Effect of home exercise intervention on functional capacity and quality of life in decompensated heart failure patients

MISSING IMAGE

Material Information

Title:
Effect of home exercise intervention on functional capacity and quality of life in decompensated heart failure patients
Physical Description:
ix, 110 leaves : ; 29 cm.
Language:
English
Creator:
Handberg-Thurmond, Eileen
Publication Date:

Subjects

Subjects / Keywords:
Exercise Therapy   ( mesh )
Heart Failure, Congestive   ( mesh )
Quality of Life   ( mesh )
Functional Residual Capacity   ( mesh )
Walking   ( mesh )
Genre:
bibliography   ( marcgt )
theses   ( marcgt )
non-fiction   ( marcgt )

Notes

Thesis:
Thesis (Ph. D.)--University of Florida, 1998.
Bibliography:
Includes bibliographical references (leaves 98-109).
General Note:
Typescript.
General Note:
Vita.
Statement of Responsibility:
by Eileen Handberg-Thurmond.

Record Information

Source Institution:
University of Florida
Rights Management:
The University of Florida George A. Smathers Libraries respect the intellectual property rights of others and do not claim any copyright interest in this item. This item may be protected by copyright but is made available here under a claim of fair use (17 U.S.C. §107) for non-profit research and educational purposes. Users of this work have responsibility for determining copyright status prior to reusing, publishing or reproducing this item for purposes other than what is allowed by fair use or other copyright exemptions. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder. The Smathers Libraries would like to learn more about this item and invite individuals or organizations to contact the RDS coordinator (ufdissertations@uflib.ufl.edu) with any additional information they can provide.
Resource Identifier:
oclc - 51555936
ocm51555936
System ID:
AA00024431:00001

Full Text









EFFECT OF HOME EXERCISE INTERVENTION ON FUNCTIONAL CAPACITY
AND QUALITY OF LIFE IN DECOMPENSATED HEART FAILURE PATIENTS





By

EILEEN HANDBERG-THURMOND























A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY

UNIVERSITY OF FLORIDA

1998














Copyright 1998

by

Eileen Handberg-Thurmond













ACKNOWLEDGEMENTS



I would like to thank my husband Mike for all of his unwavering support

throughout my doctoral program. His understanding of the demands of the

graduate program made completing it that much easier.

I would like to thank my supervisory committee. Special thanks go to Dr.

Kathleen Smyth, my chair. Her patience and support will not be forgotten.

Thanks to Dr. Joyce Stechmiller for her guidance into graduate school and her

support along the way. Thanks to Dr. Michael Pollock for allowing me to take

part in the education and learning activities at the Center. Thanks to Dr.

Hossein Yarandi for his humor and patience with statistical analysis. Thanks to

Dr. Marian Limacher for being a role model and for listening as I went through

the process. Special thanks to Dean Lockhart and my brother Roger for their

words of encouragement along the way.

Heart felt thanks to Drs. Burt Silverstein and Carl J. Pepine for being

mentors. Their encouragement, willingness to teach, and support of my

educational and professional efforts have been the cornerstone of my

development. And finally, many thanks to the patients whose willingness to take

part will always be appreciated.


iii













TABLE OF CONTENTS

page

A C KN O W LED G M ENTS.................................................................................... iii

LIS T O F TA B LE S .................................................... ........................................... vi

LIS T O F F IG U R E S ........... ...................... ...............................................vii

A B S T R A C T ..................... ... ....................................................................... .v iii

CHAPTERS

ONE INTRODUCTION...................................... ............................... 1

Background of Problem................................... ........................ 1
Conceptual Framework..........................................................4
Purpose of the Study ............................................................8
Significance of the Study............................................................8
Statement of Hypotheses...........................................................9
D efinition of Term s ................................................. ....................... 9
Scope and Limitations ......... .........................................................11

TWO REVIEW OF THE LITERATURE..................................................12

Heart failure pathophysiology........................................................12
Skeletal Muscle Function.............................................. .......15
S ym ptom s........................................................................ ......17
Medical Optimization as Therapy...........................................18
Role of Exercise Training..................................................................25
Functional Capacity ................................................................. 28
Q u a lity of L ife ............................................................................ .. 3 1
S u m m a ry .................................................................................. ... 3 3






iv








TH R EE M ETH O D S................................................................................. 35

Research Design...................................................... ..................35
Selection of Subjects................................................. ...............35
Study Protocol.............................................................. 37
P ro ce d u re s.............................. .................... ........... ................3 9
Data Analysis................................. ................ .................... 49
S um m ary...................................................... .. .... ...................49

