the final models.
Therefore, I had to make a judgment as to what variables I included in the final model.
Table 15 includes the odds ratios of the final model for thrombolytic therapy

across each age-stratum. The final model for the use of thrombolytic therapy for the

71

65 year and older age-stratum includes the following variables: admission year,
comorbidity, and age. I chose not to include the interaction between admission year
and insurance and its main effects, because their prediction of thrombolytic therapy
utilization was not statistically significant. More importantly, the inclusion of the
variables did not change the time trends in the utilization of thrombolytic therapy. The
final model for the 65 year and younger cohort includes the following: admission year
and gender. I again chose not to include the statistically significant independent
interaction between gender and race for the same reason previously mentioned. I did
assess whether race was a statistically significant predictor as a main effect in the final
model, and it did not prove statistically significant. Thus, the final model for the age-
stratum includes just adrrrission year and gender as the statistically significant predictors
for the utilization of thrombolytic therapy.

Table 16 includes the odds ratios of the final model for the use of cardiac
catheterization across each age-stratum. For the less than 65 year old cohort, no
interactions were reported as statistically significant effect modifiers, thus the final
model includes the following variables: adnrission year, comorbidity, and race. And
for the 65 year and older cohort, the final model includes the following: admission
year, age, comorbidity, and the interaction between comorbidity and age. The
interaction between comorbidity and age is statistically significant and remained as such
when included in the final model.

Table 17 includes the odds ratios of the final model for the utilization of CABG

across each age-stratum. For the 65 year and older age-stratum, the final model

72

includes the following variables: admission year, age, and race. I chose not to include
the interaction term between race and gender because it was not a statistically
significant predictor once added to the final model. I did evaluate whether gender, as a
main effect, would be statistically significant; however, once entered into the final
model, it lost statistical significance. The final model for the less than 65 age-stratum,
includes the following variables: admission year, comorbidity, gender, and the
interaction between comorbidity and gender. I chose not to include the interaction term
between comorbidity and insurance in the final model, because it was just barely
statistically significant once added to the final model. And more importantly, the
inclusion of this interaction term did not alter the time trends of admission year on the
utilization of CABG. I did assess the possibility of an interaction between gender and
insurance, and the interaction was not a statistically significant effect modifier on the
utilization of CABG.

Finally, Table 18 includes odds ratios of the final model for the utilization of
PTCA across each age-stratum. The final model for the 65 and older age-stratum
includes the following: admission year, age, and comorbidity. No interaction terms
were statistically significant among this age group. The final model for the less than 65
year age-stratum includes the following: admission year, age, and comorbidity. The
interaction term between admission year and age was just barely statistically significant,
thus I chose not to include this interaction term in the final model. More importantly,
the inclusion of the interaction term did not alter the time trends of admission year on

the utilization of PTCA.

73

The results of this age-stratified analysis confirmed that insurance and age are
not confounders of each other. Thus, I additionally assessed the best predictors for the
utilization of each of the four procedures across all ages, with the exception of
insurance. Because insurance is predetermined by age, I chose to exclude this variable
when determining the best predictors across all ages. I used a multiple-logistic
regression model to examine the independent contribution of admission year, race, age,
gender, and comorbidity for the use of each of the four cardiovascular procedures
across all ages. Tables 27 through 30 present the results of the logistic regression
analyses that predict the performance of select cardiovascular procedures across all
ages. The tables provide the unadjusted odds ratios on the utilization of each procedure
across all ages and individually adjusted by age, gender, race, and comorbidity for
other effects of admission year on utilization. While independently controlling for
race, age, gender, and comorbidity, admission year was a statistically significant
predictor (p <0.01) of the use of each of the four procedures. Again, with the
exclusion of insurance, Tables 27 through 30 confirm that there is no confounding of
the use of any of the four procedures by age, gender, race, or comorbidity.

Tables 31 through 34 provide the unadjusted and fully-adjusted odds ratios and
95 % confidence intervals for each of the four procedures across all ages. With the
inclusion of all the variables, admission year remains a statistically significant predictor
for each of the four procedures. Additionally, the odds ratios for undergoing the four
Procedures based on select demographics are also displayed in Table 31 through 34.

For assessing potential effect modification, two-way interactions were created. Tables

74

35 through 38 provide the change in chi-square, degrees of freedom, and p—values. For
the utilization of thrombolytic therapy (Table 35), the interaction between admission
and comorbidity was statistically significant. For the utilization of cardiac
catheterization (Table 36), there were no statistically significant effect modifiers.
Whereas for the utilization of PTCA (Table 37), the interaction between adrrrission year
and age was statistically significant. And finally, for the utilization of CABG (Table

38), there again were no statistically significant effect modifiers.

75

Chapter 10

Discussion

I found that for time trends, there was no effect modification by any of the other
variables of age, race, gender, insurance, or comorbidity. These variables did not
modify the effect of admission year on the utilization of thrombolytic therapy, cardiac
catheterization, coronary artery bypass grafting, or percutaneous transluminal coronary
angioplasty. Additionally, none of these variables acted as confounders for any of the
four cardiovascular procedures.

However, for the different procedures, some of the above mentioned variables
were independent predictors of utilization either as main effects only, or as interactions
between themselves. Thus, the final models vary for the different procedures, for
example, sometimes it was only gender that effected the significance and sometimes it
was age. Nevertheless, the inclusion of these significant independent predictors and
their interactions did not change my conclusion about the time trends with the
utilization of a given procedure because they were neither effect modifiers, nor
confounders for admission year.

My conclusions were based on the final models for each of the procedures for
both age-strata. For a patient less than 65 years of age, they were less likely to receive
thrombolytic therapy if admitted in 1990 or were female. This is reflective of the
actual number of patients that received thrombolytic therapy during the study period.

The use of this particular procedure increased in 1991, where it remained at a constant

76

level for the remainder of the study period. And the distribution of thrombolytic
therapy was greater for the males throughout the study period; more so during the four
remaining years of the study. For a patient 65 years and older, they were less likely to
receive thrombolytic therapy if admitted in 1990. Again, this is reflective of the actual
distribution of thrombolysis during the study period. As Figures 16-20 show,
thrombolytic therapy was not widely distributed across all of the variables of interest
during 1990. Additionally, patients were almost 2 times more likely to receive
thrombolytic therapy if aged 65 -74 years, as compared to 75 years and older, and were
least likely to receive therapy if they had additional diagnoses and/ or more severe
conditions beside an AMI. Again, both of these results are reflective of the distribution
of thrombolytic therapy during the study period.

My results for administration of thrombolytic therapy confirm current literature
for the distribution of thrombolysis across age. As literature suggests, most of the
major studies, with the exception of ISIS-2 and GISSI excluded patients greater than 70
or 75 years of age. Nevertheless, these two studies did reveal a greater mortality
reduction among the younger cohorts; however, a mortality reduction was still
observed among the treatment group in the eldest cohort. Additionally, the
recommendations for administration of thrombolytic therapy to patients with
myocardial infarction suggest that patients greater than 75 years of age (with Specific
medical conditions), could have harmful results if given this therapy. In summary, as

literature suggests, elderly patients are more at risk if given thrombolysis.

77

Whereas my results concerning distribution of thrombolytic therapy across
gender, do not agree with most of the larger studies comparing gender differences in
outcome. My findings show that gender is a statistically significant predictor for the
utilization of thrombolytic therapy among the youngest age-stratum (less than 65 years
of age). As a result, a woman less than 65 years of age was less likely to receive
thrombolytic therapy than a man of the same age-stratum. In general, studies reveal no
significant difference in the pharmacokinetics of tPA or coronary artery patency rates in
men vs. women (105). In addition, no difference is seen with the reduction in
mortality rates in both sexes. Nevertheless, there are subgroup analyses that do
conclude gender differences in mortality rates. However, gender was only a
statistically significant predictor in the younger age-stratum in my findings. And
differences in mortality among the genders is hypothesized to be due to the older age of
women presenting with myocardial infarction. This is what is suggested to be
contributors to their relatively lesser reduction in mortality after thrombolysis (106).

For a patient less than 65 years of age, they were less likely to receive a cardiac
catheterization if adrrritted in 1990, were white, or had additional diagnoses and/or
more severe conditions beside an AMI. This again is reflective of the distribution of
the procedure during the study period. And for a patient 65 years and older, they were
less likely to receive a cardiac catheterization if admitted in 1990, or had only 1
additional diagnosis beside an AMI. A patient aged 65 -74 years was 4 times more
likely to receive a catheterization as compared to a patient in the 75-101 year old

cohort. This indicates that the elderly were less likely to receive cardiac

78

catheterization. However, with the interaction between age and comorbidity, this was
no longer the case. A 65 -74 year old patient with additional diagnoses and/ or more
severe conditions was less likely to receive a catheterization as compared to a 75 - 101
year old patient having just an AMI diagnosis.

A patient aged 64 years and younger was less likely to receive a CABG if
admitted in 1990. The remaining four years of study period did not effect the
distribution of CABG among the study population. This again is reflective of the actual
distribution of the procedure during the study period. A patient in this age-stratum who
had only one additional condition was almost 2 times more likely to receive a CABG
than that of a patient in the same age bracket, who either had only an AMI diagnosis or
had more severe and/or multiple conditions. This strongly indicates that the
distribution of CABG was based on the patient’s medical condition. Gender alone was
not a significant predictor, but interacting with comorbidity, it became a statistically
significant predictor of CABG utilization. Such that, a 64-75 year old female patient
who had multiple and/ or more severe conditions, beside an AMI was more than 5 times
likely to receive a CABG. A patient 65 years or older again was less likely to receive a
CABG in 1990. This is reflective of the actual distribution of CABG over the study
period. Whereas, a patient aged 65-74 years was 2 times more likely to receive a
CABG, than that of the eldest cohort. Finally, a black patient 65 years and older was
less likely to receive a CABG. However, the actual distribution shows that black

patients admitted in 1990 and 1991 received more CABGs than the white patients.

79

A patient less than 65 years of age was less likely to receive a PTCA if admitted
in 1990, 1991, and 1992. This again is reflective of the actual distribution. Age was a
statistically significant predictor in the utilization of PTCA; however, there was no
difference in the chances of receiving a PTCA in any of the age cohorts. Additionally,
a patient less than 65 years of age was less likely to receive a PTCA if they had
multiple and/ or more severe conditions beside an AMI. A patient 65 years of age and
older was less likely to receive a PTCA, if admitted in 1990 or 1991, and had multiple
and/or more severe conditions besides their primary diagnosis of AMI. On the other
hand, the youngest cohort in this age-stratum was 2 times more likely to receive a
PTCA than the eldest cohort.

As the above information indicates, my analysis shows an obvious year effect
across all age-strata and procedures. The 1990 admission year in particular, is the year
when the patients in my study were least likely to receive a procedure. My analysis
shows that the cardiovascular procedures were widely disseminated as the years
progress. As literature suggests, increasing expertise and technological advances have
occurred with cardiovascular procedures over time. I hypothesize that these are
contributing factors for the increasing utilization of the procedures as the study
progressed.

Additionally, my analysis also shows an age effect across the 65 years and
older age-stratum for all four procedures. The eldest cohort was the least likely group
of patients in my study to receive a particular procedure. There is a paucity of data on

the effects of cardiovascular procedures among AMI patients that are 65 years or older.

80

For example, two of the larger trials of coronary artery bypass grafting only included
persons less than 65 years of age (103, 104). Thus, with the exclusion of this group of
patients, I can only recommend that additional studies be conducted that include the
elderly to effectively assess the risks and benefits of treatment in this population. The
elderly are the fastest growing segment of the population and about two-thirds of the
health care costs for heart disease in the US are for those 65 years and older. Thus, it
will continue to be an important issue to appropriately assess the most effective means
for treatment specifically among this cohort.

My data also strongly linked comorbidity with the decreasing chances of
receiving a procedure. The more severe a patient’s condition, in addition to the
presence of multiple conditions, were strong indications for not receiving a particular
procedure. As the literature review states, each cardiovascular procedure has
contraindications, and as a result recommendations have been made to assist in
evaluating the severity of a patient’s case for the distribution of cardiovascular
treatments.

In summary, for all the procedures analyzed, there is a definite trend towards
higher utilization favoring some subgroups. This is again dependent on the age cohort
and the cardiovascular procedure analyzed; however, given there are demographics that
are statistically significant predictors in my study, there is reason enough to encourage
further investigation among these groups. Such studies could provide information that
could be used to develop specific recommendations targeted to eliminate unnecessary

biases in the distribution of cardiovascular treatment.

81

I believe that my study proved informative, however, the study is limited by the
following: (1) the data study was abstracted by coding personnel, thus I could not
guarantee that coding errors did not occur; (2) I did not address the issue of patient
readmission; (3) a clinico-demographic profile was not included, and as a result, I was
not able to determine if a procedure was refused by a patient; (4) patient outcomes
were not assessed in this study; (5) my study population was insufficiently distributed
across all demographics; (6) I did not specifically address infarct location; (7) failure
to develop my own comorbidity index scale; (8) not taking into account the specific
artery used in the CABG; and (9) not addressing single vs. multiple vessel disease.

Despite these limitations, I believe that my study provides valuable information
that can be used to improve health care at McLaren Hospital. In particular is the
underuse of thrombolytic therapy. ”Increasing the number of patients that receive this
procedure is a nationwide challenge. I do not propose indiscriminate use of
thrombolytic therapy, rather I recommend the increased use in patients who probably
will benefit. Furthermore, I encourage the hospital to reevaluate following the strict
inclusion and exclusion criteria as recommended for administration of thrombolytic
therapy, because the benefits especially that for the elderly, outweigh that of
hemorrhagic risk.

Overall, the trends indicate that McLaren has widely distributed each of the four
Cardiovascular procedures as the years progress. Nevertheless, there was still evidence
of unequal distribution among certain population subgroups at the close of the study. I

would further recommend that an assessment of what might be accomplished using

82

currently available knowledge and technology be done, keeping the hospital’s patient

population in mind.

83

APPENDICES

APPENDIX A

Appendix A

ICD-9-CM Diagnosis Coding Descriptions (98)

ICD-9-CM code 410: ACUTE MYOCARDIAL INFARCTION - A severe, sudden
onset of myocardial necrosis due to formation of a thrombus in the coronary arterial
system obstruction arterial blood flow to that section of cardiac muscle.

The following fifth-digit subclassification is for use with category 410:
0 Episode of Care Unspecified

Use when the source document does not contain sufficient information for the
assignment of fifth-digit 1 or 2.

1 Initial Episode of Care

Use fifth-digit 1 to designate the first episode of care (regardless of facility site)
for a newly diagnosed myocardial infarction. The fifth-digit 1 is assigned regardless of
the number of times a patient may be transferred during the initial episode of care.

2 Subsequent Episode of Care

Use fifth-digit 2 to designate an episode of care following the initial episode
when the patient is admitted for further observation, evaluation or treatment for a
myocardial infarction that has received initial treatment, but is still less than 8 weeks
old.

ICD-9-CM code 410.0: OF ANTEROLATERAL WALL - Infarction of the cardiac
wall situated in front and below.

ICD-9-CM code 410.1: OF OTHER ANTERIOR WALL - Infarction of the cardiac
wall situated in the front.

ICD-9-CM code 410.2: OF INFEROLATERAL WALL - Infarction of the cardiac
wall situated below and to one side.

ICD-9-CM code 410.3: OF INFEROPOSTERIOR WALL - Infarction of the cardiac
wall situated below and in back.

ICD-9-CM code 410.4: OF OTHER INFERIOR WALL - Infarction of the lower
cardiac wall situated below and to one side.

ICD-9-CM code 410.5: OF OTHER LATERAL WALL - Infarction of the cardiac
wall situated to one side.

ICD-9-CM code 410.6: TRUE POSTERIOR WALL INFARCTION - Infarction of the
cardiac wall situated on the back side.

84

ICD-9-CM code 410.7: SUBENDOCARDIAL INFARCTION - Infarction situated just
beneath the endocardium.

ICD-9-CM code 410.8: OF OTHER SPECIFIED SITES - Note: Use this code when
the diagnosis as a myocardial infarction but is not listed above (410.0-410.7).

ICD-9-CM code 410.9: UNSPECIFIED SITE - Note: Use this code when the
diagnosis is identified as a myocardial infarction, but is not identified as to site, or

type.

85

APPENDIX B

Appendix B

Diagnoses & Procedures (99)

The Uniform Hospital Discharge Data Set (UHDDS), prepared under the
direction of the National Committee on Vital and Health Statistics of the US. Public
Health Service, provides 14 data items recommended as basic data for hospital
discharge statistics. Of the 14 items, diagnoses and procedures (with dates) are exactly
defined in the Coding Clinic:

Diagnoses are all diagnoses that affect the current hospital stay. The principal
diagnosis is designated and defined as the condition established after study to be chiefly
responsible for occasioning the admission of the patient to the hospital. Other
diagnoses to be designated and defined as associated with current hospital stay and are
all conditions that coexist at the time of admission, that develop subsequently, or that
affect the treatment received and/ or the length of stay. Diagnoses related to an earlier
episode that have no bearing on the current hospital stay are to be excluded.

Procedures and dates: All significant procedures are to be reported. A
significant procedure is one that carries an operative or anesthetic risk, that requires
highly trained personnel, or that requires special facilities or equipment. When more
than one procedure is reported, the principal procedure is to be designated. In
determining which of several procedures is principal, the following criteria apply:

The principal procedure is one that was performed for definitive
treatment rather than for diagnostic or exploratory purposes, or one

necessary to take care of a complication.

86

The principal procedure is that procedure most related to the
principal diagnosis.
Diagnoses other than those required in the UHDDS (principal and associated) may

appear in the medical record.

87

APPENDIX C

Appendix C
ICD-9-CM Procedure Coding Descriptions (98)

ICD-9-CM code 37.2: DIAGNOSTIC PROCEDURES ON HEART AND
PERICARDIUM

ICD-9-CM code 37.21: RIGHT HEART CARDIAC CATHETERIZATION -
The insertion of a cardiac catheter into the right heart chambers for the detection of
cardiac abnormalities.

ICD-9-CM code 37.22: LEFT HEART CARDIAC CATHETERIZATION -
The insertion of a cardiac catheter into the left heart chambers for the detection of
cardiac abnormalities.

ICD-9-CM code 37.23: COMBINED RIGHT AND LEFT HEART CARDIAC
CATHETERIZATION - The insertions of cardiac catheters into both the right and left
heart chambers for the detection of cardiac abnormalities.

ICD-9-CM code 36.1: BYPASS ANASTOMOSIS FOR HEART
REVASCULARIZATION - Restoration of coronary blood flow by a tubular surgical
bypass of an occluded coronary artery.

ICD-9-CM code 36.11: AORTOCORONARY BYPASS OF ONE
CORONARY ARTERY - Surgical anastomosis from the aorta, distal to one occluded
coronary artery.

lCD-9-CM code 36.12: AORTOCORONARY BYPASS OF TWO
CORONARY ARTERIES - Surgical anastomosis from the aorta, distal to two occluded
coronary arteries.

ICD-9-CM code 36.13: AORTOCORONARY BYPASS OF THREE
CORONARY ARTERIES - Surgical anastomosis from the aorta, distal to three
occluded coronary arteries.

lCD-9—CM code 36.14: AORTOCORONARY BYPASS OF FOUR OR MORE
CORONARY ARTERIES - Surgical anastomosis from the aorta, distal to four or more
occluded coronary arteries.

ICD-9-CM code 36.15: SINGLE INTERNAL MAMMARY-CORONARY
ARTERY BYPASS - Surgical anastomosis from one internal mammary artery, distal to
an occluded coronary artery(s).

88

. ICD-9-CM code 36.16: DOUBLE INTERNAL MAMMARY-CORONARY
ARTERY BYPASS - Surgical anastomosis from both internal mammary arteries, distal
to occluded coronary artery(s).

ICD-9-CM code 36.0: REMOVAL OF CORONARY ARTERY OBSTRUCTION
AND INSERTION OF STENT(S) - The surgical elimination of coronary artery
obstructions.

ICD-9-CM code 36.01: SINGLE VESSEL PERCUTANEOUS
TRANSLUMINAL CORONARY AN GIOPLASTY [PTCA] OR CORONARY
ATHERECTOMY WITHOUT MENTION OF THROMBOLYTIC AGENT - Dilation
of an obstructed coronary artery using a balloon-tipped catheter or the procedural
removal of a thickened coronary arterial intima, inserted through the femoral or other
artery, without infusion of a thrombus-destroying substance.