FOUR ANALYSIS OF DATA.....................................50

Recruitment Procedures................................................. ..... 50
Characteristics of the Sam ple............ ..........................................51
Patients W ithdrawn from Study ....................................................54
Hemodynamic Characteristics of 12 Patients ........ ............ ..57
Functional Capacity........................................................... 58
Hom e Intervention................................................. .... ..... ..........62
Self Reported Quality of Life........................................................66
Analysis of Data in Relation to the Hypotheses......................... 69
Sum m ary......................................................................................72

FIVE CONCLUSIONS AND RECOMMENDATIONS.............................74

C onclusions.............................................. ...................................76
Discussion of the Findings............................... ................................78
Summary........................................................... .................84
Recom m endations....................................................................... 85
Im plications for Nursing Practice.................................................86

APPENDICES

A EXERCISE INSTRUCTIONS........................................................88

B LIFESTYLE MANAGEMENT INSTRUCTIONS.............................89

C ACTIV ITY D IA RY............................... .........................................90

D SCALES FOR ACTIVITY DIARY.....................................................91

E INFORM ED CONSENT ........................................ ........................ 92

R E F E R E N C E S ......... ...........................................................................................98

BIOGRAPHICAL SKETCH................................................. ..................... 110


V













LIST OF TABLES

Table .pge

3.1 Schedule of Study Protocol Procedures..........................................40

4.1 Characteristics at Study Entry for 23 Patients ................................... 52

4.2 Characteristics of 15 Patients................................ ................. ..............56

4.3 Post Medical Optimization Hemodynamics............................................57

4.4 Cardiopulmonary Responses before and after Home Intervention...........59

4.5 Analyses of Cardiopulmonary Variables of Home Intervention Group......61

4.6 Characteristics of and Adherence to Home Intervention by Patient.........63

4.7 Changes in NYHA Classification over 8 weeks......................................64

4.8 Activity Recall at Entry, 4, and 8 Weeks ........................................ ..65

4.9 MAACL-R Traits at Study Entry............................................................67

4.10 MAACL-R State Responses at Entry, 4, and 8 Weeks...........................68

4.11 PAIS-SR Responses at Entry, 4, and 8 Weeks......................................69













vi













LIST OF FIGURES

Figure page

1.1 Roy's M odel of Adaptation ....................................................................... 6

1.2 Medical Optimization and Home Walking Intervention.............................7
as Stimuli in Roy's Adaptation Model

































vii








Abstract of Dissertation Presented to the Graduate School of the
University of Florida in Partial Fulfillment of the Requirements
for the Degree of Doctor of Philosophy

EFFECT OF HOME EXERCISE INTERVENTION ON FUNCTIONAL CAPACITY
AND QUALITY OF LIFE IN DECOMPENSATED HEART FAILURE PATIENTS


by

Eileen Handberg-Thurmond

May 1998

Chairman: Kathleen A. Smyth
Major Department: Nursing

The purpose of this research was to evaluate the effects of a home

exercise intervention on functional capacity and quality of life in decompensated

heart failure (HF) patients. Fifteen men and women who had been admitted for

medical optimization for decompensated (HF) were randomly assigned to home

intervention (n=8) or control (n=7). The intervention consisted of a progressive

walking program for 8 weeks.

Functional capacity was measured using a 6 minute walk test, exercise

testing with gas exchange to assess changes in distance walked, total exercise

time and VO2peakat study entry and after 8 weeks. Quality of life was assessed

using the PAIS-SR and MAACL-R at study entry and at 4 or 8 weeks.

Student t-test statistics and repeated measures ANOVA were used to

examine variables between and within the groups.

There were no statistically significant changes between the two groups in

total distance walked during a 6 minute walk test (t=0.64, p=0.53), total exercise
viii








time (t=-0.06, p=0.94), VO2peak (t=0.44, p=0.66) at study entry and after 8 weeks.

There were no statistically significant improvements in quality of life for either

group at 4 or 8 weeks. There was shift towards improved functional class,

although not statistically significant, in both groups at 8 weeks as demonstrated

by changes in New York Heart Association classification to II and III from III and

IV. The majority (75%) of home intervention patients were compliant with a 3

day a week program. Subjective activity recall by these patients at 4 and 8

weeks revealed that 50% reported more activity in the previous week compared

to 14% of the control group.

This study of a home intervention in patients with decompensated HF

provides preliminary data that this intervention is feasible and safe. Whether

such an intervention proves to be effective in improving physical function and

quality of life needs to be further studied on a larger sample.




















ix













CHAPTER ONE
INTRODUCTION


Background of the Problem

Heart failure (HF) is a debilitating, fatal syndrome manifested by exercise

intolerance and fatigue, which is a result in part of the heart's inability to meet

the metabolic supply demands of the body. HF (AHA, 1996) affects 1-2% of the

adult population, with the annual incidence of 400,000 new cases in the United

States. In the US alone in 1988, there were 1.8 million patients hospitalized with

a diagnosis of heart failure (English & Mastrean, 1995). Heart disease in

general is on the decrease, yet the incidence of HF is increasing and the

prognosis is poor. Conservative estimates of the annual mortality rate from this

disease range from 15-60% (Hanson, 1994, English & Mastrean, 1995).