ICD-9-CM code 36.02: SINGLE VESSEL PERCUTANEOUS
TRANSLUMINAL CORONARY AN GIOPLASTY [PTCA] OR CORONARY
ATHERECTOMY WITH THROMBOLYTIC AGENT - Dilation of an obstructed
coronary artery using a balloon-tipped catheter or the procedural removal of a
thickened coronary arterial intima, inserted through the femoral or other artery, with
infusion of a thrombus-destroying substance.

ICD-9-CM code 36.05: MULTIPLE VESSEL PERCUTANEOUS
TRANSLUMINAL CORONARY ANGIOPLASTY [PT CA] OR CORONARY
ATHERECTOMY PERFORMED DURING THE SAME OPERATION, WITH OR
WITHOUT MENTION OF THROMBOLYTIC AGENT

ICD—9-CM code 99.2: INJECTION OR INFUSION OF OTHER THERAPEUTIC
OR PROPHYLACTIC SUBSTANCE - The forcing of a fluid, or introduction into a
vein of a healing or disease-preventative substance, other than listed in (99.11 through
99.19).

ICD-9-CM code 99.29: INJECTION OR INFUSION OF OTHER
THERAPEUTIC OR PROPHYLACTIC SUBSTANCE

89

APPENDIX D

APPENDIX D

CANADIAN CARDIOVASCULAR SOCIETY (102)
AN GINA SEVERITY DEFINITIONS

Class I angina occurs with strenuous or prolonged exertion at work or recreation and
does not occur with ordinary physical activity.

Class II angina occurs with walking rapidly on level ground or a grade and with
rapidly walking up stairs. Ordinary walking for < 2 blocks on the level or climbing
one flight of stairs does not cause angina except during the first few hours after
awakening, after meals, under emotional stress, in the wind, or in cold weather. This
implies slight limitation of ordinary activity.

Class III angina occurs when walking < 2 blocks on level ground at a normal pace,
under normal conditions, or when climbing one flight of stairs. This implies marked
limitation of ordinary physical activity.

Class IV angina occurs with even mild activity, and may occur at rest but must be of
brief (<15 rrrin) duration. (If the angina is of longer duration, it is called unstable
angina.) This implies inability to carry out even mild physical activity.

APPENDIX E

Appendix E

Recommendations for Administration of Thrombolytic Therapy
to Patients with Myocardial Infarction

I

Patients Without Contraindications to Thrombolytic Therapy (3)

Class I ' t

1. Patients < 70 years of age who present with chest pain consistent with the
diagnosis of acute myocardial infarction and at least 0.1 mV of ST segment elevation in
at least two contiguous ECG leads in whom treatment can be initiated within 6 hours of

pain onset.

Class 11a

1. Patients between ages 70 and 75 years who present with chest pain consistent
with the diagnosis of acute myocardial infarction and at least 0.1 mV of ST segment
elevation in at least two contiguous ECG leads in whom treatment can be initiated
within 6 hours of pain onset.

2. Patients with acute myocardial infarction > 6 hours after symptoms onset
but with a “stuttering” pattern of pain.

3. Patients who suffer clinically apparent reinfarction in the days after
administration of thrombolytic therapy.

Class 11b

1. Patients who present with chest pain consistent with the diagnosis of acute
myocardial infarction and at least 0.1 mV of ST segment elevation in at least two
contiguous ECG leads in whom treatment can be initiated between 6 and 24 hours after
pain onset.

2. Patients > 75 years of age who present with chest pain consistent with the
diagnosis of acute myocardial infarction and at least 0.1 mV of ST segment elevation in
at least two contiguous ECG leads in whom treatment can be initiated within 6 hours of
pain onset where the impending infarction is extensive.

3. Patients who present with chest pain consistent with the diagnosis of acute

myocardial infarction with ECG changed less profound than 0.1 mV of ST segment
elevation in two contiguous leads who can be treated within 24 hours.

91

Class III

Patients who have had chest pain when:
1. Treatment cannot be initiated within 24 hours of onset of chest pain and pain has
not recurred.

2. Chest pain onset is unknown and has receded.

3. The cause of the chest pain is unclear.

92

APPENDIX F

Appendix F

Recommendations for Angioplasty
After Intravenous Thrombolysis (67)

Class I

Dilation of a significant lesion suitable for coronary angioplasty in the infarct-
related artery in patients who are in the low risk group for angiographic-related
morbidity and mortality who have a type A lesion (see ACC/ AHA Task Force Report

on coronary angioplasty 42) and:

1. Have recurrent episodes of ischemic chest pain particularly if accompanied
by ECG changes (postinfarction angina).

2. Show evidence of myocardial ischerrria while on optimal medical therapy
during submaximal stress testing performed before hospital discharge or on maximal
stress testing in the early postlrospital period.

3. Have recurrent ventricular tachycardia or ventricular fibrillation, or both
convincingly related to ischenria while on antiarrhythmic therapy.

Class 110
Dilation of significant lesions in patients who:

1. Are similar to those in class I but who have type B lesions (anticipated
success rate 60% to 85 %) (see ACC/AHA Task Force Report on coronary
angioplasty”) .

2. Are within 18 hours of onset of acute infarction and have cardiogenic shock
or pump failure. These patients should be studied and undergo reperfusion as soon as
possible.

3. Before hospital discharge in those who have survived cardiogenic shock or
pump failure.

Class IIb
Dilation of a lesion in patients who:

1. Have an occluded coronary artery after attempted thrombolytic therapy.

2. Require multivessel angioplasty.

3. Have > 90% diameter proximal narrowing of an infarct-related artery with
a large area of viable myocardium still at risk.

Class III

All patients in the immediate postinfarct period (during initial hospitalization)
who do not fulfill Class I or 11 criteria. For example:

93

1. Dilation in patients who are within the early hours of an evolving
myocardial infarction and have < 50% residual stenosis of the infarct-related artery
after receiving a thrombolytic agent.

2. Dilation of lesions in vessels other than the infarct-related artery within the
early hours of infarction.

3. Dilation of residual lesions that are borderline in severity (50% to 70%
diameter narrowing) of the infarct-related artery without demonstration of ischemia on
functional testing.

4. Dilation of the type C lesions (see ACC/AHA Task Force Report on
coronary angioplasty for definition”).

5. Undertaking angioplasty in patients in the high risk group for morbidity and
mortality (see ACC/ AHA Task Force Report on coronary angioplasty for definition”).

94

APPENDIX G

Appendix G
Recommendations for Angioplasty (3)

Early Evolving Myocardial Infarction (Initial Hours of Myocardial Infarction)
Class I:

1. All patients developing pump failure/ shock syndrome.

2. All patients suspected of developing an acute ventricular septal defect.

3. Persistent or recurrent ischenria, or both, despite thrombolytic therapy.

Class 11a:
1., When coronary angiography can be performed within the first 6 hours after the
onset of chest pain in patients who are candidates for revascularization therapy utilizing
percutaneous translunrinal coronary angioplasty or coronary artery bypass surgery (but
who are not candidates for thrombolytic therapy).
2. Patients who have had a previous aortocoronary vein graft if the graft is to the
suspected infarctrelated vessel.

Class Ilb:
1. Patients who can be taken quickly for angioplasty or bypass surgery in a facility set
up and qualification for these emergency procedures.

Class III:
1. As a routine after early intravenous thrombolytic therapy.
2. Patients with uncomplicated myocardial infarction having no evidence of ongoing
ischerrria.

Late Evolving Myocardial Infarction (Afier the Initial 6 hours up to But Not Including
Predischarge Evaluation)

Class I:
1. Patients with recurrent episodes of ischerrric chest pain, particularly if accompanied
by ECG changes.
2. Patients suspected of having acute mitral regurgitation or a ruptured interventricular
septum causing heart failure or shock.
3. Patients suspected of developing subacute cardiac rupture (pseudoaneurysm).
4. Patients with cardiogenic shock or sever pump failure.

Class 11a:
1. Patients with congestive heart failure during intensive medical therapy.
2. Patients with recurrent ventricular tachycardia or ventricular fibrillation, or both,
during intensive antiarrhythmic therapy.

Class Hb:

1. Asymptomatic patients who have received thrombolytic therapy during the evolving
phase.

95

Class III:
1. Patients with uncomplicated completed myocardial infarction in whom no acute
mechanical or surgical intervention is contemplated.

Convalescent Myocardial Infarction (Immediate Predischarge up to 8 Weeks After
Discharge)

Class I:
1. Postinfarction angina pectoris.
2. Patients with evidence of myocardial ischemia on laboratory testing: exercise-
induced ischemia (with or without exercise-induced angina pectoris), manifested by
> / = 1mm of ST segment depression or exercise-induced reversible thallium perfusion
defect or defects, increased lung thallium uptake, or exercise-induced reduction of the
ejection fraction or wall motion abnormalities on radionuclide ventriculography or two-
dimensional echocardiography.

Class 11a:
1. Patients with the need to return to unusually active and vigorous physical
employment.
2. Patients with a left ventricular ejection fiaction < 40%.

Class Ilb:
1. As a routine in patients receiving thrombolytic therapy during the evolving phase of
infarction.
2. Otherwise uncomplicated and asymptomatic patients who are < 45 years of age.
3. Patients with uncomplicated non-Q wave myocardial infarction not otherwise
manifesting evidence of myocardial ischemia on noninvasive laboratory testing.

Class III:
1. Patients judged to have a debilitating disease or conditions that preclude their being
candidates for invasive intervention.
2. Patients with coexisting disease judged to be primarily responsible for the patient’s
prognosis, with a greatly shortened life expectancy unless revascularization is
determined to be necessary to facilitate treatment of the underlying disease.
3. Patients with very advanced left ventricular dysfunction (ejection fraction < 20%)
in t he absence of angina pectoris or evidence of ischerrria. An exception is the patient
who is a candidate for aneurysectomy or cardiac transplantation.
4. Patients with ventricular arrhythrrrias who have no evidence of ischemia
symptomatically or during exercise testing, well preserved exercise tolerance and no
suggestion may be the patient with inducible sustained ventricular tachycardia.

96

APPENDIX H

Table 1: Characteristics of patients admitted to community hospital with acute
myocardial infarction diagnosis; 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
Total Admissions-no. 475 511 549 550 574
Age no. (%)
1-44 37 (7.8) 37 (7.2) 27 (4.9) 32 (5.8) 33 (5.7)
45-54 68 (14.3) 82 (16.0) 71 (12.9) 68 (12.4) 84 (14.6)
55-64 117 (24.6) 118 (23. D 135 (24.6) 140 (25.5) 138 (24.0)
65-74 139 (29.3) 120 (23.5) 166 (30.2) 183 (33.)3) 162 (28.2)
75-101 114 (24.0) 154 (30.1) 150 (27.3) 127(23.1) 157 (27.4)
Gender-no. (%)
Female 158 (33.3) 204 (39.9) 220 (40.1) 229 (41.6) 210 (36.6)
Male 317 (66.7) 307 (60.1) 329 (59.9) 321 (58.4) 364 (63.4)
Payer-no. (%)
All Other 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (0.5)
Private 6 (1.3) 11 (2.2) 8 (1.5) 4 (0.7) 3 Q5)
Medicare 252 (53.1) 281 (55.0) 331 (60.3) 320 (58.2) 329 (57.3)
Medicaid 10 (2.1) 15 (2.9) 18 (3.3) 18 (3.3) 28 (4.9)
Commercial 199 (41.9) 170 (33.3) 165 (30.1) 185 (33.6) 184 (32.1)
HMO (l-llth+) 8 (1.7) 34 (6.7) 27 (4.9) 23 (4.2) 28 (4.9)
Race-no. (%)
Black 27 (5.7) 31 (6.1) 23 (4.2) 36 (6.5) 30 (5.2)
White 448 (94.43) 480 (93.9) 526 (95.8) 514 (93.5) 544 (94.8)
Comorbidity Index-
no. (%)
0 311 (65.5) 357 (69.9) 344 (62.7) 344 (62.5) 377 (65.7)
1 119 (25.1) 116 (22.7) 141 (25.7) 132 (24.0) 139 (24.2)
2 45 (9.5) 38 (7.3 64 (11.7) 74 (13.5) 58 (10.1)

 

97

 

Table 2: No. of AMI’s by age, distributed across gender, race, insurance, and

comorbidity; 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994

Total Admissions-no. 475 511 549 550 574
(FEMALE)

Age- no. (%)
1-44 11 (7.0) 8 (3.9) 5 (2.3) 12 (5.2) 9 (4.3)
45-54 11 (7.0) 23 (11.3) 11 (5.0) 24 (10.5) 17 (8.1)
55-64 32 (20.3) 38 (18.6) 35 (15.9) 44 (17.2) 37 (17.6)
65-74 51 (32.3) 53 (26.0) 82 (37.3) 72 (31.4) 65 (31.0)
75-101 53 (33.5) 82 (40.2) 87 (39.5) 77 (33.6) 82 (39.0)
(MALE)

Age-no. (%)
1-44 26 (8.2) 29 (9.4) 22 (6.7) 20 (6.2) 24 (6.6)
45-54 57 (18.0) 59 (19.2) 60 (18.2) 44 (13.7) 67 (18.4)
55-64 85 (26.8) 80 (26.1) 100(30.4) 96 (29.9) 101(27.7)
65-74 88 (27.8) 67 (21.8) 84 (25.5) 111(34.6) 97 (26.6)
75-101 61 (19.2) 72 (23.5) 63 (19.1) 50 (15.6) 75 (20.6)
(BLACK)

Age-no. (%)
1-44 8 (29.6) 3 (11.1) 6 (22.2) 6 (22.2) 4 (14.8)
45-54 4 (12.9) 5 (16.1) 3 (22.6) 7 (22.6) 8 (25.8)
55-64 0 (0.0) 2 48.7) 7 (30.4) 9 (39.1) 5 (21.7)
65-74 3 (8.3) 9 (25.0) 9 (25.0) 9 (25.0) 6 (16.7)
75-101 1 (3.3) 7 (23.3) 12 (40.0) 5 (16.7) 5 (16.7)
(WHITE)
Age-no. (%)

1-44 29 (6.5) 33 (6.9) 27 (5.1) 29 (5.6) 32 (5.9)
45-54 65 (14.5) 77 (16.0) 69 (16.0) 59 (11.5) 77 (14.2)
55-64 111(24.8) 111(23.1) 128(23.1) 131(25.5) 126(23.2)
65-74 133(29.7) l 13(23.5) 157(29. 8) 174(33.9) 157(28.9
75-101 110(24.6) 146(30.4) 145(27 .6) 121(23.5) 152(27 .9)

 

98

 

Table 2 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994

(ALL OTHER,

PRIVATE

INSURANCE)

_Agg—no. (%)
1-64 6(100.0) 11(100.0) 8(100.0) 3 (75.0) 5 (100.0)
65-101 0 @0) 0 (0.0) 0 (0.9) 1(25.0) 0 (0.0)
(HMO)

_Age—no. (%)
1-64 3 (37.5) 25 (73.5) 16 (59.3) 22 (95.7) 25 (89.3)
65-101 5 (62.5) 9 (26.5) 11 (40.7) 1 (4.3) 3 (10.7)

(MEDICARE&

MEDICAID)

Age-no. (%)
1-64 33 (12.6) 34 (11.5) 48 (13.8) 37 (10.9) 50 (14.0)
65-101 229 (87.4) 262(88.5) 301(86.2) 301(89.1) 307 (86.0)

(COMMERCIAL)

Age-no. (%)
1-64 180 (90.5) 167 (98.2) 161 (97.6) 178 (96.2) 175 (95.1)
65-101 19 (9.5) 3 (1.8) 4 (2.4) 7 (3.8) 9 (4.9)

(COMORBIDITY

INDEX 0)

_Age-noJ%)
1-44 32 (10.3) 37 (10.4) 25 (7.3) 27 (7.8) 30 (8.0)
45-54 58 (18.6) 74 (20.7) 68 (19.8) 58 (16.9) 69 (18.3)
55-64 78 (25.1) 92 (25.8) 104(30.2) 104 (30.2) 105(27.9)
65-74 89 (28.6) 76 (21.3) 94 (27.3) 102 (29.7) 101(26.8)
75-101 54 (17.4) 78 (21.8) 53 (15.4) 53 (15.4) 72 (19.1)

 

99

 

Table 2 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994

(COMORBIDITY

INDEX 1)

Age-no. (%)
1-44 4 (3.4) 0 (0.0) 2 (1.4) 5 (3.8) 0 (0.0)
45-54 6 (5.0) 7 (6.0) 2 (1.4) 5 (3.8) 10 (7.2)
55-64 27 (22.7) 21 (18.1) 23 (16.3) 24 (18.2) 25418.0)
65-74 40 (33.6) 35 (30.2) 50 (35.5) 55 (41. 44 (31.7)
75-101 42 (35.3; 53 (45.7) 64 (45.5) 43 (32.6) 60 (43.2)

(COMORBIDITY

INDEX 2)

Age-no. (%)
1-44 1 (2.2) 0 (0.0) 0 (0.0) 0 (0.0) 3 (5.2
45-54 4 (8.9) 1 (2.6) l (1.6) 5 (6.8) 5 (8.6)
55-64 12 (26.7) 5 (13.2) 8 (12.5) 12 (16.2) 8 (13.8)
65-74 10 (22.2) 9 (23.7) 22 (34.4) 26 (35.1) 17 (29.3)
75-101 18 (40.0) 23 (60.5) 33 (51.6) 31 (41.9) 25 (43.1)

 

100

 

Table 3: No. of AMI’s by gender, distributed across age, race, insurance, and

comorbidity; 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994

Total Adnrissions-no. 475 511 549 550 574
(AGE 1-44)

Gender-no. (%)
Female 11(29.7) 8 (21.6) 5 (18.5) 12 (37.5) 9 (27.3
Male 26 (70.3) 29 (78.4) 22 (81.5) 20 (62.5) 24 (72.7)
(AGE 45-54)

Gender-no (%)
Female 11 (16.2) 23 (28.0) 11 (15.5) 24 (35.3) 17 (20.2)
Male 57 (83.8) 59 (72.0) 60(84.5) 44 (64.7) 67479.8)
(AGE 55-64)

Gender-no. (%)
Female 32 427.4) 38 (32.2) 35 (25.9) 44(31.4) 37 (26.8)
Male 85 (72.6) 80 (67.8) 100(74.l) 96(68.6) 101(73.2)
(AGE 65-74)

Gender-no. (%)
Female 51 (36.7) 53 (44.2) 82 (49.4) 72 (39.3) 65 (40.1)
Male 88 (63.3) 67 (55.8) 84(50.6) 111(60.7) 97 (59.9)
(AGE 75-101)

Gender-no. (%)
Female 53 (46.5) 82 (53.2) 87 (58.0) 77 (60.6) 82 (52.2)
Male 61 (53.5) 72 (46.8) 63 (42.0) 50 (39.4) 75 (47.8)
(BLACK)

Gender-no. (%)
Female 8 (29.6) 10 (32.3) 13 (56.5) 14 (38.9) 12 (40.0)
Male 19 (70.4) 21 (67.7) 10 (43.5) 22 (61.1) 18 (60.0)
(WHITE)

Gender-no. (%)
Female 150(33.5) 194(40.4) 207(39.4) 215(41.8) l98(36.4)
Male 298(66.5) 286(59.6) 319(60.6) 299(58.2) 346(63.6)

(ALL OTHER,

PRIVATE

INSURANCE)

Gender-no. (%)
Female 1 (16.7) 4 (36.4) 2 (25.0) 1 (25.0) 1(20.0)
Male 5 (83.3) 7 (63.6) 6 (75.0) 3 (75.0) 4 (80.0)

 

101

 

Table 3 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(HMO)
Gender-no. (%)
Female 4 (50.0) 17 (50.0) 11(40.7) 5 (21.7) 12 442.9)
Male 4 (50.0) 17 (50.0) 16 (59.3) 18 (78.3) 16 (57.1)
(MEDICARE &
MEDICAID)
Gender-no. (%)
Female 102(38.9) 134(45.3) 172(49.3) l61(47.6) 160(44.8)
Male 160(61.1) l62(54.7) l77(50.7) 177(52.4) 197(55.2)
(COMMERICIAL)
Gender-no. (%)
Female 51 (25.6) 49 (28.8) 35 (21.2) 62 (33.5) 37 (20.1)
Male 148(74.4) 121(71.2) 130(78.8) 123(66.5) 147(79.9)
(Comorbidity Index
0)
Gender-no. (%)
Female 90 (28.9) 130(36.4) 116(33.7) 132@8.4) 119(31.6)
Male 221(71.1) 227(63.6) 228(66.3) 212(61.6) 258(68.4)
(Comorbidity Index
1)
Gender-no. (%)
Female 45 (37.8) 56 (48.3) 75 (53.2) 59 (44.7) 57 (41.0)
Male 74 (62.2) 60(51.7) 66(46.8) 73 (55.3) 82 (59.0)
(Comorbidity Index
2)
Gender-no. (%)
Female 23 (51.1) 18 (47.4) 29 (45.3) 38 (51.4) 34 (58.6)
Male 22 (48.9) 20 (52.6) 35 (54.7) 36 (48.6) 24 (41.4)

 

102

 

Table 4: No. of AMI’s by insurance, distributed across age, race, gender, and

comorbidity; 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
Total Admissions-no. 475 51 1 549 550 574
(AGE 1-44)
Payer-no. (%)
AllOther, Private 3 (8& 1 (2.7) 2 (7.4) 1 (3.1) 1 (3.0)
HMO l (2.7) 7 (18.9) 2 (7.4) 4 (12.5) 3 (9.1)
Medicare& 3 (8.1) 7 (18.9) 5 (18.5) 8 (25.0) 6 (18.2)
Medicaid
Commercial 30481.1) 22 (59.5) 18 (66.7) 19 (59.4) 23 (69.7)
(AGE 45-54)
Payer-no. (%)
AllOtheg Private 2 (2.9) 3 43.7) 4 (5.6) 1 (1.5) 2 (2.4)
HMO 0 (0.0) 8 (9.8) 4 (5.6) 9 (13.2) 6 (7.1)
Medicare& 9 (13.2) 15 (18.3) 13 (18.3) 6 (8.8) 16 (19.0)
Medicaid ,
Commercial 57 (83.8) 56 (68.3) 5000.4) 52(76.5) 60 (71.4)
(AGE 55-64)
Payer-no. (%)
AllOther, Private 1 (0.9) 7 (5.9) 2 (1.5) 1 (0.7) 2 (1.4)
HMO 2 (1.7) 10 (8.5) 10 (7.4) 9 (6.4) 16 (11.6)
Medicare & 21 (17.9) 12 (10.2) 30 (22.2) 23 (16.4) 28 (20.3)
Medicaid
Commercial 93 (79.5) 89 (75.4) 93 (68.9) 107(76.4) 92 (66.7)
(AGE 65-74)
Payer-no. (%)
AllOther, Private 0 (0.0) 0 (0.0) 0 (0.0) 1 (0.5) 0 (0.0)
HMO 3 (2.2) 7 (5.8) 4 (2.4) 1 40.5) 3 (1.9)
Medicare & 123(88.5) 110(91.7) 158(95 .2) 179(97.8) 150(92.6)
Medicaid
Commercial 13 (9.4) 3 (2.5) 4 (2.4) 2 (1.1) 9 (5.6)

 

103

 

Table 4 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(AGE 75-101)
Payer-no. (%)
All Other, Private 0 (0.0) 0 (0.0) 0 (0.0) 1 (0.5) 0 (0.0)
HMO 3 (2.2) 7 (5.8) 4 (2.4) 1 (0.5) 3 (1.9)
Medicare & 123(88.5) 110(91.7) 158(95.2) 179(97.8) 150(92.6)
Medicaid ,
Commercial 13 (9.4) 3 (2.5) 4 (2.4) 2 (1.1) 9 (5.6)
(BLACK)
Payer-no. (%)
All Other, Private 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0)
HMO 1 (3.7) 0 (0.0) 0 (0.0) 0 (0.0) 1 (3.3)
Medicare& 11( 40.7) 19 (61.3) 15 (65.2) 18 (50.0) 16 (53.3)
Medicaid
Commercial 15 (55.6) 12 (38.7) 8 (34.8) 18 (50.0) 13 (43.3)
(WHITE)
Payer-no. (%)
AllOther, Private 6 (1.3) II (2.3) 8 (1.5) 4 (0.8) 5 (0.9)
HMO 7 (1.6) 34 (7.1) 27 (5.1) 23 (4.5) 27 (5.0)
Medicare & 251(56.0) 277(57.7) 334(63.5) 320(62.3) 341(62.7)
Medicaid
Commercial 184(41. 1) 158(32.9) 157(29.8) 167(32.5) 171(31.4)
(FEMALE)
Payer-no. (%)
All Other, Private 1 (0.6) 4 (2.0) 2 (0.9) 1 (0.4) 1 (0.5)
HMO 4 (2.5) 17 (8.3) 11 (5.0) 5 (2.2) 12 (5.
Medicare & 102(64.6) 134(65.7) 172(78.2) 161(70.3) 160(76.2)
Medicaid
Commercial 51 (32.3) 49 (24.0) 35 (15.9) 62 (27.1) 37 (17.6)
(MALE)
Payer-no. (%)
AllOther, Private 5 (1.6) 7 (2.3) 6 (1.8) 3 (0.9) 4 (1.1)
HMO 4 (1.3) 17 (5.5) 16 (4.9) 18(5.6) 16 (4.4)
Medicare/Aid 160(50.5) 162(52.8) l77(53.8) 177(55 . 1) 197(54Q
Commercial 148(46.7) 121(39.4) l30(39.5) 123(38.3) l47(40.4)

 

104

 

Table 4 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(Comorbidity Index
0)
Payer-no. (%)
AllOther, Private 6 (1.9) 10 (2.8) 8 (2.3) 441.2) 5 (1.3)
HMO 3 (1.0) 30 (8.4) 19 (5.5) 19(5.5) 24 (6.4)
Medicare& 152(48.9) 166(46.5) 175(50.9) 175(50.9) 201(53.3)
Medicaid
Commercial 150(48.2) 151(42.3) 142(41.3) 175(50.9) 147(39.0)
(Comorbidity Index
1)
Payer-no. (%)
AllOther, Private 0 (0.0) l (0.9) 0 (0.0) 0 (0.0) 0 40.0)
HMO 4 (3.4) 4 (3.4) 5 (3.5) 2 (1.5) 3 42.2)
Medicare& 81 (68.1) 97 (83.6) 116(82.3) 105(79.5) 110(79.1)
Medicaid
Commercial 34 (28.6) 14 (12.1) 20 (14.2) 25 (18.9) 26 (18.7)
(Comorbidity Index
2)
Payer-no. (%) _
AllOther, Private 0 (0.0) 0 (0.0) 0 (0.0) 0 40.0) 0 (0.0)
HMO 1 (2.2) 0 (0.0) 3 (4.7) 2 (2.7) 1 (1.7)
Medicare& 29 (64.4) 33 (86.8) 58 (90.6) 58 (78.4) 46 (79.3)
Medicaid
Commercial 15 (33.3) 5 (13.2) 3 (4.7) N 14 (18.9) 11 (19.0)

 

 

 

 

 

 

105

 

Table 5: No. of AMI’s by race, distributed across age, gender, comorbidity,
and insurance; 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994

Total Adnrissions-no. 475 51 1 549 550 574
(AGE 1-44)

Race-no. (%)
Black 8 (21.6) 4 (10.8) 0 (0.0) 3 (9.4) 1 (3@
White 29 (78.4) 33 (89.2) 27(100.0) 29 (90.6) 32 (97.0)
(AGE 45-54)

Race-no. (%)
Black 3 (4.4) 5 (6.1) 2 (2.8) 9 (13.2) 7 (8.3)
White 65 (95.6) 77 (93.9) 69 (97.2) 59 (86.8) 77 (91.7)
(AGE 55-64)

Race-no. (%)
Black 6 (5.1) 7 (5.9) 7 (5.2) 9 (6.4) 12 (8.7)
White 111(94.9) 111(94.1) 128(94.8) 131(93.6) 126(91.3)
(AGE 65-74)

Race-no. (%)
Black 6 (4.3) 7 (5.8) 9 (5.4) 9 (4.9) 5 (3.1)
White 133(95.7) Il3(94.2) 157(94.6) 174(95.1) 157(96.9)
(AGE 75-101)

Race-no. (%)
Black 4 (3.5) 8 (5.2) 5 (3.3) 6 (4.7) 5 (3.2)
White 110(96.5) 146(94.8) 145(96.7) l2l(95.3) 152(96.8)
(FEMALE)

Race-no. (%)
Black 8 (5.1) 10 (4.9) 13 (5.9) 14 46.1) 12 45.7)
White 150(94.9) 194(95.1) 207(94.1) 215(93.9) 198(94.3)
(MALE)

Race-no. (%)

‘ Black 19 (6.0) 21 (6.8) 10 (3.0) 22 (6.9) 18 (4.9)
White 298(94.0) 286(93.2) 319(97.0) 299(93.1) 346(95.1)

(Comorbidity Index

0)

Race-no. (%)
Black 18 (5.8) 18 (5.0) 14 (4.1) 21 (6.1) 19 (5.0)
White 293(94.2) 33 (95.0) 330(95.9) 323(93.9) 358(95.0)

 

106

 

Table 5 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(Comorbidity Index
1)
Race-no. (%)
Black 4 (3.4) 10 (8.6) 3 (2.1) 9 (6.8) 7 (5.0
White 115(96.6) 106(9l.4) 138(97.9) 123(93.2) 132(95.0)
(Comorbidity Index
2)
Race-no. (%)
Black 5 (11.1) 3 (7.9) 6 (9.4) 6 (8.1) 4 (6.9)
White 40 (88.9) 35 (92.1) 58 (90.6) 68 (91.9) 54 (93.1)
(ALL OTHER,
PRIVATE
INSURANCE)
RACE-no. (%)
BLACK 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0)
WHITE 6(100.0) 11(100.0) 8(100.0) 4(100.0) 5(100.0)
(HMO)
RACE-no.4%)
BLACK l(l2.5) 0 (0.0) 0 40.0) 0 (0.0) 1 (3.6)
WHITE 7 (87.5) 34(100.0) 27(100.0) 23(100.0) 27(96.4L
(MEDICARE&
MEDICAID)
RACE-no. (%)
BLACK 11 (4.2) 19 (6.4) 15 (4.3) 18 (5.3) 16 (4.5)
WHITE 251(95.8) 277(93.6) 334(95.7) 320(94.7) 341(95.5)
(COMMERCIAL)
RACE-no. (%)
BLACK 15 (7.5) 12 (7.1) 8 (4.8) 18 (9.7) 13 (7.1)
WHITE 184(92.5) 158(92.9) 157(95.2) 167(90.3) 171(92.9)

 

107

 

Table 6: No. of AMI’s by comorbidity, distributed across age, gender, race, and

insurance; 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(WHITE)

Comorbidity Index-

no.(%)
0 293 65.4) 339(‘E.6) 330(62.7) 323(62.8) 358(65.8)
1 115(25.7) 106(22.1) 138(26.2) 1234239) 132(24.3)
2 40 (8.9) 35 (7.3) 58 (11.0) 68 (13.2) 54 (9.9
(FEMALE)

Comorbidity Index-

no. (%) .
0 90 (57.0) 130(63.7) 111(52.7) 1324576) 119(56.7)
1 45 (28.5) 56 (27.5) 75 (34.1) 59 (25.8) 57 (27.1)
2 23 (14.6) 18 (8.8) 29 (13.2) 38 (16.6) 34 (16.2)
(MALE)

Comorbidity Index-

no. (%)
0 22 (69.7) 227(73.9) 228(69.3) 212(66.0) 258(70.9)
1 74 (23.3) 60(19.5) 66 (20.1) 73 (22.7) 82 (22.5)
2 22 (6.9) 20 (6.5) 35 (10.6) 36 411.2) 24 (6.6)
(ALL OTHER,

PRIVATE)

Comorbidity Index-

no. (%)
0 6 (100.0) 10 (90.9) 8 (100.0) 4 (100.0) 5 (100.0)
1 0 40.0) 1 (9.1) 0 (0.0) 0 (0.0) 0 (0.0)
2 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0)
(HMO)

Comorbidity Index-

no. (%)
0 3 (37.5) 30 (88.2) 19 (70.4) 19 (82.6) 2 (85D
1 4 (50.0) 4 (11.8) 5 (18.5) 2 (8.7) 3 (10.7)
2 1412.5) 0 (0.0) 3 (11.1) 2 (8.7) 1 (3.6)

 

108

 

Table 6 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(WHITE)

Comorbidity Index-

no.(%)
0 293(65.4) 339(70.6) 330(62.D 323(62.8) 358(65.8)
1 115(25.7) 106(22.1) 138(26.2) 123(23.9) 132L243)
2 40 (8.9) 35 (7.3) 58 (11.0) 68 (13.2) 54 (9.9)
(FEMALE)

Comorbidity Index-

no. (%)
0 90 (57.0) 130(63.7) 111452.7) 132(57.6) ll9(56.7)
1 45 (28.5) 56 (27.5) 75 (34.1) 59 (25.8) 57 (27.1)
2 23 (14.6) 18 (8.8) 29 (13.2) 38 (16.6) 34 (16.2)
(MALE)

Comorbidity Index-

no. (%)
0 22 (69.7) 227(73.9) 228(69.3) 212L660) 2584709)
1 74 (23.3) 60(19.5) 66 (20.1) 73 (22.7) 82 (22.5
2 22 (6.9) 20 (6.5) 35 (10.6) 36 (11.2) 24 (6.6)
(ALL OTHER,

PRIVATE)

Comorbidity Index-

no. (%)
0 6 (100.0) 10 (90.9) 8 (100.0) 4 (100.0) 5 (100.0)
1 0 (0.0) 1 (9.1) 0 (0.0) 0 (0.0) 0 (0.0)
2 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0)
(HMO)

Comorbidity Index-

no. (%)
0 3 (37.5) 30 (88.2) 19 (70.4) 19 (82.6) 2 (85.7)
1 4 (50.0) 4 411.8) 5 (18.5) 2 (8.7) 3 (10.7)
2 1 (12.5) 0 (0.0) 3 (11.1) 2 (8.7) 1 (3.6)

 

109

 

Table 6 (cont’d):

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CHARACTERISTIC 1990 1991 1992 1993 1994
(MEDICARE&

MEDICAID)

Comorbidity Index-

no.(%)

0 1524580) 166(56.1) 175(50.1) 175(51.8) 201(56.3)
1 81430.9) 97432.8) 116(33.2) 105(31.1) 110(30.8)
2 29411.1) 33 (11.1) 58 (16.6) 58 (17.2) 46 (12.9)
(COMMERCIAL)

Comorbidity Index-

no. (%)

0 150(75.4) 151(88.8) 142(86.1) 14608.9) 147(79.9)
1 34 (17.1) 14 (8.2) 20 (12.1) 25 (13.5) 26 (14.1)
2 15 (7.5) 5 (2.9) 3 (1.8) 14 (7.6) 1146@

 

110

 

._o>£ mod 05 “a ugawaflm u can 350$:me 82 o
ufimouoEEoomm 8:885 98 no $325888 ”BE? .88 GEE cocaow who» 3-? some 3&3 mac» coining
3338 3 2a 83~5> 65 not“ 3:on 855%: 9:. n :od v am He 389:3» 2a 838 ago 62865 83:28 32:3 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

0 Ron. - - - - - eggflj
o 3%. - - - - - 02m
a go. - - - - -
m
- o NEE - - - - a
- a 88. - - - - - a
saga
- - a 8R. - - - final
00mg
- - - 2%. - - cease
HOE—00
- - - - - - ES
- - - - - - 3R
- - - - G at. - was.
- - - - a Sea. - $1 .
AmHMQCdu
o 2:. o as. o KR- o 8&1 u was. it owns. mama
o 384 ӣ83 0 ~23 o 2:: 0 was; a $8; 82
a Raw 0 new. 0 new. a 38. o 3.8. o 88. $2
laws. 2%. man 8:. 8%. Ram. omfl
11233 was. mafia?
-m 85235 43638600 Bumahc<oomm -5980 Bum=€<bw< BEER—5 83wt~>

 

 

52:35: no use.» Gamma? no 38%» .55: .Su 8.55mi new $329588 .88 cocoon due .3 683?:

Ego—.385 can .oua mo E8» we 3 a: 35:3 .5. 55.35: 3325 33.3525 .8 :6 8:2 move ESQ—FED "h 935.

111

._o>o_ mod 2: “a ~588me c 28 385:9.“ “oz 0
88888 3 8:835 93 no 583888 ”BE? .88 BEE £88» “88» 87$. .68 3&2 .82“ 838va
330:8 8 8a 838:; 05 88 museum 8:888 25. n :06 Va 88 25888“ 8.» 8:8 88 .3868 85850 82:: a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

o wvvo. - - - - - 850 _
< 8:88:

- movm. - - - - N

- vmvm. - - - - H
3658800

- - o womm. - - - 88m
895

- - - o 33. - - oREom
Sociom

- - - - wvfl .N - Shmo

- - - - - - $-mm

- - - - - - v99.

- - - - - - Si
8

0 Sam; 6 wwwm; G 3mm; 0 cmmmg 0 3mm; 0 «mam; 33

o Gama; o wNNmA o mbvmg o wag.“ 0 05mm; 8 Emma; 82

o memo; o memo; 8 move; o 834 o 3:; o Sumo.— 32

mwam. mmwm. mwam. Eon. comm. can. 83
88> 83883.

88:2 Easiest Bases.
-< 68835 43658800 8am=€<-o8m -8880 BLSFTom/x 832.883 8388>

 

 

.8535: no 88» 86886: no 88:0 8:8 8.. 8:88.: Ea .§Ea..o88 .88 .8ch» due .3 8.95.:

386385 E: .82: ES 88.» me 3858. .5.— oemaaufiao 3805 833885 :e a... 838 move 88:85 "a 03.2.

112

.522 85 2: a 28$:me u 23 usage? 82 o

.RSBEEoo .m 85.5”:— EE 5 .bfiéofioo .323 .88 GEE .uoccow 58> 3- mm .0? .33 £8» Sam—Eva
{6:8 3 Ba 83%? 2: H8 3:on 8:20on 2:. n. ..8 ov m H8 Enocawa- 2a 858 83 @8865 9.25550 32:: a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

o 38 - - - 3382]

u 82 - - - - - 02m
0 GE. - - - - - seal

m 00

- 8E. - - - - N

- o :2. - - - - - H
J?
- - we? - - - 18E!

8

- - - o 9.3 - - %efl
Hun—~00

- - - - - - v20

- - - - - - flaw

- - - - 0 «RS - v09.

- - - - 0 E3 - $1 -
E83 um

a £84 0 em? 4 o %M ammfillqanmfifill|wafil
9%. m5. 8:. a fig]! |~mflll

$9.. 83. max :3. :9. 8?. $2

Ila; man. 8%. ”39 2%. «ad Jag
58% 8%

II'HIBSE |8§a< 8132
um 0055.2: -b—m—umDuO—Eoo Buw=HU<100NM Luvs—0o Bumnmb<now< Bum—game: mO—DNE>

 

 

 

 

4:53:55 no .89» nova—5.x no 38...? .65: .5.— oonanafi «Ea $322338 .88 can .3 335?: 2.2.2365
ES can .8 E8» 3. 3 a: $55.:— ..8 E5353 5:3?»853 2.5.8 .8 a:w 83a.— meuo 1895.25 "a 939—.

113

._o>o_ mod 05 E .Swofifimm : :5 ”Snow—Ema 82 o
”88:68 3 85:85 :5 no 563888 ”HEB .86 “2:8 £35» 3:?» ST? .0»: ”39 £8» :0???“
332:8 m: 0:: 833:3 05 :8 3:8» 8:282 2F : :odvm :8 Enema»: 2: 8:8 3:: .Bfifivfi 85.850 32:: :

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

o 83: - - - - - 550
< 8:82":

- 8mm. - - - - N

- 83.. - - - - _
£29558

- - o 88. - - - .32:
8|.

- - - u 9.x». - - 2.50:
50:00

- - - - 85m - $8

- - - - - - 3-3

- - - - - - - $9.