Patients in the general population with heart failure have a 50% 5 year survival,

while those with advanced heart failure have a 50% 1 year survival (Poole-

Wilson, 1993).

Heart failure is characterized by low cardiac output due to impairment of

the myocardium to contract. This impairment in central hemodynamics may be

caused by 1) scar from previous myocardial infarctions or ischemia; 2) chronic

volume overload due to hypertensive or valvular heart disease resulting in


1







2

generalized dilation; 3) viral syndromes which result in global hypokinesis; or 4)

idiopathic or unknown causes resulting in global hypokinesis (Smith & Kampine,

1990). Regardless of the etiology of the heart failure, central hemodynamic

compromise results in both short and long-term compensatory mechanisms to

preserve cardiac output. These adaptations occur both centrally and

peripherally and lead to reduced function. There is no treatment available to

completely reverse the physiological insult to the myocardium. Nevertheless

pharmacologic therapy is used to optimize cardiac function and reverse or

attenuate some of the adaptive mechanisms with a goal of improving function

and reducing mortality and morbidity (Cohn et al, 1986; The SOLVD

Investigators, 1991; The SOLVD Investigators, 1992).

In spite of the beneficial effects of these pharmacologic interventions

patients gradually reach end-stage heart failure unless they are transplanted.

End stage HF is characterized by worsening of dyspnea, fatigue, and edema

resulting in more frequent hospitalizations for acute medical management until

patients are refractory and the heart fails. Current acute in-hospital therapy

consists of optimization of central hemodynamics through diuresis and afterload

reduction with standard therapy (diuretics, digoxin, and angiotensin converting

enzyme (ACE) inhibitors) combined with inotropic infusions such as milrinone,

dobutamine, or dopamine (Costanzo et al, 1995). This aggressive therapy may

result in noticeable improvements in central hemodynamics and is accompanied

by a reduction in symptoms of dyspnea, fatigue, and edema. In addition, there









may be a delayed improvement in exercise tolerance lasting up to 10 weeks

after treatment (Pickworth, 1992). Once discharged from the hospital, these

patients improve but gradually they begin to deteriorate and their symptoms

return, in spite of optimization of medical therapy.

The treatment costs associated with a diagnosis of HF are staggering.

Over 10 billion dollars are spent annually for hospitalizations, outpatient care,

and medical therapy (English & Mastrean, 1995). In a recent survey, 30 day

readmission rates for HF in five hospitals ranged from 10-23%, with the 90-day

readmission rate between 22-42% (English & Mastrean, 1995). Recent

evaluations of HF management strategies suggest that aggressive medical

management can result in significant savings. The savings are realized as a

result of optimization of medical therapy provided to patients as inpatients and/or

outpatient services which result in significant reductions in repeat

hospitalizations (Cintron, Bigas, Linares, Aranda, & Hernandez, 1983; Kegel,

1995).

The effect of this optimization, a period of improved functional capacity

and clinical status, has not been evaluated to determine if additional non-

pharmacologic interventions could be beneficial. This investigator has

hypothesized that a home exercise intervention could take advantage of the

improved central hemodynamics and reduction in symptoms to encourage

patients to increase their activity which would help them to achieve improved

functional capacity through improvements in their level of conditioning and









partial reversal of peripheral dysfunction by improving skeletal muscle

metabolism. While exercise training in HF patients is more accepted in stable

patients, the use of a home exercise intervention has not been tested in this

medical optimization treatment period immediately after hospital discharge. In

addition to the physiological adaptations to HF and possible interventions to

reverse or attenuate those mechanisms, the role of psychosocial adaptations

that take place during periods of decompensation in chronic illness needs to be

assessed in order to determine the role it plays in the willingness of patients to

participate in additional activities that may affect their level of functioning.

Conceptual Framework

Roy's Adaptation Model (Roy, 1984) was chosen to guide this research.

This is a systems model that focuses on adaptations to stress. This adaptation

process is a response to stress which triggers behaviors which are either

effective or ineffective. This model is particularly applicable to this patient

population of decompensated HF because the chronic nature of the disease

requires constant adaptation. Roy's model defines adaptation as the human

systems capacity to adjust effectively to changes in the environment and, in turn

to affect the environment. Adaptation in the system occurs within four modes:

physiologic, self-concept, role function, and interdependence. Patients with HF

clearly have undergone significant physiologic adaptations due to the central

and peripheral circulatory changes which result in changes in function. In

addition, these changes in function directly affect role function, self-concept, and

interdependence within the system.