- - - - - - 3.;
mm:

o 8%. :5. 0 mg. 0 8%. c :5 o 8%. 82

89.. on? $9.. $9.. 9.9.. $5.. 82

8a.... 39.. .89.. 39.. 89.. as. 83

05.. $9.. ”3.. 83.. can. 89.. 82
:8? :ommm_EU<

8.3.8... 8.8.6... 32.6...
.< 005335 JGBBHOEOU B~m3€<éo§ Jaw—50 Bam=€<uow< BamzwvmcD mozatdxr

 

 

£3235: :: :8.» ::_mm_.::: a: 38:: .35: :8 8:235 :5 #329588 .82 63:0» an: .3 @825»:

35.223: 6:: .52: 6:: E8.» me 8:33: :8 553:5: 53323058 2.5.8 :: a... 85:.— mct: 13952:: 5— e35.

114

._0>0_ nod 0.: a: 8:85:me : :8 3:88:03 82 0
88:08:80 .m 00:83:: :8 .0 588888 .083 .88 .03: .:0::0m .380.» :0. mm .0w: .83 .80» 8338::
£388 a: 0:: 83:53 05 :8 8:08 8:080: 05. n. :o. ov m :8 888—83. 0:: 8:8 8:: 608088 023850 32:0 :

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

u mmoo. - 9888302].—
0 2mm- - - - - - 02$
[.88. - - - - - .0
m 8:8
- 0 mac; - - - - N
- : 3mm; - - - - H
- - o 8.: - - - 88]
8mm
- - - 0 2% - - 0
8:80
- - - - - - 3-8
- - - - 0 g. - «.va
- - - - 0 $3.. - 3”; r
6803 0:

, 0 8N4 0 boom; 0 N538 d .2qu 0 can; 0 33.: mag
Ilia? o 8:. 0 381818. a as. :81
0 mom“; 0 mefi: 0 3E; o 28.8 0 $.34 : $34 $2
: wmoo. : mmdm. “ENG. : mNG. : mmG. : 5.2:. 0mm:

8 .83 88
:03=._:< :03:_.:< 831.3.
-m 8:838 32:38:80 388.8888 -:0::00 :03:.n:<-0m< 833:8: 83:83

 

 

 

 

 

 

 

 

 

.8335“: 8 .80» :88: .8 300.80 :05: :8 00:83.8 :8 88:58:80 .008 .880» .0»: .3 833:: 3:88.388
::: .0»: .8 080» we 3 a: 8:002— ..8 80:80: “:88” 00:93 80...: 8:880 8 A..: 088.. 0:8 88:08: "2 03:8

115

”0880:: ”< 8:885 :8 no 583858 ”0:23 .88 "2:5 8:8» v.8» 87m: .0»: "32 .8» 888::

:22 8.: 2: a 288:: v :5 €888 :oz o

8328 m: 0:: 858:8 05 :8 88:» 88:80: 0::. a 20.0 V m :8 88:8»: 0:: 8:8 8:: 62885 0.8388: :85: :

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

0 8R. - - - - - :28
< 8:835
- o .83. - - - - a
- o 08. - - - - :
82:55.6
- - c :8. - - -
- - - u 8:. - -
- - - - 82.: -
o 8:. o 8:. o 8:. o 33:. o 8:. o 8:. m8:
.0 m8. :0 8:0. :0 SS. 0 m8. :0 :8. :0 m8. 8:
:0 N8. :0 $8. :0 $00. a 88. o :8. u :8. 8:
8m. 8%. 8m. 3m. 8mm. 38. 8o:
:8 > 8883:
8:8: 8:33. 88.8
-< 00:83:: 4:858:80 8:884:08”: -:0::00 :0:m=_.:<-0»< 862.880 m03::::>

 

 

.8588 8 :8: 8:8: :0 300:0 :05: :8 00:88 :8 585858 .008 8:8» .0»: .3 888: 2:28:85
:8 £020 :8 8:0: 3 80:8 :8 8:88: 828» 8%: ~23:: 8828 :0 A:.: 8:8 8:0 88:8: "8 0.8:.

116

.35 86 as a unseema c 2a usage»; 82 o
”382:an mm 82835 cum 6 .menHoEoo ”BE? .88 “owe .825» ”an?” 3-3 .owa 3&9 can» :0???
532—8 3 8a mofiacg 05 H8 33on 855%“ 05. n :odv m Re “58$:me 2a 8:8 v.26 68885 8_Eofio 30:5 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

c mvwo. - - - - - v. .
0 3mm. - - - - - 02m
0 £54 - - - ‘ - - dad!
a m 8
- :E. - - - - N
- movm. - - - - - H
flag,
- - o mmmo‘ - - - 483'
8
- - - o 98; - - oifium
Hugo
- - - - - - Ewe
- - - - - - $-mm
- - - - £va - v99.
- - - - veg. - $1 >
6533 em
0 moms. u 83. o axon. 0 Sch. 0 SP. 0 coon. mama
a snug. mmww. wwG. u 3%. n 8%. c whmo. Na
mwmm. Row. Row. $.31 Sow. $9.. 52
gm mmmm. %dm.‘ whom. 5 mm. whom. amm.
H8? 5%
llnofi:.€< Bum=€< Bas€<
-m 8:8sz -bEEBEoU Bu:.€<-8«m -5950 Ba:.€<-om< 853.823 833:3

 

.8535: .8

.89» Exam—£3 he 38:». .35: .5 85:85 can .EEicEcu .88 £88» Jug 3 @8253 2:52:65 can can he 28.»

a. 3 a: 3833 .5 8:35: @3335 E558 gas—88a 385.2% .5 a; 8:8 me? 83:25:: “2 2.3.

117

42,2 85 as a 688% u 25 359:2“ 82 o

”88:88 3. 8835 can no 5658088 ”823 .88 BEE .885» $8» 5T3. ans ”3% .88» comma?
”36:8 8 8m .8285; 05 BM 3:on 8:888 25. n "86 VA 88 “585:?" 8d 838 £60 .3885 Sméofio 82.5 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ma: - - - - - 25
< 883:

- :8. - - - - m

- 8mm. - - - - 8
365858

- - o 3%.. - - - “.85
8|

- - - o :5. - - 22.8
809.50

- - - - 8N: - 8-8

- - - - - - «can

- - - - - - $9

- - - - - - 3:
m3

o 88. o 88. o 88. 0 98. c :5. o 05. 82

o 2:. 0 ER. 0 88. o 88. o 8%. o 8:. Se

2%. 8?. 33¢. £3. 3%. 89.. $2

$3. $3. 88. $8. a? 88. 82
88> coma—SE

8:33 87.33 was?
-< 8:835 -bEESEoU Ba:.€<-8mm -8850 353c<bw< 883.:ng 838.8>

 

455.35: E.

88.» 5:38;... .3 38:» 85c 88 8:835 25 565.888 .88 £85» .0? .3 6895.: 2.8232: can .82: 83

£3» me 85:3 .5 8585:. 52388: 82.28 355383 2.85328 .3 a; 8:8 88 use—ESE "E «38.

118

 

fizdamv. :

“83.35.:

 

 

 

 

 

 

 

 

 

Ea; 22 .N - - v56
- - - - 3-?
38.1853 .
- - - o bomb. $9.
68.3ng
- - - 0 8a. El
uw<
953.203 aoodmmgq $2.383 $2.383
u v23 0 EN? 0 8%.. 0 8K. 82
33$va aa._.§w.v $8.133 sawimofl
o :53 0 $2; 0 e :2 0 $8; 89
@3383 33.1853 Emi§3 $0333
0 28; o :3; o 35. o 88. 52
38.389 285.3%; Gownia. .v 39:82 .v
82. can. can. 2%. 82
382 BE BEES 382 35m @2362: 30> .5253

 

 

 

 

52o Ea own he a8» we

 

own go E8.» we :9: $3

 

 

§€E>

 

.35.: ES... 05 ms 533:5: .5 .39» Exam-E; no 38...? .55: n8

988:5...“ 383m 3.33338 3 @3953 E5 5:35:— 3305 £33825 .8 a... 838 m2! team—5:25 "mu 935—.

119

._o>o_ mod 05 .a Exam—Ema 6 v5. 35.518582 0 “30quan .m 39235 "28:68 .< 353% no .»=E€qaoo

“833 .38 316 £025» £020 and E3» no E8 E3» 3T5. d E8» no 53.. 82 .8“ E8» v0.3 .0? “33 can» gamma—vs

“36:8 an 98 33%;; 05 .8.“ 3:2» 8:20on 2:. a ”5.0 V n— he Baum—Ens Ea WEE $3 62865 832050 man—:3 a

 

 

 

 

 

984.9%;

- - - 0 2?. 2305282
Goo._.mmwm.v

- - - o 88. 035
88.153

- - - o 65. 550

m 0059—35
33.1333
- 0 $5. - - §=o

 

< 8:9sz

 

830. .mmmmd

Eggs;

$8.388;

 

 

 

 

 

 

 

8%. RR. - 0 3%. N
sawgmi sawhwosé Snagmwmg
mam. Sow. - u 8%. _
»:E€oEoU
AEQSdWMS 5m._.wo$.v
- 8mm. - 0 BR. Vega
8mm
fianfismi Gawdvmi 95$..2m3
- o 88. 2%. c mam. 220m
30:00

 

 

 

 

 

 

55:03 m» 03!».

120

 

Acowfi 63.9

5: .899

 

 

 

 

 

 

 

 

 

 

 

 

 

884V ~93 Sumo
I I I I 3-2
I I I 53 .893
0 ca: v3
53 .3wa
I I I o 88; Si
mmfl
~88. 5%: $84 .85 $2”. 653 $8. .53
u mac. 0 8%. 0 an? 0 ~33 82
9.9%. "$89 fine. £me ABS. .88; 59. £83
N3. $3. 2:. £3. 82
A83. .Swfi 98m. 683 28m. .58 $8. .583
$9.. a9. 8%. 89. 3%
92m. :83 8%. .983 3%. .829 82%. 983
3%. RS. 8%. van. 8%
382 Bi 38.62: .252 ii gamma: :3» SEE?
520 ES own we 38> no ammo $8» mo 55 v.84 833.5;

 

 

 

 

43.2: =3... 2: ma :3» sign—ca ac Soho .55: .Su £33195

ESE—Em ESESSm .3 @8953 ES 5535:. states-26 cam—=8 :e a; 33s.. mcuc townie—=5 "3 93:9

121

 

8:; .382

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

o 88. cab§§2
I €84 €83
I I o 8;. 02:
I ANS; 58$
I I a $8. 550
m 8523:—
I 53 .283
o 83. I I 550
< 3533.5
$8. .33 95.. .283 an? 5ng $5. .853
a £8. 23. mg. 0 8%. a
6th .8me 5%. .823 as; 535 98.2 583
3%. 3.5V. 0 m8». SQ. _
§Eeoeoo
I $8.2 £33 awww. £23 658.1829
0 38. 2. gm. n Sam. fism
3am
I 83a. .33 I 624 553
u 52.. o 38. 220m
“OE—00

 

 

"€3.33 3 039—.

122

._o>o_ mod 05 .a .535:me c was ”iguana 32 0 “380888 .m 3% “23308 .< 39565 no .mefioEoo

"BE? .02: “2a.: .528» "820 v5 88» me By E3» 87: d E3» no 55 32 he 9:3» v93 69. "gm— ..3?» domain—3
626:8 3 03 83.353 05 .5“. 3:8» comeback 25. a Sod Va “8 Edema—Hm 2a not! 3.5 .3339: unstofio 9.2:: a

 

 

 

 

as.» .53 I I I
u 8.3. I I $-83
an: $83
0 :8; I I I I I Same:
as»: ow<l
3:25:28

 

 

 

 

 

 

 

 

”€3.58 3 03:9

123

 

85.383

68.13me

atagdfifl

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

0 5R. 0 Saw. 0 $8. 23E
.5950
92 5.de $85.35. s
cm»? Boom - - Eé
- - - - «9%
28.1853
- - - o in. $9
$34.95:
- - - 0 39. xi
ow<
$93on9 $2,933 wadamfi $5.233
0 Si. 0 ”an. u we: o 863 82
$8.5m: Ammwo..:3.v an... _ .033 3mm. _ .8me
c £8. u 9%. o :3. o 33. 82
535% $5,239 A3368: 5:52:
o 8%. c %B. 0 ma: 0 EN: 82
@38qu Sovdomfi $3.839 €3.35
58. 3%. u 3%. c Rs. 89
382 BE 33.62: 382 RE 33.62: “8» SE53
.520 can owm MO 38% we Nmm mo mug we can: 33 833.23,

 

 

 

 

.35.: .SE 2: ma Exams—ca .8 398% .55.. .8. £333.:—

EauEuumm 3:83ng 3 68955 E:— nouanaus “£ch 82:: 9.8.5 ~£55.59 E. :8 8:“.— ncuo toga—.55 "5 ~35.

124

._o>o_ no.0 on. 3 «58555 U can ugocimi .02 o “Eugen—Eco .m 8:235 "9:3ng .< 855%: no .bmfleofig
”BE? .38 BEE .525» £020 was 9.3» we 8m 38» 37mm a. $on no 55 mm»: .8 2qu v0.3 6”.“ 3&3 .58» 5.31:?
326:8 ms 25 832:; on. .8 Knew 8:232 2:. 3 :90 V m Eu 335%; 2a 39: ago .32365 35,350 32:: a

 

Amadfiommgv

 

 

 

- - chhmfi I 225%.,“
32.1229
- I 0 $9.. - 223E:
“06:00
3.65558
2mm.1osm.v
- o 2%. - - 550

 

< 8:83:—

 

83.1203

2 Siam;

$2.539

 

 

 

 

 

 

- 0 $8.“ 0 mac. 0 33 N
$8.383 Abmoaimd g: .Niod
- o 38. £3; u «33 _
3655800
29a; 8: .V 333.5% .v 591$me
c :8. u 29.. - 0 $3 5%
comm

 

 

 

 

 

 

"€3.58 S 933,—.

125

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

236.30.: axing. :
8mg Moog - - g8
- - - - 3-2
350.35% fixtmwod
- - 0 wow: u $8; $3
€84,803 $3.33
- - 0 NE. 0 8mm. 3:
nom<
68.1353 85.583 82.3me A8362?
0 2 S. 0 amp. 0 ER. 0 83. 82
as . _ .89; $8. _ wow: 6mg..ooov.v 9.8. _ «5.3
0 SE. 0 8:. 2%. .0 $8. 82
82;.83 $85.6me @amm..§§.v 8%;va
3%. 8%. was“. $8. 52
sapamgv among: 5 $80.33 agnébfi
$9. 8?. 83. mam. 82
382 :35 8,362: 382 Em 8.3.62: :3» 85223
520 E; %O 38% no owm we 38% we :9: $01— moEwtm>

 

 

 

.355 ESL 2: ma 533:5: :c .5?» Emma—nus .3 88:0 .55: he anumuoa 2.35:“? 3.353% .3

‘83:; 25 35.55: baa—mafia: i828 Baas—mafia 38:3:23 E. :6 832 m2... noun—52:5 "3 ~35.

126

._o>o_ mod 05 as Edema—Em a EH 3505:»? .02 0 ”380588 .m 85:53 ”83:68 .< 85:35 6 .mefioEco

"233 .32 "oin— .._ov=ow row—o an: E8» we 8% E3» 373. on E3» no 55 mm“: .8» ES» 3.3 .0? ”32 can» domain—ca

332—8 ma 2.. $335; 2: 5.. 3:2» 8:952 2: a Sod V n— ..8 Enema—ma 93 8:2 £45 .3322: 83.558 mun—=3 a

 

 

 

“coco;moom¢

- - - u $3 23328:
Aofim;.nb~mg

- - - ovaw 02m
AVmw.~.mo¢v.v

- - - omo_a. .ogxu

 

m 8:335

 

Aofiv.~.ofiob.v
onowm;

_o;xu

 

< 852:2:

 

Awmnm;~m__g

Ammvm;woofig

Aommv;m_o_¢

Acmbv;bm__g

 

 

 

 

 

 

 

owow. mfiofi. “gem. cam“. m
mwwOm;Nnmmg Amvnv;wmvm¢ A~_mm;oommg A_omm;wwmmg
c_om. momm. movm. mwmm. _
bBéoEoU
Amfi_;.mmo~q Amoog.ovomg
- oewbv. - ochvc. xogm
00mm
AmomgwfimOFQ Abmm;,mooh¢
- o 88. - o 88; 225m
.5956

 

 

 

 

 

 

"€3.58 2 2:5.

127

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

onwovHVoono N 83 afieosaotoucoo
85.3382 m 92 8523510200
89¢an “86 M 9.3 Sumtocaoo
85.3382 N 83 avail
6950 5:: 550825
Shovmvfimd w 3: 5658582424311
onwovmvsfio S 8”,: 0%
85.3383 v 32 8§*=o§_§<
$53382 v 83 $898253
803383 w § .3 ”$23253
commmmfivax 5MB 8:088:—
o=_~>-m Eocooc mo moommwn Emmam-EU ago oEmtm>

 

 

 

 

 

can a: 88.» we 8 a: 3532. .Su 9.2.5-30 E «9:50 “322E. 33389.5. .3 523:5 "3 ~35.

128

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

oomd V a V owmd N 35d ofio_c02*b€m€o~=oo
oofidvmvfiod a $3 8§* “65858
o2 .o v a v owed N m2 .m Houzomkzvmfiofioo
5655:80 55 530885
09 .onVomod N ~86 %EOEoU*mm<|.
SmonvOmfio _ mad 0%
Snovavfimd _ 83V 84%
353382 _ om; 5%
o < 53, 230825
ommdvavoed w med 36385983!
Rodvmfiveod v 3.: 0%
Shovavfimd v \ m2.“ 82*8353
Padvmvfiqo v 23 520023353
8m.ovgv%~.o v :2. $53
=ofi£Ec< 2:3 :ouofiefi
on??? Eovooc mo 32wa BusmWEU E owSfiD 033:3

 

 

 

 

 

on“ me was?» me :2: 98:. 3532. 3.. 0.5.5930 5 owns—.0 “REEF £33585. .3 553:5 5N «Sun.

129

 

8m.oquom~.o

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

w «New 8535* “63858
cmmd V a V o2 .o N Sud omm*b§€oEoU
o2 .0 V a v 086 m Ema 5950... 638800
op.ovmv8m.o v a? a
£282.50 55 88885
ammonvSS N 23 >3
oofioVaVomod N 39m 8:83:7023
Sodvmvgd fl Sod %«ml
omovaquo a mid omflmowmll
comm 53 5:22an
madvsoad w 33 §Eeoeoo*%
036 V a V 09 .o S :52 35:27:23?le
mad V a V omod v pod oomMEBmmmEEx
cow .o V a ommd v 03.4. 5300223?va
80on v 82 w 5.x 43%
=o_mm_Ec< £3 5:088:—
83?“ Eocoot mo moowmwa Busmméo E mwfifio oEatm>

 

 

 

 

 

on: no E8.» 8. 8 a: 3533 he Ea=am.EU E owns—U Hagar—89:30 93an a: £5.55: SM 225—.

130

 

 

 

 

 

 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Ombd V a V 8m .o N 8N; oho_uo§*§|E€oEoU

opovgvoomd N v85 ou§*§2eoeou

omhvavSmd N 9.3 3880

638800 55 8:228:—

036 V a V nNod N 8V6 :EfioEoUE <

oomd V a V ommd fl vavd ogomvoszw<

oooanVOmhd H God oomM*ow<

8nd V Q V OmNd _ Red hoccoo*ow<
H035? g

8%ng v om; w 83 Eaeoaooéefieg
ammonvSfio v BE 0%

com .o V AWV OWNd v mmvN oo~m*:o_mm_Ec<

omod V a V ooad v awe; gov—BOEBEEE‘
oomdvmVomNd v Now.m 3%
[5%

039d 8030c mo 88on 8m:mm-£0 E owaacu Egan;

 

 

 

 

 

can .3 28.» me .55 22: 35:2. .8. 25.5-20 E onus—U 83.3.5855 25:5 .3 5.23:5 "NN 035—.

131

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

o2 .o v m V owed N_ of .2 uofihsmarcoammefii
onwovmv 89o v mam a
cmNvaVoSd v End 52%
emNdVaVoowd w 250 a
; coafleg. 53, 85885
cow .o V a V omNd w mobs =o_mm_Eu<* :EfioEoU
85.0 V a V 8nd v SmN o <... :EfioEoU
33qu ES m 252 8:835... 65858
mood va Sod N va.N_ 5300*.5658800
omodeVooQo N 8N6 oo§*§l
3655950 .23 88885
Sigh Egon: mo $0..wa oE:mm-EU @525 033:;

 

 

on: .3 was?» we 8 a: 3:3an 58 9:35.30 5 swan—5 8.5.8.9 3.5.3 E32 358.50 .8 53355 "nN 935—.