5

Roy's model has focused on nursing interventions that can be utilized to

facilitate adaptation. Using the model, the first step is the assessment of the

patient and situation in order to identify focal, contextual and residual stimuli that

influence behaviors that may affect the patient's ability to adapt. Focal stimuli

are those factors which provoke the situation and demand attention; contextual

stimuli are other stimuli which contribute to the focal stimuli. Residual stimuli are

more vague in nature, and their influence cannot be fully appreciated (Blue et al,

1994).

HF is a chronic process which results in a series of adaptations over time,

both physiological and psychological. The period of decompensation studied in

this research results in a significant focal stimuli which requires the subjects to

seek immediate medical attention. The focal stimuli is a result of changes in

physiological function which result in the inability to perform activities of daily

living, and are accompanied by severe symptoms such as dyspnea, fatigue, and

reduced exercise tolerance. The prescribed medical treatments may or may not

improve function and, as a result, may require additional short and long term

adaptations.

Adaptation to stressors is achieved by utilizing coping mechanisms--

regulator and cognator. Regulator coping mechanisms are used to deal with

physiological stimuli, while cognator mechanism are used to deal with cognition,

judgement, and emotion. The regulator mechanisms most often are not directly

perceived by the patient, but can result in cognitive awareness. For










decompensated HF patients who have received medical optimization, the

resulting improved hemodynamics lead to improvement in symptoms and

increased energy.

Patients respond to stressors with adaptive behaviors that either

contribute to survival, growth, or mastery and are considered adaptive, or

behaviors that are maladaptive and ineffective. Figure 1.1 illustrates Roy's

model in terms of the person as the adaptive system.



Input Control Effectors Output
processes
Stimuli Coping D Physiological function Adaptive
Adaptation > mechanisms Self-Concept 0 and
level Regulator Role function Ineffective
Cognator Interdependence responses

<- Feedback

Figure 1.1. Roy's Model of Adaptation. From "Introduction to Nursing: An
Adaptive Model" by C. Roy, 1984, p. 30. Copyright 1984 by Prentice Hall.



Applying Roy's model to decompensated HF patients illustrates how the

implementation of a home walking intervention can positively affect change.

Nursing interventions, such as the home walking intervention, are a way patients

can directly participate in health care treatments which may result in

improvements in self-concept, role function, and interdependence. It was

assumed that patients willingly entered the health care system for medical

optimization of their HF. The medical optimization treatment is a stimulus from








7

which adaptation may result on a physiologic level. It serves as an internal

stimulus which affects both the regulator and cognitive processes through

improvement in central hemodynamics and changes in functional capacity. It is

expected that the patients are then more receptive to additional external stimuli



Input Control Adaptations Outcomes
processes

Stimuli Adaptive
Responses

Functional
Medical .. Capacity
Optimization > Regulator -Physiological Function lHemodynamics
Cognator .. RExercise time
Walking lVO2peak
Intervention ->
Self-Concept I QOL
Role function ,
Interdependence

3= 3= FEEDBACK = .

Figure 1.2. Medical Optimization and Home Walking Intervention as Stimuli in
Roy's Adaptation Model.

such as the walking intervention, which can result in further adaptations both

peripherally and psychosocially resulting in changes in functional capacity and

quality of life.

The variable of functional capacity as measured by total exercise time,

oxygen consumption, and 6 minute walk assesses patients' ability to adapt to

changes in physiological stimuli. The psychological adaptation of these patients

is measured by two instruments. The Psychosocial Adaptation to Illness Survey

(PAIS) was designed to examine the responses to chronic illness in seven








8
domains: health care orientation, vocational environment, domestic environment,

sexual relationships, extended family relationships, social environment, and

psychological distress. These represent areas of measure that can be used to

define responses in terms of role function, self concept, interdependence

(Derogatis & Derogatis, 1983), in addition the Multiple Affect Adjective Check

List-Revised (MAACL-R) was designed to assess changes in affect over time

(Zuckerman & Lubin, 1985).

Purpose of the Study

The purposes of the study are a) to determine the efficacy of medical

optimization on functional capacity at study entry and 8 weeks later, b) to

examine the effects of a home exercise intervention on functional capacity at

study entry and 8 weeks later, c) to measure the effects of medical optimization

and home exercise intervention on quality of life at study entry and at 4 and 8

weeks, and d) to determine the safety of a home intervention initiated

immediately upon hospital discharge.

Significance of the Study

Patients with decompensated HF have intolerable symptoms of dyspnea,

fatigue, and edema which result in exercise intolerance and changes in their

quality of life (QOL). The goal of HF management is prevention of

decompensation, improvement of functional status, lessening of symptoms, and

reduction in morbidity and mortality (Poole-Wilson, 1993). Medical optimization

has been reported to reduce symptoms, improve exercise tolerance, and result









in fewer hospital readmissions (Smith, Fabbri, Pai, Ferry, & Heywood, 1997). It

is anticipated that this period of improved cardiac function can be further

extended by a home exercise intervention that is designed to increase daily

activity levels. Increased levels of activity during this hemodynamically

improved period may result in improved skeletal muscle function, and a partial

reversal of the muscle atrophy. If this testing of a home exercise intervention is

safe we may expect increases in activity levels that may lead to improvements in

functional capacity and quality of life.