132

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

oomd V a V omNd v 83. u§_82*=o_m£Ec<
85.on v 82 w 83 56353

Sadvavomho V SS H8598???
%fiovgvoomd v $3 3
tr :BmEES‘ 53 8:22an

80o V m V cmNd v $06 :8? =o_mm_Ev<*oo~m

coho V a V cmNd N as: EEEoEoUEonm
863383 fl :2 a
8m.ovavOmN.o H E: [0%
mNoanVSOd H N86 hocaowuwooflml
08¢ .23 530885
omNdvavSfi .o a wmva §u_eo5oo..mm<|
863383 e 83 so» SEEEEW
853382 H mm; [0%
85.3383 _ 83 52090.31]

85.3382 H Ed 8&3?
mm< 5? E5082:—

o:_w>-m Eovooc No 80.1de 2w: $-20 E Mmflwdo oEmtm>

 

 

 

 

 

on: .3 Eu?» me :2: 98:. 3:05am you 9:35.30 5 onus—U 3:286 magma tori E3930 he 55355 #N 035.

133

 

 

 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

oomd V a V cmNd m N2 .0 85:35,. “6:58:80
Snovmvond N SNN 83:. £3858
omNvavOe .o N Na; agooazaenfiolul
\ 3:938:50 5S, canon—85
853383 w wmmN $258509» <
ogovmvoog o a: a
8w.ovav%N.o N NwoN 0%
Sqovaomfio N 0N; 52%?
o < 55 couofiefi
8m.ovav%N.o w :3 565:3
mgovavfiqo N: MEN i3
3:338: v RNd 8%
Sqovnvofid V 8: HoocooEolaalefl
$9on v mNod w Naé mmfceésg
tr commmmEv< £3, 83885
03?: E082... No 883D 0545-50 5 MMSEU 032:3
oua .3 E8.»

we 3 a: 3:33: :8 9:55-30 :_ owe—«:0 mafia—nc_w:< b.3980 3552888 38:33.3.— ..c 553:5 "mN 035,—.

134

 

 

 

  

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

conovavode N E: 0382... 55558
89o V a V cmmd m woo.“ comm... :EfioEoO
8nd V a V Ommd N 9 Nu 6200*bfifiofioo
EEBSEoU 55 5:09:85
ommd V mv OS .0 N 2 m.m mefioEoUEw’w
omdeaVoomd fl N2 .o 050m82§om<
8:338: _ NEN oo§*om<
oP.ovmv8m.o : 2.3 5%
mw< £5 :28825
Smovmvofld w 8% 36543
ooad V a V omhd v won; o§_82*=omm£:6<
3.33%: v $3 a
$5.0 Vd V omad v owed 5:50.13
813383 v $3 4%?

 

 

 

33>:

 

Eovooc .3 89on

 

 

.9 :ommmmEEN. 53> 850885

 

usamméo E owsfi

 

03E;

 

 

on: a: v.8»

me :2: 95:. 8:33: :8 9:35-50 :_ mug—.0 “mama—:cmu:< #8530 3352829 38:8..on a: 55355 new 033—.

135

.35 mod 2: a “58$:me u ea 9.85:? 82 o a .Eaeoes

ER ”233 .88 SEE qocuow 3:3» 873. .oma ”33 :8» so??? 332—8 3 2a 83~E>
05 8m .32on 85.8%.— 2F n ”Ed V m H8 Encamcwu 2a 838 max. .Bfiomcfi 3.5.858 33.5 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

38. - - - - a
Em. - - - - _
$2.558
- o 89. - - - ~85
- - 3%. - - oaaom
.5950
- - - E: .N - $8
- - - 3.3 - $3
- - - ~22 - $9
- - - ~33 - «I
03
o 8:: 0 £8. 0 Ex: 0 83. o 83. 82
can: 382 one: £82 £82 82
0 3a. 0 88. o 28. o 9.8. o 88. 82
£3 £8. 83 En. «new. 89
5% :OmmmmEc
32.3 332
-bfieoaoo 3333““ -328 8.3.2.0? 3288: 8359

 

 

 

 

 

 

 

A8335:— 5 .39» 5mg: .3 38....» .85: 3.. aging—=3 can .39. cuts» 6? E 1895:“

£33315 ES .89“ =a 889a .3335: .382: 333825 .8 ai 83a.— 3? €895.25 RN 035—.

136

.33: 85 as 3 “58558 c 2a 3.382% 82 o a 58.358

88 ”323 .88 6:8 .630» ”88» 87m» .owa ”33 .88» :23qu 826:8 3 8a 838g
05 88 3:8» 8:888 2F c Sod v m 88 885:me 8a 838 33 68868 85.85o «823 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Sea. - - - - N
2 S. - - - - _
36888
- o 28. - - - «85
00
- - 88 - - 32.8
58.06
- - .. Rafi - «who
- - - a3.“ - a»?
- - - 83.0 - 8-9
- - - an: - «3
M3
0 83. o 28. 0 $8. o «3. o 38. 82
was. 8:. 8:. 83. 8:. 82
2.3. :3. $3. $9. 82.. 82
39. $9.. 83.. an. 89.. 82
a; 8352
385 33.3
-afieoaoo 383-88 -528 Bmac<.om< 32.68: 8§E>

 

 

 

 

 

 

 

5.53:5: .8 .82» 5383 he 38...? .65: .5. bfiaéficu ES .88 .338» can .3 53253

38.3365 ES .8? =« 889a 8535.: 55.588058 8:83 :o a... 83:.— mEx. Pam—5.85 "an ~35.

137

42,2 85 as a asmema u as €85:me 82 o a éseces
93 ”BE? .08» ”2a.: Cow—Em 33% 57? 6mm 3&2 53» gamma—um 332—8 3 03 83mg;
05 8% 3:ch 8:20on 05. a ”56V m we 28:23». 2m 89E ago 68865 83550 32.5 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

0 Eu ._ - - - - a

38. - - - - _
afifioaou

- 0 NE. - - - x35
83:

- - c Em - - oaaom
How—.00

- - - 33mm - Sumo

- - - «$3 - 3-3

- - - ems; - «we.

- - - o «9.2 - 3:
1%

£3. 0 88. 0 E3. 0 Ea. o 88. 82

2?. 0 8K. 0 an“. u 2:. o 8?. 82

m3. o 85. o 93. o 83. 0 mg. 82

RS. 25.. 2:. ~81 GS. 82
so» 8353

383 32?
-bfieoeou B.m=.e<-8& .328 333.»? 33.68: 83~E>

 

 

 

 

 

 

 

£8235: :c .39» again: a: 58.5 .55: 8.. 583.888 ES .83 .865» Jug .3 ©3253 3.33.5.3
can .8»: =a 89.8 5:35.: «:53» 2.9.3 but: E388 E. a... 838 m2... 36:?83 "am «Sun.

138

.35. nod 2: “a “58¢?me v 23 £chme 82 o no $339888
23 ”SE? .092 638 53% and?» STmh Jam ”32 :3» so??? $338 3 2m 83mg;
05 H8 3:8» 8:80.?— ofi. a :odV m 8% 285:? 2a moun— mvco .3322: 85.650 32.5 a

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Ru. - - - - m

omhw. - - - - fl
$288.8

- o 3%. - - - ~83

- - o5. - - unsun—
H0950

- - - 28.~ - «we

- - - o3? - «can

- - - 8:3 - 3-9.

- - - 88a - 11
«3

32.. u £8. c 3.3. u an“. n 2E. 82

$3. 88. 3e. 88. $8. 82

89.. 53. 8:. as. £8. 32

awn... 83. 05. 29. 82.. 82
3.» SEEE

38:2 383
-bfieoeoo 333-8% .388 33.2.»? 33.62: 8§E>

£335...

E. .39» gamma—ca .8 3820 .65: 8.. 583.838 2:. .33 .865» .0»: .3 6395.: E56355 ES
.8»: =: 883 mama—:8»: 3328 35822.8“ 38:359—2— E. oi 8:8 n25 team—5:3: 5n 035.

139

Table 31 : Unadjusted and fully-adjusted odds ratios 39" on thrombolytic therapy

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

utilization across all ages.
Variables Unadjusted F ully-adj usted
Admission Year
1990 .3632 .3468
(.2496, .5284) (.2373, .5066)
1991 .9799 c .9799 c
(.7309, 1.314) (.7267, 1.321)
1992 1.1037 c 1.1217 c
(.8318, 1.465) (.8405, 1.497)
1993 .9897 c .9940 c
(7427, 1.319) (.7415, 1.332)
__Age (years)
1-44 2.6941 2.1564
(1.753, 4.140) (1.374, 3.383)
45-54 2.2439 1.7386
1.586, 3.175) (1.204, 2.510)
55-64 2.8521 2.3775
(2.114, 3.848) (1.736, 3.257)
65-74 2.1216 1.9457
(1.574, 2.860) (1.433, 2.642)
Gender
Female .7171 .8333 c
(.5844, .8806) (.6717, 1.034)
Race
Black .7321 c .7226 c
(4604, 1.164) (.4498, 1.161)
Comorbidity Index
1 .5193 .6068
(.40311, .6689) (.4649, .7920)
2 .3779 .4567
(.2517, .5673) (.3003, .6946)

 

 

 

 

 

a Unless otherwise indicated, odds ratios are significant for P < 0.01; b The reference
groups for the variables are as follows; admission year, 1994; age, 75-101 years;

gender, male; race, white; and comorbidity, 0; c Not significant; and d Significant at
the 0.05 level.

140

Table 32: Unadjusted and fully-adjusted odds ratios 39" on cardiac
catheterization utilization across all ages.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Variables Unadjusted Fully-adjusted
Admission Year
1990 .4552 .3758
(.3538Q8SD (.2856, .4943)
1991 .4622 .4027
(.3608, .5921) L3073,.527¥8)
1992 4788 .4316
(3754, .6106) (.3309, .5629)
1993 .9164 c .8877 c
(.7133, 1.177) (.6761, 1.165)
Age (Lears)
1-44 6.7780 5.6866
(4.611, 9.964) (3.788, 8.537)
45—54 6.1827 5.0931
(4.676, 8.175) 43.773, 6.876)
55-64 5.2177 4.6146
(4.137, 6.581) (3.602, 5.912)
65-74 3.8422 3.6276
3.092, 4.775) (2.890, 4.554)
Gender
Female .6738 .9395 c
(.5752, .7893) (.7856, 1.123)
Race
Black .7016 d .5814
(.5029, .9788) (.4030, .8391)
Comorbidity Index
1 .4271 .5748
(.3553, .5134) (.4686, .7050)
2 .2759 .3670
(.2117, .3598) (.2741, .4915)

 

 

a Unless otherwise indicated, odds ratios are significant for P < 0.01; b The reference
groups for the variables are as follows; admission year, 1994; age, 75-101 years;

gender, male; race, white; and comorbidity, 0; 0 Not significant; and d Significant at
the 0.05 level.

141

Table 33 : Unadjusted and fully-adiusted odds ratios 39" on coronary artery
bypass grafting utilization across all ages.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Variables Unadjusted Fully-adjusted
Admission Year
1990 .4751 .4587
(.3414, .6611) Q3286, .6402)
1991 .8429 c .8845 c
(.6321, 1.123) (.6610, 1.184)
1992 .7527 c .7393 d
(.5647, 1.003) (.5529, .9884)
1993 .9769 c .9382 c
(.7413, 1.287) (.7093, 1.241)
Age (years)
1-44 1.50000 1.6218d
(9535,2360) (1.012, 2.598)
45-54 1.5987 1.6651
(1.138, 2.247) (1.161, 2.387)
55-64 2.0305 2.1028
(1.524, 2.706) (1.556, 2.843)
65-74 2.3061 2.3762
(1.753, 3.034) (1.795, 3.146)
Gender
Female .8144 d .8469 c
(.6679u9931) (.6887, 1.041)
Race
Black .7247 c .6886 c
(.4596, 1.143) (.4341, 1.092)
Comorbidity Index
1 .9660 c 1.0827 c
(.7695, 1.213) (.850’L 1.378)
2 1.1412 c 1.3587 c
(.8406. 1.549) (.9836, 1.877)

 

 

8 Unless otherwise indicated, odds ratios are significant for P < 0.01; b The reference
groups for the variables are as follows; admission year, 1994; age, 75—101 years;

gender, male; race, white; and comorbidity, 0; 0 Not significant; and d Significant at

the 0.05 level.

142

 

Table 34 : Unadjusted and fully-adjusted odds ratios a,b on percutaneous
transluminal coronary angioplasty across all ages.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Variables Unadjusted Fully-adj usted
Admission Year
1990 .4623 .4182
(3.478, .6145) (.3098, .5645)
1991 .4678 .4073
4.3544, .6175) (.3035, .5466)
1992 .6689 .6446
(5174, .8646) £4901, .8478)
1993 .7586 d .7457 d
(.5892, .9767) (.5693, .9767)
Age (years)
1-44 3.7075 2.6881
(2.466, 5.572) (1.753, 4.123)
45-54 6.2114 4.6243
(4.531, 8.515) (3.302, 6.476)
55-64 4.4166 3.5656
(3.308, 5.897) (2.626, 4.841)
65-74 2.6063 2.2841
(1.948, 3.488) (1.690, 3.089)
Gender
Female .7860 1.1382 c
(.6558, .9421) (.9318, 1.390)
Race
Black .6854 c .6154 d
(.4523, 1.039) (.3955, .9576)
Comorbidity Index
1 .2826 .3575
(.2196, .3636) (.2744, .4656)
2 .1667 .2085
(1067, .2606) (.1318, .3300)

 

 

 

a Unless otherwise indicated, odds ratios are significant for P < 0.01; b The reference
groups for the variables are as follows; admission year, 1994; age, 75-101 years;

gender, male; race, white; and comorbidity, 0; 0 Not significant; and d Significant at
the 0.05 level.

143

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

0%.onng 3. Es serge]
Seovevfiod a $3 a
lame as. ea
omodvaav Rod N 83 call
2:.on v owed a as; been? “63858
Shavmv ommd w sod mw<s§aec5co
3638500 55 8:08an
Shovevfimd a $3 coasts???
owed V a V 0% .o v omv.~ coccuwaaommflefiz
omNdVQVoofio E wNVdN a
owed V m V mmod w cow . m m QEEeEoUEoEflEc<
Seas? swag
039d :5ch mo 82on 0323-20 5 omfifio Spawn;

 

 

 

 

 

Baa E. 39.3 Eggrfiu 5 ens—:0 “382:. £3.35; he E5355 ”mm 03:.

144

detuwaffiairflh .. 1......» his...

a!!! snag! sunfish...

l»! - . x . t it
.. . x . .: , ”.5».a_.

l. I 11.111111.

. . ....-.t.«.u_C.~w¢~.~ .

it‘vlrj

ESE.

   

,u... ,a... you?)

t .. Il‘.'l..rt'l II.

.R ... to ... U...
.1 0.1.. . a

 

   

.
.
- t I. . . . . y. . n...“ fiwnthflf. fluke]
. .r. .. MM...
11.. .~.. . .
t1. . . .t . .5....
v‘ .I. ..n .. 1.1.. $3.11....“ .V .s ..
t a . l . c 1.. l-..— . v. .
C 'I‘
g r v.

 

 

8nd V a VOmNd

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

_ we» . _ coccoosoonm
08M £5 53082:—
madvq v83. a mad negate?
8%on v82 e 8e... cce|m|=coto <
o < 5:; 530385
85.on v82 N 8: ceeecoEfiecEcu
o2 .ovavaod m 25.2 $3363.28
oood v m v £3 a Sod cougabssscso
£29950 5?» .5308an
omeoqusod a 22. 52822253
omNdvevOS .o 8 six engages?
Sod v a v own .9 w mmw .v bfifiofioutcemmfleg
8%on vow; a 22 Seats???
1. =06£Ev< 53 530825
039,5 Eouooc he 82on oaazmméo E omSEU oEaE>

 

 

 

 

 

 

 

8»: =a $9.2. Enigma—5 E 99.25 ”Effie—82.30 cam—:50 he 553:5 "on 933—.

145

...VJ ..

115.1!E..:.1 e. .....-t... _ .

.28.”

l. .11.! v. [WWW-‘5‘»; .

1-10:1! .11.I.

 

 

     
  

     

  

 
  

71--....19 . - . ”1,111.3”. . .
. _ .. .. 4:... . - - ..--.. 135.9:

m . 1.7.9.2....u .3... gm . ......

                

 

t I..t..¢'ll

eds... .... 5.880

.I' 0.1111.

3.». . . . M1309

_ . .. ...ufl.-....m...c.z.....~
, .. ....H... «1.53.;

, t, t «vigwctwslit. _
r. .. L11...N.Me¢. ., . .. fix...

'1: to. . .

1 1 1.1.1.

.. .. .57....

  

.1111:- l

 

{"11

7321.13» . .

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

803333 _ 83. 152.0%
08¢ 55 530825
%fioanS. .o v 83 0%
2.32.535 v ~85 .85de
o < 53» 83082:.
oe .ovAH Von; N 83 528.565.38
cmngvSno m wan $5565.28
02.338. .o N S? Bamazzeoeou
365.850 .23 5:082:—
25va Vow; v $2 52.0%
83v? mad 2 :38 3
25.3383 w 83 36.9.2898???
8a.ngVoP.o v 23 855%
cofimmE—z 5?» 550885
263..— Eovooc Mo 82wa assuming 5 any asst—g

 

 

 

 

 

“on: =a 89.8 2.5—$-50 5 owns—.0 “baa—nomflJ. E5550 35539.2... 38:3:th no 553:5 Rm 635,—.

146

..r...
DI. - ‘h
’3')? r :0 s

tI'VAU, ti.l\.!'

, r

Ito {vl’V “:3r(.|,..
"L9"~ .v.l...pt

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ommdvmvsfio v was 0850?

853383 v we.” 523...» <
oohonVommd w Sad €2€oElo9Mm<l
mw< .23 55825

Smd V a V ommd v mom.m commuxcofifleg‘

ombd v m v oow .o v awe . N 5200* :o_mm_Ev<

85.3383 2 £0: omfcefieg

awhovmv 82 w $2 afieoEoquEEE
SEE—3‘ 55 530885

nigh =5ch ‘8 moohwwm 2d: WED E o :20 033:;

 

 

8mg =a v.83“ 85.5.30 5 yuan—.0 mun—EEO $3.3 Devi b.5980 no 553:5 "an 035—.

147

APPENDIX 1

      

3*

‘ ‘6’...“ ..‘.o-

.2’ .. 7- “7. :A

 

~

I

, .

V, -
, .‘
u . 1‘
I ‘h V
D “il"'t
I‘ -

g _

-‘ M9 an
4. ., .

. a» .
.~ ,M: _’

..x

u ,l
.| ‘

g.

 

 

Deaths per 100.000

i White male

Black male - ‘ ‘

   

 

Black female

 

White female

 

 

0‘
19801981198219831984198519861987198819891990
Year

Figure 1: Age-adjusted death rates per 100,000 for ischemic heart disease by gender
and race: United States.

Source: Gillum, RF. Trends in Acute Myocardial Infarction and Coronary Heart
Disease Death in the United States. American College of Cardiology 1994; 23: 1274.

400-

Men

300‘

 

  

Mortality (per 100.000)

01.11 of hospital

  

 

30 I I I I
1970 1975 1980 1985 1990

 

Figure 2: Trends in Mortality Due to Coronary Heart Disease from 1970 to 1990,
According to the Location of Death, among Residents of the Twin Cities Area Who
Were 30 to 74 Years of Age.

Source: McGovern PG, Pankow J S, Shahar E, et 3.1. Recent Trends in Acute
Coronary Heart Disease. The New England Journal of Medicine 1996; 334:886.

148

milk”
..m w

I?

   

[W1 01 U" V} via-.5 Lax1 “an-J4 1.5. ”21$ f AU M“
ed?! 53.": ennui :uw'l :48 :c- l;.1.- m mums msfl b

9199‘ 0:10am.” waded is P " mien}: 11w M.
938 231391?! arr-mast! 30:21. i . 5de all“? '

 

 

Number (thousands)

I Bl/Pass E Angioplasty ..,,__

 

 

1985 1987 1988 1990
Year

Figure 3: Number of coronary artery bypass graft (ICD-9-CM 36.1) and coronary
angioplasty procedures (removal of coronary obstruction, ICD-9-CM 36.0): United
States.

Source: Gillum, RF. Trends in Acute Mycardial Infarction and Coronary Heart
Disease Death in the United States. American College of Cardiology 1994; 23: 1276.

Thrombolytic
therapy

PTCA i

 

 

0 2'0 4‘0 60 8b 100
Patients Treated (%)

Figure 4: Trends in Acute Medical Care for Residents of the Twin Cities Area, 30 to
74 Years of Age, Who Were Hospitalized for Definite Acute Myocardial Infarction in
1985 and 1990.

Source: McGovern PG, Pankow J S, Shahar E, et a1. Recent Trends in Acute
Coronary Heart Disease. The New England Journal of Medicine 1996; 334: 888.

149

. “Xv,
ISVM": . . '1

      

, .w. 56-.TM‘H
.. - . -. , ”rpm“. '5'}.an-
. Ah”? ( ‘ W“ -}m 1” .’
r , a , .

.9 _ A _' Q“ ,1. 3317': .' {WI-chad} “it.“ w

 

 

FIGURE 5

    
    

 

 

 

 

AMI ADMISSION BY AGE
1990-1994
I I AGE
I 75101
E E 6574
m 5564
- 4554
' ' - - [II 144
199° 199‘ 1992 1928 1994
AUVISSIOV YEAR
FIGURE 6
AMI ADMISSION BY GENDER
l 990- 1994
ml
E ml
43' GHQ]?
23- E] ME
I Fame

 

 

150

 

 

FIGURE 7: % 65 YEARS OF AGE & OLDER
AMI ADMISSION BY INSURANCE, 1990-1994

1CD|
g):
ml
70!

ml
ml
Ql

 

 

 

 

so" INSLRAME
:: I MEDICARE
0 - - e _ r CI ALONE?
1990 1991 1am 19a; 1994
AUI/ISSICNYEAR

FIGURE 8: % LESS THAN 65 YEARS OF AGE

8

WIT
8888858

.3
CO

 

 

 

19:30 1991 7 1532 1593 1994

ADVISSU‘I YEAR

151

      

tandem _

 

1

 

 

FIGURE 9
AMI ADMISSION BY INSURANCE, 1990-1994
100‘ 1115mm:
83' I moo-mm
E 001mm.
E memo
I moms
I: PRIVATE
MOTHER

 

 

 

1% 191 1g 1% 1%

ADVISSICN YEAR

FIGURE 10
AMI ADMISSION BY RACE, 1990-1994

PERCENT

 

 

ADMISSION YEAR

152

FIGURE 11
AMI ADMISSION BY COMORBIDITY
1990-1994

 

1G)

ml

ml

 

 

 

 

 

 

 

 

or

 

 

ml

 

 

 

153

 

 

FIGURE 12: % RECEIVING THROMBOLYTIC THERAPY
AMI ADMISSION, 1990—1994

20- IRecEIvamz

 

 

n , , DDDNOI’REDEVE

 

FIGURE 13: % RECEIVING CARDIAC CATH
AMI ADMISSION, 1990-1994

OARJACCA‘n-I
Inacavaaza4
CIREZENEZH
MDDNOTREENE

 

 

154

 

 

...H
M
.. p
m.

.\. .

NH

FIGURE 14: % RECEIVING CABG
AMI ADMISSION, 1990-1994

1113'

ml

E:

ml

 

 

0|

 

1% 1&1 19.12 1% 194

ADVISSICN YEAR

FIGURE 15: '% RECEIVING PTCA
AMI ADMISSION, 1990-1994

 

 

Inmavanz

 

 

 

- _ _ CI DDNOTREEVE
mo 1991 m2 1993 1991

AUVISSIOI YEAR

155

 

. 1mm»?

 

‘. ..I; v.
1%.”: . .

a... ...
.....1

. . .

.. .. w.

‘2

u r. .
.1» l.
4... .
:2 - .

 

1
I
1 .

1‘.

.1? ‘ he. I
:3

.
. 5:53:37: '5 l” 3f

1.
."

 

1am it"-

  

 

FIGURE 16: % RECEIVING THROMBOLYTIC THERAPY

 

AMI ADMISSION BY AGE, 1990-1994

 

   

.. x... . 1.......................... ... ....
, ................ . . . . .. . . . . .
.............................. m

 

AEMSSKNYEAR

FIGURE 17: % RECEIVING THROMBOLYTIC THERAPY
AMI ADMISSION BY GENDER, 1990-1994 ’

 

 

 

 

 

 

 

 

 

ADi/ISSION YEAR

156

 

FIGURE 18: % RECEIVING THROMBOLYTIC THERAPY
AMI ADMISSION BY RACE, 1990-1994

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1o| . MOE
I Iapae
o. _I__ __I [:Iw-nes
19m 1991 11m 11m
ADWSSICNYBAR

FIGURE 19: % RECEIVING THROMBOLYTIC THERAPY
AMI ADMISSION BY INSURANCE, 1990-1994

 

a: II‘SLRAME
Imon-aa

%PRNATE
Iwmcme

 

 

1

 

 

 

 

N
\;

/

 

 

 

157

 

 

FIGURE 20: % RECEIVING THROVIBO THERAPY
AMI ADMISSION BY COVIORBIDI'IY, 1990-1994
3)

_ T

 

 

 

mm W
“1
.2
Clo

 

 

 

 

 

 

 

 

 

 

an 191
AWSSWYBAR

158

 

 

% RECEIVING CARDIAC CATH

AMI ADMISSION BY AGE, 1990-1994

FIGURE 21:

 

 

 

 

AEMSSICNYEAR

FIGURE 22: % RECEIVING CARDIAC CATH
AMI ADMISSION BY GENDER, 1990-1994

 

 

 

 

ACMSSIONYBAR

159

  
   

1' ¢ '

l!
r'PIuJCIA nu ' '

I

 

_, , - . Kit-JD“.
.,, ,. .. *1:qu INA

   

71/45 1' ‘KI’«3«11.6

 

 

AMI ADMISSION BY RACE, 1990-1994

FIGURE 23: % RECEIVING CARDIAC CATH

 

RACE
.aAoKs
_ Dw-mss

 

 

 

 

 

 

ILII

 

 

mmmmmmwo
g

194

1

Q1

1

19m

Am YEAR

 

 

 

§§§§

I
_===.__==_==_===_=====_

1Q

AWSSICN YEAR

§§

191

§\\\\\\\\\\\\\\\\\\

1m)

V\\\\\\\\\\\\\\\\\\\\\\\\\\

FIGURE 24: % RECEIVING CARDIAC CATH
AMI ADMISSION BY INSURANCE, 1990-1994

 

 

          

160

 

A
.__.
é
,

|
‘( kmw
-_:-_q-,~. -

.' A"

l:

"-43
{I

 

% RECEIVING CARDIAC CATH

FIGURE 25
AMI ADMISSION BY COMORBIDITY, 1990-1994

 

 

 

...-1......
..-

 

 

 

 

 

 

1Q
AUVISSKN YEAR

1

161

 

FIGURE 26: % RECEIVING CABG
AMI ADMISSION BY AGE, 1990-1994

 

AGE
.1-44
.4554
.5664
@544
D5101

 

 

 

FIGURE 27: % RECEIVING CABG
AMI ADMISSION BY GENDER, 1990-1994

8

 

 

 

 

162

   

II I’IIA Im“ I

u. -1:, .
~ v» .
. ." v n. ' _' ,
”I, ‘1 #313 ‘
5 ‘1. . .‘ ,
’~* 3 , ,

n"; ..'

b" ,. :- .
'IIII'g r , 3% 1
, l‘ ' b
:1, l

   

FIGURE 28: % RECEIVING CABG

AMI ADMISSION BY RACE, 1990-1994

 

 

 

 

 

 

 

 

 

 

AEMSSKW YEAR

% RECEIVING CABG

AMI ADMISSION BY INSURANCE, 1990-1994

FIGURE 29:

l‘BLRAME

.monm

Imam

%PRNATE
NEJCARE

 

 

Imam.
._ Dl-MQI-LTI-H)

 

             

:EEEE_a:z=E:_E:=_==_======_

 

:_==__=_==_======_===5:

_____.___________.___________======

 

_=___=___=_==_=_==_=====_==_=

 

ADVISSICNYEAR

163

 

I 4

   

.- «CIA INA
I;
I
I

 

n
w in 2 2,“:
., Q .. Jot ,

w 2 ._.:2..%r.:._., . -, 2,2

I I ‘.
, . 3 3.2V... .2 :_
r.. 35.5..“ .. -.
I I, .

V ,. Trev”. w“
_. .1222. .

 

3v. 2
.1»
I 2‘ w
.2 , y a
2 I . i
E .
, u A
_ .v
. .2 .

FIGURE 30: % RECEIVING CABG
AMI ADMISSION BY COMORBIDITY, 1990-1994

 

WOW INJEX

 

 

 

 

ADVISSDN YEAR

164

 

FIGURE 31: % RECEIVING PTCA
AMI ADMISSION BY AGE, 1990-1994

 

AE
I144
I654
I564
@1574
[175101

 

 

FIGURE 32: % RECEIVING PTCA
AMI ADMISSION BY GENDER, 1990-1994

 

 

 

 

165

 

FIGURE 33: % RECEIVING PT CA
AMI ADMISSION BY RACE, 1990-1994

 

RAG
I was

 

 

 

 

 

 

 

 

 

     

1Q

AUVISSICN YFAR

FIGURE 34: % RECEIVING FICA
AMI ADMISSION BY INSURANCE, 1990-1994

 

IBSLRANE
§ maria
PRIVATE
I NEJCIRE
I mo
I W
D I'MQI-LTH-r)

 

 

 

 

 

 

166

 

 

FIGURE 35: % RECEIVING PTCA
AMI ADMISSION BY COMORBIDITY, 1990-1994
50

 

__ T—

 

 

 

 

 

 

 

 

 

 

 

 

 

 

190 191

AEMSSKN YEAR

167

LIST OF REFERENCES

 

‘1'"- - -"

LIST OF REFERENCES

l. Margolis JR, Kannel WB, Feinleib M et al: Clinical features of unrecognized
myocardial infarction-silent and symptomatic: eighteen year follow-up: the
Framingham study. Am J Cardio. 32:1, 1973.

2. Solomon CG, Lee TH, Cook EF, et a1. Comparison of Clinical Presentation of
Acute Myocardial Infarction in Patients Older than 65 Years of Age to Younger
Patients: The Mulitcenter Chest Pain Study Experience. The American Journal of
Cardiology. 1989; 63:772-776.

3. Gunnar RM, Bourdillon PDV, Dixon DW, et a1. ACC/AHA Guidelines for the
Early Management of Patients With Acute Myocardial Infarction. A report of the
American College of Cardiology/ American Heart Association Task Force on
Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee to
develop guidelines for the early management of patients with acute myocardial
infarction). Circulation 1990; 82(no.2):664-707.

4. CDC, Trends in Ischemic Heart Disease Mortality, 1980-1988. MMWR 41(1992):
548-56.

5. National Center for Health Statistics. health, United States, 1992. Hyattsville,
(MD): Public Health Service, 1993.

6. National Heart, Lung and Blood Institute. Advance Report of Final Mortality
Statistics, 1990. Monthly Vital Statistics Report, Vol 41, No 7, Suppl, Hyattsville,
(MD): Public Health Service, 1993.

7. Gillum R.F., Feinleib M. Cardiovascular disease in the United States: mortality,
prevalence and incidence. In: Kapoor AS, Singh BM, editors. Prognosis and Risk
Assessment in Cardiovascular Disease. New York: Churchill Livingstone, 1993; 49-
59.

8. Goldberg RJ, Gorak El, Yarzebski J, et al. A community-wide perspective of
gender differences and temporal trends in the incidence and survival rates following
acute myocardial infarction and out-of-hospital deaths due to coronary heart disease.
Circulation 1993;87:1947-53.

9. Sempos C, Cooper R, Kovar MG, McMillen M. Divergence of the recent trends in

coronary mortality for the major race-sex groups in the United States. Am J Public
Health 1988;78:1422-7.

168

    
 
   
  
 
   
  
  
  
  

Ilf"0:"11i“! ...
" .' £111.4de
-I ”'.WI

1 :11! , ' '

‘ 4‘5nm'i H
. .1259"

":I-IZ'I MI

.' ‘ 'l" ."_111. '1 , a.“
‘ ' ‘ - ' . '. ' .‘ . . '2'; 1 ‘.‘~.;-"';-LI-'>fl‘ M
“I I -‘ " . " ' mfiil ..‘It.erM)li§

. ‘7 |._.‘-';‘ 2.11“” _' ,, ””1,.,, .' _ _ -,-u_ _; (1'1": L11 “fl; .u.
. 1 ' xiv-3.1..-'./:.1;;°.._..u~,;.-.. ‘ ': ‘ fir“. 27:/”.13: ban '-
-~..b«.1.. wad ware-91;.) -; ..2 f. (.42.).- ' WW1 3 ‘.. :'~ -u":. maintain” ' '

.=arm:€am."
’3,

:1 mm: moor. ed; 111”“ motif] M nun: v" ‘. UH «we )1 mm
211?“ Mm r068 15.12.153.11 m mm 13 new 91.4.1 W ”Nd
X

J-

aw.» ~~‘

 

10. McGovern PG, Pankow JS, Shahar E, et a1. Recent trends in acute coronary heart
disease mortality, morbidity, medical care, and risk factors. The New England Journal
of Medicine. 334(14); 1996:884-890.

ll. Asaf AR, Lapane KL, McKenney JL, et a1. Possible influence of the prospective

payment system on the assignment of discharge diagnoses for coronary heart disease.
N Engl J Med 1993; 329:931-5.

12. Gillum, RF. Acute myocardial infarction in the US, 1970-1983. Am Heart J.
1987; 113:804-11.

13. Roig E, Castaner A, Simmons B, et a1. In-hospital mortality rates from acute
myocardial infarction by race in US hospitals: findings from the National Hospital
Discharge Survey. Circulation. 1987; 76:280-8.

14. National Center for Health Statistics. Health, US, 1992. Hyattsville (MD):
Public Health Service, 1993.

15. Graves FJ. National Hospital Discharge Survey: Annual Summary, 1990.
Hyattsville (MD): National Center for Health Statistics, 1992: Public Health Service
(Vital & Health Statistics: Series 13, No. 112).

16. GISSI: Long-term effects of intravenous thrombolysis in acute myocardial
infarction: final report on the GISSI study. Lancet 2:871, 1982.

17. Rogers WJ, Baim BS, Gore JM et al, for the TIMI 11A Investigators: Comparison
of immediate invasive, delayed invasive and conservative strategies after tissue-type
plaminogen activator. Results of the Thrombolysis in Myocardial Infarction (TIMI)
phase IIA trial. Circulation 81:1457,1990.

18. Forssmann W: The catheterization of the right side of the heart. Klin
Wochenschr, 8:2085, 1929.

19. Brannon ES, Weens HS, Warren JW: Atrial septal defect: study of
hemodynamics by the technique of right heart catheterization. Am J Med Sci.
210:480, 1945.

20. Zimmerman HA, Scott RW, Becker NO: Catheterization of the left side of the
heart in man. Circulation 1:357, 1950.

21. Sones FM Jr, Shirey EK: Cine coronary arteriography. Mod Concepts
Cardiovasc Dis, 31:735-738, 1962.

169

 

 

 

    
      
  
   
  
  
    
     
  

‘ w, :5 w r} ,?i #Utlifl .G‘!
‘ ‘ . ' . ‘7 u: mm nmifimm .Y ' ,
Md. 3:1J9l HUN];

"I m' )i 20,561.] .“

, m 1,: I.» v” m "w (a

3‘. g, {“51 W‘ 'q‘

'.-l [X , ut‘ “-
:MOBLEN

an .5! sad.
wnyz .- .
fl, _

‘ ’ [snaiflyh f)"
" 4:133}! ‘ ' "

- ‘U.._.
A .

‘nlo

2"
1..! ovnO ‘
film '. ;K
5;? mix.“ 3‘"

., ~24ng m

up. that .. ,

-L . 4.." ,IW
”LI-ani
'vc fi-zmma -

35$}, 3a,} " _ 5..-”‘0. «Jawgmr-ufi‘f) ;‘ *' raj-34:5! (2'51 No.92 ,AH _
um .TrF Momma ‘
. ‘ 1.9..

gm ,sef; 4:ng -

"1390036“ {mgmguzmhs 2'5,u:..1r_:3 ‘30:“) :33 W53

A,‘
- .
‘ _ "z:
. . ;_- ' '
r ‘ . ‘
~ v ' ‘ . v
A- u ~ ,‘M. 'l .6 .‘

 

 

22. Heupler, F Jr. Coronary Arteriography and Left Ventriculography: Sones
Technique in Coronary Arteriography and Angioplasty by Spencer B. King 111 and John
S. Douglas, Jr. McGraw-Hill Company, 1985.

23. Califf RM, O’Neill W, Stack RS, et al: Failure of simple clinical measurements
to predict perfusion status after intravenous thrombolysis. Ann Intern Med
108:658,1988.

24. Kulick DL, Rahimtoola SH: Assessment of the survivors of acute myocardial
infarction: the case for coronary aniography, p. 429. In Gersh B, Rahimtoola SH
(eds): Myocardial Infarction. Elsevier, New York, 1991.

25. Crawford MH, O’Rourke RA: The role of cardiac catheterization in patients after
myocardial infarction. Cardiol Clin 2(1):105, 1984.

26. O’Rourke RA: Clinical decision in post infarction patients. Mod Conc
Cardiovasc Dis 55:55, 1986.

27. Kelly DT: Clinical decisions in patients following myocardial infarction. Curr
Probl Cardiol 10(1). 1,1985.

28. Bamrah VS, and Warm LS. Cardiology in Concise textbook of Medicine.
Elsevier, 1990.

29. O’Rourke, RA. Invasive and noninvasive risk stratification of postmyocardial
infarction patients, pg. 135 In McCall, David (ed): Acute Myocardial Infarction.
Churchill Livingstone, New York, 1991.

30. GISSI: Effectiveness of intravenous thrombolytic treatment in acute myocardial
infarction. Lancet 1986; 1:397-402.

31. GISSI: Long-term effects of intravenous thrombolysis in acute myocardial
infarction: Final report of the GISSI study. Lancet 1987; 2:871-874.

32. ISIS Collaborative Group: Randomized trial of intravenous streptokinase, oral
aspirin, both or neither among 17,187 cases of suspected acute mycardial infarction:
ISIS-2. Lancet 1988; 2:349—360.

33. Wioox RG, von der Lippe G, Olsson CG, Jensen G, Skene AM, Hampton JR.
Trial of tissue plasminogen activator for mortality reduction in acute myocardial
infarction: Anglo-Scandinavian study of early thrombosis (ASSET). Lancet 1988;
2:525 -30.

170

 
   
     
 
  
 
   
    
  
   

..mnu" 1“ V
,4

v-rrl NM

1“, ~35.ij J‘

i

-‘ 'IIM‘O m ‘ r;
-|' |. --.';?) {View 4r:

. .74. , "
549‘ _djm“ .
«(:nvgfiivu 7- 'l

v'.

.7 , . .: —. . 7 . '. ,, J.“ ' ”Win“! “‘7"
. '54 , .1; I’gl .- ‘~n.x;iltfm

,4 . ‘. . (A . nu- ...: .. --.i..' 1: .. ‘ ‘ V 'V "Jul; ”WW . ' i
.u; .31.! ‘. . . I. ~ g1... . ; awn-Mu ”mm“
-... sari .8201

"ht. Y‘j’.’ ,1. ‘th‘uf “a 30.379931 ‘t‘g‘lfl‘n ‘6‘!” «wt-£1339 mfll‘lnm ‘ (U...
.‘IJ‘Q; imeu: Vii?!“ .2 ewwlmmdl vl’ws .6 «an; N33”? ' ' i “

“A! I: lit-7* 3.5.1 3.15.4? Q) -_—._‘_.:~3¢_ ,i!’ - mar?!“ .0 “5"" ”I ’ ' '

- .l
~A .r
on .
77 31; J P".
‘ V _f _ l‘

 

34. Bassand J -P, Machecourt J, Cassagnes J, et a1 and the APSIM Study Investigators.
Multicenter trial of intravenous anisoylated plasminogen streptokinase activator

complex (APSAC) in acute myocardial infarction: effects on infarct size and left
ventricular function. J Am Coll Cardiol 1989; 13:988—97.