Statement of Hypotheses

The research hypotheses of this study were as follows:

a. Medical optimization in patients with decompensated HF results in an

increase in functional capacity after 8 weeks.

b. Home exercise intervention will result in significant improvement in

functional capacity at 8 weeks when compared to controls.

c. Home exercise intervention will result in significant improvement in quality

of life when compared to controls at 4 and 8 weeks.

d. Home exercise intervention in patients with decompensated heart failure

who have received medical optimization is feasible and safe.

Definition of Terms

Exercise intervention is participation in a program of exercise of

prescribed frequency, intensity, duration and mode of activity aimed at improving

cardiorespiratory fitness.








10
Functional Capacity is the maximum oxygen uptake that one can utilize

under the most strenuous exercise that is reflective of the overall oxygen

transport system and can be predicted with relative accuracy from a graded

exercise test.

Quality of Life is a multidimensional concept that addresses a person's

feelings about their health, physical function, psychological function, and social

interactions.

Medical Optimization is the improvement in symptoms such as dyspnea,

fatigue, paroxysmal nocturnal dyspnea, and peripheral edema, and/or

physiological measurements such as increase in blood pressure, reduction in

heart rate, increase in cardiac output, and reduction in pulmonary capillary

wedge pressure after adjustment of medical therapy which can include short

term infusions of inotropic therapy.

Functional Class is the assessment of current activity level as defined by

the New York Heart Association Classification system (Criteria Committee,

1964).

Operational Definition of Terms

Functional capacity can be measured using multiple tools to assess

exercise capacity. In this study functional capacity was measured using three

testing strategies: total exercise time which was the time to reach symptoms or

85% of an age predicted heart rate maximum while participating in a graded

exercise stress test using a standardized exercise protocol, oxygen consumption









through gas exchange during exercise testing at peak exercise, and distance

walked during a 6 minute walk test.

Quality of Life was measured by two paper and pencil tests, the Multiple

Affect Adjective Check List Revised (MAACL-R) (Zuckerman & Lubin, 1985), and

the Psychosocial Adjustment to Illness Scale-Self-Report (PAIS-SR) (Derogatis

& Derogatis, 1990).

Medical Optimization was determined by self report and improvements in

selected physiological measurements: blood pressure, heart rate, cardiac

output, and pulmonary capillary wedge pressure.

Functional Class is the assessment of current activity level achieved with

or without symptoms using the New York Heart Association Classification system

(Criteria Committee, 1964).

Scope and Limitations

This study was limited to recruitment of subjects from a large tertiary

referral center in the southeast. The home exercise intervention was felt to

potentially limit the full potential of participants to achieve maximal gains in

functional status due to lack of direct supervision, and low intensity of the

activity.













CHAPTER TWO
REVIEW OF THE LITERATURE

This chapter deals with the pathophysiology, hemodynamics, skeletal

muscle function, symptomatology, medical interventions and non-pharmacologic

treatments, and quality of life of patients with heart failure.

Heart Failure Pathophysiology

HF is a result of the body's inability to meet the metabolic demands of the

body. It is considered to be a syndrome with many causes as opposed to a

specific disease (Smith & Kampine, 1990). HF is characterized as a high

cardiac filling, low output state due to the impairment of the ventricle. The

impairment may stem from the presence of a scar secondary to myocardial

ischemia or infarction, remodeling of the myocardium after a large infarction,

generalized hypertrophy or dilatation because of chronic volume overload due to

hypertension or valvular heart disease, or global hypokinesis due to viral or

idiopathic causes (English & Mastrean, 1995). Early studies that evaluated

incidences of heart failure, like Framingham, reported the primary etiology to be

hypertension (Ho, Pinsky, Kannel, & Levy, 1993). Currently, in the majority of

patients with HF (approximately 70%), ischemic heart disease is the primary

etiology (Bourassa et al, 1993; Garg, Packer, Pitt, & Yusuf, 1993; Costanzo et al,

1995). Regardless of the etiology, changes in the pressure and volume

12








13
relationship of the myocardium in HF result in both acute and chronic

compensatory mechanisms being activated in order to preserve function. These

mechanisms affect the myocardium, fluid balance, bioenergetics of the

cardiovascular system and the peripheral circulation (Smith & Kampine, 1990).