35. Verstraete M, Bernard R, Bory M, et al. European Cooperative Study Group for
Recombinant Tissue-Type Plasminogen Activator: Randomized trial of intravenous
recombinant tissue-type plasminogen activator versus intravenous streptokinase in acute
myocardial infarction. Lancet 1985; 1:842-847.

36. Chesebro JH, Knatterud G, Roberts R: Thrombolysis in Myocardial Infarction
(TIMI) trial, Phase I: A comparison between intravenous tissue plasminogen activator
and intravenous streptokinase. Circulation 1987; 76:142-154.

37. An international randomized trial comparing four thrombolytic strategies for acute
myocardial infarction. The GUSTO investigators. N Engl J Med 1993; 329: 673-82.

38. The effects of tissue plasminogen activator, streptokinase, or both on coronary-
artery patency, ventricular function, and survival after acute myocardial infarction.
The GUSTO Angiographic Investigators. N Engl J Med 1993; 329:1615—22.

39. Bonnier HJRM, Visser RF, Klomps HC, Hoffman HJML and the Dutch Invasive
Reperfusion Group. Comparison of intravenous anisoylated plasminogen streptokinase
activator complex and intravenous streptokinase in acute myocardial infarction. Am J

Cardiol 1988; 62:25-30.

40. National Center for Health Statistics: 1986 Summary: National Hospital Discharge
Survey. Advance Data from Vital and Health Statistics. No. 145. US Dept of Health
and Human Services publication No. (PHS) 87-1250. Public Health Service.
Hyattsville, Md, National Center for Health Statistics, 1987.

41. Graves El. National Hospital Discharge Survey: Annual Summary, 1991. National
Center for Health Statistics 1993; DI-IHS publication (PHS):93-1775;44.

42. Dotter, CT and Judkins, MP: Transluminal treatment of arteriosclerotic
obstruction: Description of a new technique and a preliminary report of its application.
Circulation 30: 654, 1964.

43. Dotter, CT, Rosch, J, Anderson JM, et al: Transluminal iliac artery dilation: Non-
surgical catheter treatment of atheromatous narrowing. JAMA 230: 117, 1974.

44. Porstmann, W: Ein neuer Korsett-Ballonkatheter zur transluminalen Rekanalisation

nach Dotter unter besonderer Berficksichtigung von Obliterationen an den
Beckenarterien. Radiol Diagn (Berl) 14:239, 1973.

171

   
   
  
  
   
  

, . w. warms.
1W» at .
' If!“ r

wartwd .M ..

i' 3:591?

_:- um
trlltl'iTM'

~n-, .- ..mq.
".pfrn'gnfi. (.r

. “URN
allow.) '
.l'l'. l‘)‘

.u‘ 1’0 ‘

us: ., . 7‘ . , m -." ‘4‘“ buy")
1‘1"} ~ .; ' «U U ' ‘ ' 1".

~ ‘ (H;- I“; .,._.L “first“

.' - ". i' mi '.I‘H I WEE-M1 a“ .

ism-«3.24 3'3“ ’,..’..,‘12’ i; . 4.1.3; 5.? 7.5.1“,an r:

2".“ '2 m

fibuv... ‘5 11. 3.307.] a .vIJ’tflM; ”'3 jut .«rlqmll hm .
.WJJu-g. a is) ,2):th ' (.n‘ ' WI; 5 V‘.‘H'U‘1 'J '1 10

W :m‘cstib ham: 36:37 Seaway-run? 7.»: w ,M& mutual: ,! .“n
#99} ,Yilrflfl 9.547491 _suirwmm: mummmiu - - '

WW 1w: immvwml m i
M m; WM) m1 33W“ .
{we .rzrru autumn

 

45. Athanasouleis, CA: Percutaneous transluminal angioplasty: General principles.
AJR 135:893, 1980.

46. Grfintzig, A and Kumpe DA: Technique of percutaneous transluminal angioplasty
with the Griintzig balloon catheter. AJR 132:547, 1979.

47. Grfintzig, A: die perkutane transluminale Rekanalisation chronischer
Arterienverschliisse mit einer neuen Kilatiationstechnik. Gerhard Witzstrock, Baden-
Baden, 1977.

48. Gruentzig, AR, Myler, RK, Hanna, ES, et al: Coronary transluminal angioplasty
(abstr.) Circulation 56 (Suppl 3):84, 1977.

49. Gruentzig AR. Transluminal dilation of coronary artery stenosis. Lancet 1978;
1:263.

50. Dotter CT, J udkins MP. Transluminal treatment of arteriosclerotic obstruction.
Circulation 1964; 30:654-70.

51. Hill JA, Margoli JR, Feldman RL, et al. Coronary arterial aneurysm formation
after balloon angioplasty. Am J Cardiol 1983; 52:261—4.

52. Castaneda-Zuniga WR, Forrnanek A, Tadavarthy M, et al. The mechanism of
balloon angioplasty. Radiology 1980; 135:565-71.

53. Lee G, Low RI, Takeda P, et al. Importance of follow-up medicare and surgical
approaches to prevent reinfarction, reocclusion, and recurrent angina following
intracoronary thrombolysis with streptokinase in acute myocardial infarction.
American Heart Journal. 1982; 104:921—4.

54. Meyer J, Merx W, Schmitz H, et al. PTCA immediately after intracoronary
streptolysis of transmural myocardial infarction. Circulation 1982; 66:905-13.

55. Swan HJC. Thrombolysis in acute myocardial infarction: treatment of the
underlying coronary artery disease. Circulation. 1982; 66:914-6.

56. Fitzgerald DJ, Catella F, Roy L, Fitzgerald GA. Marked platelet activation in
vivo after intravenous streptokinase in patients with acute myocardial infarction.
Circulation. 1988; 77:142-150.

57 . Sebuski RJ, Ohlstein EA. Attenuation of platelet responsiveness to prostacyclin
(PGIZ) after tPA. Circulation. 1987; 76:(Suppl IV):IV-338.

172

 

. . . . t
. ‘«.-'l'l\~~‘.

   
   
  
  
   
   
 
  
  

n: ' ".cwslomwfl”
‘1 '.Y. . A‘l"'flhfi .-‘

.1 ' im‘ ..un- 93 ‘

fl
' ‘ ""1" . LB 14 = W

.“H‘J‘

.-" (129.31”

u” EH*na£,
.alaenRQIl.

i‘L- {veal -

‘ .‘ ~ ‘ a & ..vzy' h 1:fid.i’”‘
-‘.»~ ' .1 . 453mm”. _'T)‘?n§m]

:21“ rwz. . , ' ii~--3~ J‘MvwdnvndT .
’ "NJ-43 ‘ .'- was»: {Vim ‘ ' _-
‘E U‘rl’f-\ a" hu‘flfi’“ 1}}- "'."IV J- ’ ‘ 1355' hi: ‘i‘ h 1533“? 0'.”
.Irtiib‘ss‘tn. ....v? w .. .5.me 9 u Norma} r ‘ ’I’amiultpil '7 ',
Adi-3H???-

 

58. Topol EJ, Califf RM, George BS, et al. A randomized trial of immediate versus
delayed elective angioplasty after intravenous tissue plasminogen activator in acute
myocardial infarction. N Engl J Med 1987; 327:581-8. .

59. TIMI Research Group. Immediate vs delayed catheterization and angioplasty
following thrombolytic therapy for acute myocardial infarction: TIMI IIA results.
JAMA 1988; 260:2849-58.

60. Ryan TJ, Faxon DP, Gunnar RM, Kennedy JW, King SB 111, Loop FD, Peterson
KL, Reeves TJ , Williams DO, Winters WL Jr, et al. Guidelines for percutaneous
transluminal coronary angioplasty: a report of the American College of

Cardiology/ American Heart Association Task force on Assessment of Diagnostic and
Therapeutic Cardiovascular Procedures. Circulation 1988; 78:486-502.

61. Gruentzig AR, King SB HI, Schumpf M, Siengenthaler W. Longterm followup of
percutaneious transluminal coronary angioplasty: the early Zurich experience. N Engl J
Med 1987; 316: 1127-32.

62. Leimgruber PP, Roubin GS, Hollman J, et al. Restenosis after successful coronary
angioplasty in patients with single-vessel disease. Circulation 1986; 73:710-717.

63. Kent KM. Restenosis after percutaneous transluminal coronary angioplasty. Am J
Cardiol 1988; 61:67G-7OG.

64. Leimgruber PP, Roubin GS, Anderson HV, et al. Influence of intimal dissection
on restenosis after successful coronary angioplasty. Circulation 1985; 72:5 30-5 .

65. Lam JYT, Cheseboro JH, Steele DM, et al. Deep arterial injury during
experiemtnal angioplasty. Relationship to a positive 111 indium-labelled platelet
scintiram, quantitative platelet deposition and mural thrombus. J Am coll Cardiol 1986;
8: 1380.

66. Meier B, King SB, Gruentzig AR, et al. Repeat coronary angioplasty. J Am Coll
Cardiol 1984; 4:436.

67. Sipperly, Mary Ellen. Expanding role or coronary angioplasty: Current
implications, limitations, and nursing considerations. Heart & Lung 1989; 18:507-13.

68. Dorros G, Cowley MJ, Simpson J, et al. Percutaneous transluminal coronary
angioplasty: report of complications from the National Heart, Lung, and Blood Institute
PTCA Registry. Circulation 1983; 67: 723-30.

69. Detre K, Holubkov R, Kelsey S, et al. Percutaneous transluminal coronary

angioplasty in 1985—1986 and 1977-1981. The National Heart, Lung, Blood Institute
Registry. N Engl J Med 1988; 318:265-270.

173

 

 

   
   
  
 
   
  
    

V'. .s , wai 0" “M
:‘i. y‘lw’u‘wm

’yn'Y 5" IN V ’V

" 5‘. 11.1 ,IJVI‘J) :

~. x . , _ 3 ' 231.121}?!
.- 3 . . . a. manger.
;. . g . a. ,1 .; ‘n Human”.
'f

-:.,-I , IV 1 I" 1191‘" 1‘ ’7 '; ‘., .. :“‘i,’~:1'~‘1' 3(- ”8A {a . I
.ottr:8‘ ‘ ‘

‘nérm‘ '1 . H?" -.._-.w’ ._‘::;r:A. ‘ 2'. ,: 11131- "‘ .; 1231151 (3“
H The; 2:989 Jam‘s»: .r..;r 12:/«"1 gr.» «m 13:18 W

913.321“ , 3mm: m: s") i”, 5 3.; . i. 'vtldszfi .881 gal-090:3
'38:}?!er 91:01.51 and , fur}: Tm tale 1.. «no .9 zm‘rérufllmm in”;
2;}; r"_'.‘ '4 [393 M "

~

“mix. mum! an: r! -‘ -aznsmmtr' 1!». '3 .2 102163 .3
new Me! 358.} .muh' museum 1.896 EV?! -
m2 awe .8011

«r .

70. Galan KM, Deligonul U, Kern MJ, et al. Smoking increases the risk of restenosis
following coronary angioplasty (PTCA). Circulation 1986; 74: II-281.

71. Cowley MJ, Dorros G, Kelsey SF, Van Rader M, Detre KM. Emergency
coronary bypass surgery after coronary angioplasty: The National Heart, Lung, and
Blood Institute’s PTCA Registry Experience. American Journal of Cardiology. 1984;
53:22C-26C.

72. Bredlau CE, Roubin GS, Leimgruber PP, et a1. In-hospital morbidity in patients
undergoing elective coronary angioplasty. Circulation 1985; 72: 1044-52.

73. Sinclair IN, McCabe CH, Sipperly ME, et al. Predictors, therapeutic options and
long-term outcome of abrupt reclosure. American Journal of Cardiology. 1988;
61 :615-66.

74. Kent KM, Bentivoglio LG, Block PC, et al. PTCA: Report from the Registry of
the National Heart, Lung, and Blood Institute. American Journal of Cardiology.
1982; 49:2011-2020.

75 . Falk, E: Plazue rupture with sever pre-existing stenosis precipitating coronary
thrombosis : Characteristics of coronary atherosclerotic plazues underlying fatal
occlusive thrombi. Br Heart J 50: 127, 1983.

76. Cohn LH, Gorlin R, Herman M, et al.: Surgical treatment of acute coronary
occlusion. J Thorac Cardiovasc Surg 1972; 64:503-13.

77. Phillips SJ, Kongtahworn C, Skinner JR, et al: Emergency coronary artery
reperfusion. A choice therapy for evolving myocardial infarction. J Thorac Cardiovasc
Surg 1983; 86:679-688.

78. Phillips SJ, Kongtahworn C, Zeff RH, et al: Emergency coronary artery

revascularization. A possible therapy for acute myocardial infarction. Circulation
1979; 60:241.

79. DeWood MA, Notske RN, Berg R, Ganji JH, Simpson CS, Hinnen ML, Selinger
SL, Fisher LD. Medical and surgical management of early Q wave myocardial
infarction. I. Effects of surgical reperfusion on survival in recurrent myocardial
infarction, sudden death and functional class at 10 or more years of follow-up. J Am

Coll Cardiol 1989; 14:65-77.

80. DeWood MA, Leonard J, Grunwald RP, Hensley GA, Mouser LT, Burroughs
RW, Berg R, Fisher LD. Medical and surgical management of early Q wave
myocardial infarction. H. Effects on mortality and global and regional left ventricular
function at 10 or more years follow-up. J Am Coll Cardiol 1989; 14:78-90.

174

‘_ 7. ._":~ . '- 35.1. -- X2" ..9-1'151 A”
E»; '7 '::-~' fi' tin. ,- t .vz ~..-nbsu . ‘ ..
. ' Ir ...,
t“ '- an???“ :11 kWh-aw ~= '- Iv: ‘ 0.1”" team-I 7 . .

.41 “I;

14* r' .

Niki"

.1 ‘l E]
Toni-3

v‘W‘m ’

"1:;7521} 9m.
fi'mt

unsivrgmd .12 ‘ ‘
mu: 3:11:13 A
.f-f‘N‘ VITO” q "

I ' . ' '1’ ?!1’13912 “u

r. ’ . ‘ - b V“ A .81.”

.1 ‘ r

. - ’ .- . ,— . .a ,r.
‘t" \' ‘J‘M . , ‘;?}4 ..‘r‘"" .’- '1' *'

a
1
- 1

4.133. mm ,H :‘woid 3... must“ ‘-‘ Mama; .1. mm}. ‘

rat:

 

' 2w ’.‘ uh"; tr: "cm W4 m" V08 01' 1 3&3“ M
as“? flat 135909;» em: “data has iriimmr; no my
.Mé-i mmmrwmrmm ":

 

mi

  
  
  
 
  

 

 

81. Alderman EL, Bourassa MG, Cohen LS, Davis KB, Kaiser GG, Killip T, Mock
MB, Pettinger M, Robertson TL (CASS Investigators): Ten-year follow-up of survival
and myocardial infarction in the randomized Coronary Artery Surgery Study (CASS).
Circulation 1990; 82:1629-1647.

82. Califf RM, Harrell FE Jr, Lee KL, Rankin JS, Hlatky MA, Mark DB, Jones RH,
Muhlbaier LH, Oldham HN Jr, Pryor DB: The evolution of medical and surgical
therapy for coronary artery disease: A 15-year perspective. JAMA 1989; 261:2077-
2086.

83. Loop FD, Lytel BW, Cosgrove DM, Stewart RW, Goormastic M, Williams GW,
Golding LAR, Gill CC, Taylor PC, Sheldon WC, Proudfit WL: Influence of the
intemal-mammary-artery graft on 10-year survival and other cardiac events. N Engl J
Med 1986; 314:1-6.

84. Bourassa MG, Fisher LD, Campeaur L, Gillespie MJ, McConney M, Lesperance
J: Long-term fate of bypass grafts: The Coronary Artery Surgery Study (CASS) and
Montreal Heart Institute experiences. Circulation 1985; 72:V-71-V-78.

85. Grondin CM, Campeau L, Lesperance J, Enjalbert M, Bourassa MG: Comparison
of late changed in internal mammary artery and saphenous vein grafts in two

consecutive series of patients 10 years after operation. Circulation 1984; 70(supp I):I-
208-1-212.

86. Kirklin, JW, Blackstone, EH, Califf, RM, et al. ACC/AHA Guidelines and
Indications for Coronary Artery Bypass Graft Surgery. A report of the American
College of Cardiology/ American Heart Association Task Force on Assessment of
Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Coronary
Artery Bypass Graft Surgery). Circulation 1991; 83(no.3):1125-1173.

87. Pocock SJ, Henderson RA, Rickards AF, et al. Meta-analysis of randomised trials
comparing coronary angioplasty with bypass surgery. Lancet 1995; 346: 1 184-89.

88. CABRI Trial Participants. First-year results of CABRI (Coronary Angioplasty vs
Bypass Revascularization Investigation). Lancet 1995; 346: 1179-84.

89. RITA Trial Participants. Coronary angioplasty versus coronary artery bypass
surgery: the Randomised Intervention Treatment of Angina (RITA) trial. Lancet
1993; 343: 573-80.

90. King, SB, Lembo NJ, Kosinski AS, et al. A randomised trial comparing coronary
angioplasty with coronary bypass surgery. N Engl J Med 1994; 331:1044-50.

175

 

  
    
  
  
   
   
  
  
 
  

am A.
'2 out?“ ‘
1,: ’.i ‘u hull“ '<
;.-~ M ii! ‘

. ' M 1.1M
’ ‘5' ...-19.)”.

'l'

1911“)...”

‘ru'nr

't-n'. wall

6» .M') M.-
. V >
' "1‘9“ in t- r
{341" ‘.-r (m

. ' » ‘ ..., ,‘ I..Ie-'J;1x'J fl ':
L .‘ r ‘ ‘ .’ 1, 151 ”#31772“? n
) r! . (i 3'" ’1'. m1 9‘

.. ' v ;.;:.' 3 . . ‘. a" _l ‘ "-111M '8 .
‘~ :. ' ‘i‘, Mug-’11,“ . .. " ‘.""' 13.1313.“ 1 V

..32'2..>r:‘-. -‘:2".:“ z ‘CJ. ‘ ' ." ‘7 . lfi'fl’flfi‘mtd:

3.): -. . :_.: f .14: x..; ww- mi u u-

e-IWG rain 4;). mm; ~34 {NaZWm frown} ...MOM
3.21.! 6:91;} 1.31125" ...-199;.“ : mmtm'f‘mmbvmll '- '. _

may.» scream-mist), matrix: I: k. r: .31“ tm A“
cram: m 589mm; {gm-w mama-

' . ' Dfo
p1 , ..i .
L. . .3
_ ._ vat 1. r 1.4.. ‘

91. Hamm CW, Riemers J, Ischinger T, et al. A randomised study of coronary
angioplasty compared with bypass surgery in patients with symptomatic multi-vessel
coronary disease. N Engl J Med 1994; 331: 1037-43.

92. Puel J, Karouny E, Marco F, et al. Angioplasty versus surgery in multi-vessel
disease: immediate results and in-hospital outcome in a randomised prospective study.
Circulation 1992; 86 (supp I):372.

93. Hueb W, Arie S, Oliveira SA, et al. The Medicine, Angioplasty or Surgery Study
(MASS): a prospective randomised trial for single proximal left anterior descending
artery stenoses. J Am Coll Cardiol (in press).

94. Goy J -J , Eeckhout E, Burnand B, et al. Coronary angioplasty versus left internal
mammary grafting for isolated proximal left anterior descending artery stenosis.
Lancet 1994; 343:1449-53.

95. Rodriguez A, Boullon F, Perez-Balina N, et al. Argentine randomised trial of
percutaneous transluminal coronary angioplasty versus ccoronary artery bypass surgery
in multi-vessel disease (ERACI): in-hospital results and l-year follow-up. J Am Coll
Cardiol 1993; 22:1060-67.

96. Fitzgibbon GM, Leach AJ, Kafka HP, Keon WF. Coronary bypass graft fate:
long-term angiographic study. American Journal of Cardiology. 1991; 17: 1075-80.