The cardiac muscle has the ability to compensate for changes in volume

and pressure. The force or tension of the contracting muscle can be increased

by prestretching the muscle when presented with increased volume. The Frank

Starling law describes this relationship and is expressed as a curve where

increasing end diastolic volume results in increasing ventricular pressure (Smith

& Kampine, 1990). This relationship can be affected by many mechanisms,

shifting the curve to the right or the left. Neurohormonal activation shifts the

curve up and to the left, because of the influence of the sympathetic nervous

system. Different pharmacological compounds can also alter contractility, which

is defined as the ability of the heart muscle to generate power, either positively

or negatively. Pathological factors such as myocardial ischemia or viral

syndromes can negatively affect this volume pressure relationship and shift the

curve down and to the right. Starling (Smith & Kampin, 1990) demonstrated that

if the ventricle is stretched beyond the physiological limit the systolic pressure

will decline, indicating impending failure.

The short-term response to volume overload is the activation of the

sympathetic nervous system. Release of norepinephrine results in immediate

increases in heart rate to increase contractility and preserve function (Zelis,








14
Sinoway, Leuenberger, Clemson, & Davis, 1991). In addition there is an

increase in systemic resistance that is thought to occur at the level of the

vascular bed and be mediated by the endothelium (Poole-Wilson, 1993). If the

impaired function is chronic, more long-term adaptations take place. In the heart

muscle itself, chronic volume overload results in left ventricular hypertrophy to

maintain stroke volume. While initially effective, the increase in muscle mass

results in more oxygen demand, and the increased afterload further impairs the

failing heart. The development of hypertrophy can also be accompanied by

myocardial cellular fibrosis leading to ventricular stiffness, which in turn results

in diminished compliance. As a chronic adaptation, ventricular dilation can also

occur. Initially this increase in size allows the ventricle to generate a larger

stroke volume with less muscle shortening. The continued dilation with chronic

HF results in an inability to compensate stretching beyond the physiological

limits.

While initial sympathetic stimulation increases myocardial contractility,

chronic stimulation leads to down regulation of beta receptors, which leads to

attenuation of their effects (Zelis, Sinoway, Leuenberger, Clemson, & Davis,

1991). In addition, excessive sympathetically mediated vasoconstriction occurs

because of increased norepinephrine spillover and impaired clearance (Drexler,

Munzel, Riede, & Just, 1991). The renin-angiotensin system is activated,

resulting in sodium and water retention, and strong peripheral and renal

vasoconstriction result in order to maintain plasma volume (Drexler, Munzel,








15

Riede, & Just, 1991). These changes maintain homeostasis. Chronic activation

of renin-angiotensin and its resulting sodium retention can result in limiting the

metabolic vasodilatory capacity of vessels both centrally and peripherally.

All of these mechanisms affect the central circulation. Chronic HF, in

spite of these adaptive mechanisms, is characterized by low cardiac output,

primarily due to reduced stroke volume and increased pulmonary pressures and

elevated venous pressure. In addition to the adaptive mechanisms that affect

the central circulation, there are adaptations in the peripheral circulation that

occur in response to the low filling state that can play an important role in HF

management.

Skeletal Muscle Function

Drexler et al (1992) looked at the structure of skeletal muscle in 57

subjects with HF. The results demonstrated that patients with HF developed

significant abnormalities of skeletal muscle, which reflected a depressed

oxidative capacity of working muscle. The volume density of the mitochondria of

skeletal muscle were reduced by approximately 20%. Capillary length density

was reduced and fiber type shifted from type I (slow twitch) to type II (fast twitch).

These changes reflect the late occurring compensatory mechanisms to maintain

adequate tissue perfusion both centrally and peripherally.

The short term response to inadequate tissue perfusion is sympathetic

stimulation, resulting in the release of norepinephrine, causing systemic

vasoconstriction. The activation of the renin-angiotensin system preserves







16
plasma volume by increasing sodium and water retention. However, chronic

volume overload and chronic sodium and water retention lead to impaired

vasodilatation and vascular wall stiffness, which compromises skeletal muscle

function and metabolism. The changes to the peripheral vascular structure

result in alterations that contribute to impaired peripheral vasorelaxation

(Drexler, Munzel, Riede, & Just, 1991). This adaptation of the skeletal muscle

results in reduction in oxidative metabolism and decrease in mitochondria and in

capillary density. In addition to the changes that result from decreased tissue

perfusion due to a low flow state, additional changes occur due to the effects of

deconditioning and atrophy. As a result there is a decrease in muscle mass and

a shift of fibers from type I or slow twitch to type II or fast twitch. These changes

reflect the shifting reliance from aerobic to an anaerobic pathway to maintain

force (Lipkin, Jones, Round, & Poole-Wilson, 1988; Sullivan, Higginbotham, &

Cobb, 1988).

It has been demonstrated that during exercise, peripheral blood flow

(Zelis, Sinoway, Leuenberger, Clemson, & Davis, 1991) and skeletal muscle

metabolism are abnormal in patients with HF (Weiner et al, 1986; Wilson et al,

1985). Minotti et al (1991) demonstrated that HF patients have impaired muscle

endurance that was independent of muscle blood flow, indicating that there are

parallel peripheral, that is, skeletal muscle, adaptations that occur in HF.

Muscle metabolism can be assessed directly by 31P magnetic resonance

spectroscopy. This technology allows for the continuous monitoring of skeletal







17

muscle inorganic phosphate, phosphocreatine, adenosine triphosphate (ATP),

and pH during imaging. The ratio of inorganic phosphate to phosphocreatine

(P/PCr) correlates closely with adenosine diphosphate (ADP), the principal

regulator of mitochondrial oxidative metabolism. The method has been shown to

be sensitive to cellular oxygen availability, and therefore it is possible to

examine changes in oxygen delivery to skeletal muscle (Wiener, Maris, Chance,

& Wilson, 1986). Using this direct measure, it has been shown that patients with

HF have impaired skeletal muscle metabolism (Mancini et al, 1990), particularly

with exercise (Massie et al, 1987b; Weiner et al, 1986). Intracellular pH declines

more rapidly during exercise in CHF patients, which together with a more rapid

rise in venous lactate is indicative of an earlier onset of anaerobic glycolysis.

The more rapid decline in phosphocreatine and rise in inorganic phosphate

during exercise indicates impaired oxidative metabolism (Minotti and Massie,

1992). Similar changes in skeletal muscle metabolism have been demonstrated

in healthy sedentary adults indicating that changes in skeletal muscle function in

heart failure patients may be a consequence of deconditioning (Chati et al,

1996), leaving open the opportunity for interventions that promote conditioning.

Symptoms

Considering the variety of adaptations and abnormalities that result from

chronic HF it is not surprising that there may be multiple mechanisms involved in

the symptoms associated with this syndrome (i.e., exercise intolerance,

dyspnea, fatigue, and edema). Exercise intolerance is due in part to reduced







18
cardiac output, which may actually result more from deconditioning and its

skeletal muscle adaptations, such as reduced muscle mass, loss of oxidative

capacity and shifting of fiber types. Fatigue, while thought to be related to

volume overload and impaired cardiac output, may also be a result of skeletal

muscle metabolism (Massie et al, 1987a). The pathophysiological mechanisms,

whether due to central or peripheral causes, that result in symptoms of fatigue,

exercise intolerance, and dyspnea are the targets for therapy in this population.

Medical Optimization as Therapy

Medical therapy for HF has as its goal to improve the contractility of the

myocardium and to reduce afterload and preload in order to reduce the workload

and improve cardiac output. More recently medical therapy has been focused on

prevention, for example, preserving function through decreasing myocardial

infarction size and optimizing myocardial remodeling after myocardial infarction

and ischemia (Pfeffer et al, 1992). Treatment of heart failure has progressed

from diuretics and cardiac glycosides, to preload and afterload-reducing agents,

and most recently angiotensin converting enzyme (ACE) inhibitors (Smith,

1991). ACE inhibitors have made the biggest impact in HF treatment. Initially

the benefit was thought to be related to reductions in blood pressure. They have

now been shown to reverse endothelial dysfunction in subjects with CAD

indicating effects across the entire vasculature. ACE inhibition may work by

interference with the renin-angiotensin system by reducing circulating and

vascular angiotensin II levels or by reducing vascular sodium content. These







19

changes then improve oxygen availability of working muscle and improve

systemic oxygen consumptions (Drexler et al, 1989). In their study of 21

patients, the systemic and peripheral effects of long term ACE strongly

resembled those observed after 6 months of endurance training. Long-term

ACE increased oxygen consumption at similar workloads during exercise, which

may be in part due to increased exercise training. ACE inhibition appeared to

reverse in part some of the abnormalities of the peripheral circulation, the

inability of vessels to dilate adequately during exercise.

Current standard medical therapy for HF consists of digoxin, diuretics,

and ACE inhibitors (Williams et al, 1995). In addition, new agents are currently

being developed and evaluated, and already approved cardiovascular agents

such as beta blockers are being evaluated for use as new indications for heart

failure (Fisher et al, 1994; Packer et al, 1996). In spite of improvements in

mortality and morbidity with triple therapy, and the further improvement with

newer compounds, the underlying disease is not cured and despite intensive

therapy, patients gradually decline in spite of optimal therapy. In patients with

refractory HF, therapy is geared towards optimization of medical therapy to

achieve improved exercise tolerance and palliation of symptoms such as

dyspnea and fatigue and to maintain a reasonable quality of life. In addition to

optimizing oral therapy, newer intravenous medications are often added acutely

to rapidly change central hemodynamics in order to reduce to acute problem of

volume overload.