97. Loop FD, Lytle BW, Cosgrove DM, et al. Influence of the intemal-mammary
artery graft on ten-year survival and other cardiac events. New England Journal of
Medicine. 1986; 314: 1-6.

98. The international classification of diseases. 9th Revision. Clinical modification.
2nd ed. Washington, DC: Department of Health and Human Services, 1980. (DHHS
publication no. (PHS) 80-1260.

99. Coding Clinic May/June 1984; pg. 9-14.

100. Charlson ME, Pompei P, Ales KL, and MacKenzie CR. A new method of
classifying prognostic comorbidity in longitudinal studies: development and validation.
J Chron Dis 1987; 40(no.5): 373-383.

101. Cox DR. Regression models and life tables. J R Stat Soc. 1972; 34:187-220.
102. Campeau, L: Grading of angina pectoris. Circulation 1976; 54:522-523.

103. CASS Principal investigators and their associates. Coronary artery Surgery

Study (CASS): a randomized trial of coronary artery bypass surgery. Survival data.
Circulation 1983; 68:939-950.

176

... _1 , a: <- luaqmo‘lpm
.s'wl‘t'bis.’ ’32:, .:l: J" -'

 

  
    
   
  
  
 

(it"lloo'i-H¢ ‘ m I
, ' ..z‘f’fl mfll' ‘
99'. 1th u

v . .0111 ..o W;
. ‘ emu: 4hr
I I (a “s :m
' [1 mm ,W

' Jami

u]- '

o

1-. ‘_.‘(.

“@137“:
"v‘mflmé ( magnum 9n

.- v.40: name» 5‘»
D

C-E‘S- I 'L.“C'é; 30! 1...? 3i

92,:ch ...- (5 has aiaqun room
{32 ”got .4991 maxim 3 menu; ”can” M~

M? an: mur‘ when“ “and: has M ’
a!» ‘rwmd .M «and ram VW 30 m

104. European Coronary Surgery Study Group. Long-term results of prospective
randomized study of coronary artery bypass surgery in stable angina pectoris. Lancet
1982; 2: 1173-1180.

105. Becker RC. Coronary thrombolysis in women. Cardiovasc Dis Women.
1990;77(suppl 2): 1 10-123.

106. Eysmann SB, Douglas PS. Reperfusion and Revascularization strategies for
coronary artery disease in women. JAMA. 1992;268(14): 1903-1907 .

107. Talley JD. Review of thrombolytic intervention for acute myocardial infarction-
is it valuable? Journal of the Arkansas Medical Society. 1994;91(2):70-79.

108. Van de Werf F, Arnold AER. Intravenous tissue plasminogen activator and size
of infarct, left ventricular function and survival in AMI. Br Med J. 1988;297:1374-
1379.

109. AIMS Trial Study Group: Effect of intravenous APSAC on mortality after AMI:
Preliminary report of a placebo-controlled clinical trial. Lancet. 1988;1z545-549.

11o. Malone ML, Sial Shahid, Battiola R], e al. Age-related Differences in the
Utilizatio of Therapies Post Acute Myocardial Infarction. Journal of American
Geriatric Society 1995; 43 (no. 6): 627-633.

111. Udvarhelyi IS, Gatsonis, C, Epstein AM, et al. Acute Myocardial Infarction in
the Medicare Population. J AMA 1992; 268 (no. 18): 2530-2536.

112. Wenneker MB, Weissman J S, and Epstein AM. The Association of Payer With
Utilization of Cardiac Procedures in Massachusetts. JAMA 1990; 264 (no. 10): 1255-
1260.

113. Ayanian, I Z and Epstein AM. Differences in the Use of Procedures Between
Women and Men Hospitalized for Coronary Heart Disease. The New England Journal
of Medicine 1991; 325 (no. 4): 221-225.

114. Wenneker, MB and Epstein AM. Racial Inequalities in the Use of Procedures
for Patients With Ischemic Heart Disease in Massachusetts. JAMA 1989; 261 (no. 2):
253-257.

115. Grines CL, De Maria AN. Optimal utilization of thrombolytic therapy for acute
myocardial infarction: concepts and controversies. J Am Coll Cardiol. 1990; 16:223-
231.

116. American Heart Association. 1991 Heart and Stroke Facts. Dallas, Tex:
American Heart Association; 1991.

177

 

A' , _ my mi, midefilefiQl .

   
   
    
   
    
    
   
     
   
  
 
  

a ... ~22" ,y (aw.
J. ..L Ami .>
I!"

w" "'uufl'lul) ”i
.v‘: 0mg:

2‘. antih-

'.-; at!“

D 'l’ ”1",! ',
‘3'

‘ I
3.» I

‘3‘” 80“"
gnungn-x 3:31 . .,

A211; m

I fish?) n

,3

J
”1'
V .
',x, L
' Z. ‘

n-A‘ :; . i. ' wt . " . ' - , f. in he". 1 km.” 51,
M u «1.2? ' . . :»j£§-1-.‘£mztpi‘vfl ”I
C ‘1'. ‘42,.m} (Ci, {lat

refinerien‘I u) 3". r ‘. "I:.'-:.-..'.'-'.-n' ‘enmr Vt) 36241454318“

:(f 'mi 363:: j‘fi‘." "JV? .- - - M 'Ttuv' a.“ at {(122251 .733“ 1340‘“

sure; ml W fltvmfi‘! to {common ammo MA and! fir {Vi-1:11,“
'45571‘1.M w 903 mA I .vmmum’w be; m ‘

 

117. Smith SC Jr, Gilpin E, Ahnve S. Outlook after acute myocardial infarction in
the very elderly compared with that in patients aged 65 to 75 years. I Am Coll
Cardiol. 1990; 16:784-792.

118. Adolph R]. The elderly, the very elderly and traditional practice patterns. J Am
Coll Cardiol. 1990; 16:793-794.

119. Topol El, Califf RM. Thrombolytic therapy for elderly patients. N Engl J Med.
1992; 327: 45-47.

120. Collins R, for the ISIS Collaborative Group. Optimizing thrombolytic therapy of
acute myocardial infarction: age is not a contraindication. Circulation. 1991; 84:11-
230. Abstract.

121. Peto R. Which patients to treat with fibrinolysis: overview of ISIS-3 and Estudio
Multicentrico Estreptoquinase Republicas de America del Sur. Presented at the 40th
annual scientific session of the American College of Cardiology; March 3, 1991;
Atlanta, Ga.

122. Pepine CJ. Thrombolytic use in the elderly. J Myocardial Ischemia. 1991; 3: 10—
12.

123. Rich MW. Acute myocardial infarction in the elderly. J Myocardial Ischemia.
1991;23:10-12.

124. Robers WJ, Bowlby LJ, Chandra NC, et al. Treatment of myocardial infarction
in the United States (1990 to 1993). Observations from the National Registry of
Myocardial Infarction. Circulation. l994;90(4):2103-2114. Abstract.

125. Tobin JN, Wassertheil-Smoller S, Wexler JP, et al. Sex bias in considering
coronary bypass surgery. Ann Intern Med. 1987; 107:19-25.

126. Whittle J, Conioliaro J, Good CB, et al. Racial differences in the use of invasive
cardiovascular procedures in the department of veterans affairs medical system. The
New Engl Joum of Med. 1993; 329(9): 621-627.

127. Maynard C, Litwin PE, Martin J S, et a1. Characteristics of black patients
admitted to coronary care units in metropolitan Seattle; results from the Myocardial
Infarction Triage and Intervention Registry (MITI). Am J Cardiol. l991;67(1): 18-23.

128. Loop FS, Golding LR, MacMillan JP et al. Coronary artery bypass surgery in

women compared with men: analysis of risks nad long-term results. J Am Coll
Cardiol. 1983;4z383—390.

178

 

rm! , "tam-a at):
'T 'W-h .m-*\a-n.( ‘ I ;‘
arr me: All» "

, Maw: m! mm?”
»"H ai-"qr AWE m

’. v

'-!

7‘ my; amt J
“n.4,.‘1 (9‘ ‘g:
3’;

. ”H ‘ TC! ..9 7911M.) '\ . I
”llil‘uCJUVN m , ‘
“ma at ,g'

h I

V ..r ,; 03" .m. ‘I‘. ‘

‘rZ " ‘.' ’ HJ‘I‘HTMk
mm. tan 5 .

w') .mil’fl '

v ' . NH": 2) ._.m{f,fl m:. -

m -
-'.'|,-V;)\ WM M- 4" " .' 
mom; ~ ‘

Hun .IW much!
”a?" 1 male Inn'uU -

x mm»! 216.]!!! ‘1-

:gr'xn“ ‘ ~ .- ~ ‘ .r ‘ “z’ :1"::-::2.3.a'll .141 0”}:
In m... 3931.12135qu ‘

' yo
'nsz‘m "c': _: '6» '7‘», al,-v1 ’m’. . -" ' .1. ' ‘ (mi-3’01?) {31m '
..ft raft.» :. Ann, 'u," . 1:25.. a; :- .75»;an . - . '
; 1‘5” :"M manmufl'
I.

mum \-.,..,tmmm- mmw am an; mu. Raw 3  ‘

., £15ng 4:3? Wm :“wxr 4.3 m mit- 3,33 m m mm; ”W“
£932 ~:(I Kai“: 1 an): M am; (""31 mm ml in”
.. £1
me- a! . *1 1mm: mb‘h .1:st “ms!
fin‘)m1 Mama!" Mviim‘ vo Walsh sun“

~ np,” '

 

   
    
 
    
    
    
  
    
   
  
  
  
   
 
  
   
 
   
   
  
   
  
  
 
  
  

129. Tyras DH, Barner HB, Kaiser GC et al. Myocardial revascularization in women.
Ann Thorac Surg. 1978; 25:449-453.

130. Killen DA, Reed WA, Arnold M, et al. Coronary artery bypass in women: long-
term survival. Ann Thorac Surg. 1982;34:559-563.

131. Hall RJ, Elayda MA, Gray A, et al. Coronary artery bypass: long-term follow-up
of 22,284 consecutive patients. Circulation. 1983;68(suppl II):20-25.

132. Myers W0, Davis K, Foster ED, et al. Surgical survival in the Coronary Artery
Surgery Study (CASS) Registry. Ann Thorac Surg. 1985;40:245-260.

133. Douglas JS, King SB, Jones EL, et al. Reduced efficacy of coronary bypass
surgery in women. Circulation. 1981;64(supp12):11-16.

134. Baker ED, Kronmal R, Kennedy JW, et al. Comparison of long-term,
postsurgical survival of women and men in the Coronary Artery Surgery Study
(CASS). Am Heart J. 1989; 117:71-81.

135. Davis KB. Coronary artery bypass graft surgery in women. In: Eaker ED,
Packard B, Wenger NK, et al, eds. Coronary Artery Disease in Women. New York,
NY: Haymarket-Doyma; 1987:247-250.

136. Clark RE, Edwards FH, and Schwartz M. Profile of preoperative characteristics
of patients having CABG over the past decade. Ann Thorac Surg. 1994;58(6): 1863-
1865.

137. Gersh BJ, Kronmal RA, Frye RL, et al. Coronary arteriography and coronary
artery bypass surgery: Morbidity and mortality in patients aged 65 years or older.
Circulation. 1983;67:483-491.

138. Montague NT, Kouchoukos NT, Wilson TAS, et al. Morbidity and mortality of
coronary artery bypass grafting in patients 70 years of age and older. Ann Thorac Surg.
1985;39:552-557.

139. Loop FD, Lytle BW, Cosgrove DM, et a1. Coronary artery bypass graft surgery
in the elderly. Cleve Clin J Med. 1988;55:23-24.

140. Hibler BA, Wright JO, Wright CB, et al. Coronary artery bypass surgery in the
elderly. Arch Surg. 1983; 118:402-404.

141. Homeffer PJ , Gardner TJ , Manolio TA, et al. The effects of age on outcome
after coronary bypass surgery. Circulation. 1987;76(supp1V):6-12.

179

   
   
  
    
  
  
 
 
   
 
   
    

' I. :4inme
~ , .. «"0! as,

gm f‘. [- u‘l {-45 .Ag
“.1: m‘ufls‘: (KIA

A.“ .l\' fii‘. u u

'»' J 10'4be

‘.'M an!”

.4 v {more

:‘i.'

‘"l

in .c'. ml“

Wm

. 5)! (lawelfi ~

.:. ‘ H.131.“ m; .

1 to" p. - ,. 3‘4 ”l‘ig'liiv" a ‘.

1*. ' ‘ ‘ ' Ivan I'm

1!“ "a W" five-amt”
.‘V- .1-.' 5.“,- I

g 245.. angry. -' w‘ .4 . ' » 4* ‘21:..‘4. My“.

r_.-,. .-

:5;... .~ _' ...-:5. ., = , .. _ ... .. n..- l ‘r‘vm,,5_az..ud m. by»: .
.V. .'

IV’rgflM 31.1,“: L:___'§’I;'_ 1,353“, (1;; ‘ ;' I _ ~, ;) 14'” ,. :fitc ' .‘ {Hi “Incl m fink":
.-.-. 540133! .mldltll113m, .;

9:5 .3 nae-.m- twirl Yams ‘f‘tzal-TC I Is 75:; .5" "WW" 0i IW'

.«f-e Fit-‘43” $1501.”

must-shutout? in: M W ,t‘rw
SIEIV W731 .WJ .

- ,.¢
. '1, r ,1,

   

__.

142. Matangi MF, Strickland JA, Burgess JJ, et al. Elective aortocoronary bypass
grafting in the elderly. Can J Cardiol 1987;3z342-244.

143. Mohan R, Amsel BJ, Walter P]. Coronary artery bypass grafting in the elderly-a
review of studies on patients older than 64, 69 or 74 years. Cardiology. 1992;80:215—
225.

144. Kern MJ, Deligonal U, Galan K, et a1. Percutaneous transluminal coronary
angioplasty in octogenarians. Am J Cardiol. 1988; 61:457-458.

145. Holmes DR Jr, Holubkov R, Vliestra RB, et al. Comparison of complications
during perccutaneous trnsluminal coronary angioplasty from 1977 to 1981 and from
1985 to 1986: the NHLBI Angioplasty Registry. J Am Coll Cardiol. 1988; 12:1149-
1 155.

146. Harman EL, Kilbum H Jr, O’Donnell JF, et al. Interracial access to selected
cardiac procedures for patients hospitalized with coronary artery disease in new york
state. Medical Care. 1991;29(5):430—441.

147 . Gillum RF. Coronary artery bypass 5 surgery and coronary angiography in the
United States, 1979-1983. Am Heart J. 1987;113:1255-1260.

148. Cowley MJ, Mullin SM, Kelsey SF, et a1. Sex differences in early and long-term
results of coronary angioplasty in the NHLBI PTCA registry. Circulation. 1985;71:90-
97.

149. Holt GW, Sugrue DD, Bresnahan JF, et al. Results of percutaneous transluminal
coronary angioplasty for unstable angina pectoris in patients 70 years of age and older.
Am J Cardiol. 1988;61:994-997.

150. Dorros G, Janke L. Percutaneous transluminal coronary angioplasty in patients
over the age of 70 years. Cathet Cardiovasc Diagn 1986;12:223-229.

151. Hartzler GO, Rutherford BD, McConahy DR, et al. “High-risk” percutaneous
transluminal coronary angioplasty. Am J Cardiol 1988; 61:336-37G.

152. Cowley MJ, Kelsey SF, Costigan TM, et al. Percutaneous transluminal coronary
angioplasty in women: gender differences in outcome. In: Baker ED, Packard B,
Wenger NK, Clarkson T, Tyroler HA, eds. Coronary Artery Disease in Women. New
York, NY: Haymarket-Doyma; 1987;251-256.

153. Scott NA, Kelsey SF, Detre K, et al. Percutaneous transluminal coronary
angioplasty in African-American patients (the National, Heart, Lung, and Blood
Institute 1985-1986 Percutaneous Transluminal Coronary Angioplasty Registry).
Am J Cardiol 1994; 73(16): 1141-1146.

180

.qufl'

'. . .i: mhv‘fi‘fi"! 4'; . writ-r7} :4 .-,. nun. 1:: 44311.73 11!: 233-” '

:-..-.._-. - - - - -

'- ‘ ' 5m imam

   
  
   
 
  
 
    
 
   
     
   
  
 
 
 
 
 
 
 
  

1f
. 1.1; rt 2 ....n’uu.) .1M EM

3.. . ; .1.""§Ub‘dfl‘

,1 ,. , ... . l~\‘ l- .51 t“ ..V
. . . 5.: : :1. f"! 33:51:39.)“. '
a:

,I‘.’_)‘.i ..‘l- I!“ cw"

. a ~ 1.1". ..cmioH l“
' . ‘ amimnvq 305w.

.. ,551; 13:-.1an Cm
1?.”

l'w." 1"; v ..glr‘ .Y"
51,: 5:14;? rum-U . "

’ 5.;~ @1003 .9“ .
... ......mno ulna” .
5,” a":

A"

.‘ J
11.5.1.1!!! ! _.-...-;’; _ .‘z. ' , . 7' " ' ' "Q “1“")"mm a

0.; ";".'7. ; ~ -- ' '. ‘ war; ((""IJ3§‘“‘
..~.~:~:-3;

. w... k, ' ‘.>..’f.' ' . \I . ‘ 1:1 2: :wiufil .00 M‘ .~-’--7‘

i! .. ‘ ... 5 r mud. _ . ‘. :1.“ H: mm; Wm >100 fi‘

("kt-TIM. '.'Zf‘vj~EL.':.‘.{-r.".‘3 ,;._.mm;L. .' ") .Ni £33390”: 4' (5 “"' I'M fl”
4 rename Ill 5
my! sash-‘5’ :1an mm ‘g'pavro'l .42): A?! 5:150:11 , 111021147 ' ?v_ ~, A '

gzqutfg'm.“ mum-551.1 few: '

; y wwwukrmdamram'uwrr "A has Am! ‘45 W5:_.
'- ; vamlmmmmmmmm-fl‘
‘ ' WWWWMMW

 

. ‘-'.\ 5",. ._ , '10?-

 

i

:, .arrzm !;:'n.'u::er.n:.“:i.~uufi1hd;’ .. is H- 53:3: mo} 42: (be: )1 [MM
,3 mafiw‘é, (1! my? :ni 'xA’ --.r3ir£ 11. man namb mam; masticati-

wvx 2mm” :1 team-(l 113512.33me 2c. AH 1601.1.an

~t=:.-.‘-.; .-. 5 A— .‘5..~5. . -3» > . 5‘r‘1.v»:smslflwma-

   
   
 
    
  
 
  
 
    
    
 
  
  
   
 
    
  
  
   
  
  
  
 
  
 
  
 
   
  

...“.
.;.-:' .‘ .5 '. ' m 5341.111; .1143“
- - : - 5.: 55:.-.r.aamd

,'5- .... 5 -i|-' 'l-‘1A,HOM
- .‘ ' ~ .. ~- (“1:111:1va .
4 ‘r

1 . jl‘dl,‘ ,1”: ”M 5““ t
can 5.; WW",

1 P41 Y‘JMIO“ .W
«16310731 W
.551; mm; 5» rm .-

am

. mam .0“
"want mm
..%'-‘:M m

5‘51‘1 “4' mum TN '
5, 9' . 25M? herma- 7.“
, u ; .

u... . '- '- 5 35' -‘: 1M MWOD .OM.

..., . . . , 35.-gum rlcmnrnmmi, '

_ . 5 . -. . .. :5 «anon m
_‘ 5 . - .f‘ '51}:er
: rota-05 ."

15.1.3"?

0‘- '1 i 1382-; . .. 5- ,;- (fir/wt)? 'lusga‘

 

I’dh;
anal; ‘ ...:t; 5 1: 5 -‘. .ih‘ hf..:I.-.'-ndlt;x 00 M? ,
-'- "- 5 ~‘ —'.¢Er-;>1.:2.5 ' mmgfia 1!?le . "

;:v_s-:?,:::.': {mu-1M ,
vmimrmfismimwmze‘l .1313 ..hamt’] 18w.- :7”:
mummtauflinwnsmnn .' ;,,;‘_,V.__

. mgmwlm‘mtmfl‘ 5 '

am nit --:-~

ӣ54

 

 

"7'11 @fifl'fliflifl @‘Wfl'flflmfiflr