20

HF is a dynamic disease process that requires constant assessment and

evaluation of medical therapy in order to maintain hemodynamic balance.

Patients can require frequent adjustments of medical therapy, due to increases

in plasma volume related to dietary indiscretion, effects of over the counter

medications, or changes in pump function. HF patients often present with acute

exacerbations of HF requiring hospitalization and aggressive diuresis and

afterload reduction. In this situation short-term intravenous (IV) infusions of

inotropic agents such as dopamine, dobutamine and milrinone has been used to

improve hemodynamic function (Pickworth, 1992). Short-term inotropic therapy

has been used to improve central hemodynamics, to improve symptoms, as a

bridge to transplantation, and as a last resort medical therapy when intensive

medical therapy is no longer sufficient to keep a patient out of the hospital

(Pickworth, 1992).

Dobutamine is an inotropic agent that increases cardiac contractility

through B, adrenergic stimulation and causes vasodilation through B2 adrenergic

stimulation with little change in heart rate. It is a relatively short-acting

compound with a half-life of 2.4 + 0.7 minutes in patients with Class IV New

York Heart Association (NYHA) classification. Dobutamine is rapidly metabolized

and is excreted in the urine (Pickworth, 1992). The indication to use agents

such as dobutamine is to improve central hemodynamics, which results in short-

term improvements in symptoms such as hypoxemia, dyspnea, fatigue, and

peripheral edema. The treatment is generally short-term for acute







21

exacerbations, or in severe cases as intermittent or continuous therapy in the

outpatient setting. The administration of vasodilators or positive inotropes such

as dobutamine causes immediate improvement of hemodynamics but does not

result in immediate improvement in exercise duration or maximal oxygen

consumption. Conversely there is a delayed effect on exercise duration that

manifests within 4-8 weeks of therapy (Drexler, Munzel, Riede, & Just, 1991).

There is evidence (Unverferth, Blanford, Kates, & Leier, 1980a;

Unverferth, Magorien, Lewis, & Leier, 1980b; Liang et al, 1984) that a short term

infusion of dobutamine results in immediate hemodynamic effects and long term

improvement in symptoms. Leier et al (1982) demonstrated a sustained effect

on functional class for 1 week in 17 patients who had received a 72 hour

infusion. Unverferth et al (1980a, 1980b), in two studies, demonstrated long

term benefit. In the first study of 38 patients, 43% had an improvement in NYHA

class for up to 10 weeks after the infusion. In another study of 23 patients, after

a 72 hour infusion, 11 patients had an improvement in NYHA class 2 months

after the infusion and 3 were improved after 6 months. Liang et al (1979), in a

double-blind study of dobutamine, demonstrated improvements after 4 weeks in

functional class, EF, and exercise tolerance in 6 of 8 patients who received

dobutamine. The improvements in functional capacity that have been reported

are in studies that used high doses of dobutamine (10-25mcg/kg/min)

(Unverferth et al, 1983; Liang et al, 1984; Adamopoulos et al, 1995). These high

doses of dobutamine do result in a significant increase in heart rate which may








22

explain some of the beneficial effects that resemble a training effect. This effect

was studied by Sullivan et al (1985) in 24 healthy men who were randomized to

saline or dobutamine 2 hours daily or exercise on a stationary bicycle.

Dobutamine was given in doses to increase resting heart rate by 20% for 1 hour,

40% for 45 minutes, and 60% for 15 minutes. Otherwise those patients were on

complete bedrest. Oxygen consumption during exercise fell significantly in the

bedrest and saline group but was unchanged in the dobutamine and exercise

groups.

Dobutamine has also been shown to affect the mitochondria of cardiac

muscle. Unferverth et al (1983) examined endomyocardial biopsies in 16

patients with CHF after 3 days of bed rest and then 4-18 hours after a 3-day

dobutamine infusion. At a high dose of dobutamine (15 mcg/kg/min) there was a

significant increase in the crista:matrix ratio indicating an increase in ATP and a

decrease in electron dense particles, which indicate a reduction in degenerating

myocardial cells.

Milrinone is a positive inotropic drug that has a different mode of action

than dobutamine. It belongs to a class of drugs called phosphodiesterase (PDE)

inhibitors. Milrinone inhibits PDE III in both the myocardial and vascular smooth

muscle. This inhibition results in the breakdown of cyclic adenosine

monophosphate (cAMP) leading to higher concentrations in the myocardium,

which then increase contractility by augmenting calcium entry. This increase in

cAMP results in vascular smooth muscle relaxation (Colucci, 1991). Milrinone







23

has been shown to both increase contractility and reduce afterload due to

arterial vasodilatation. Positive chronotropic effects reflect the action of

milrinone on the calcium channel activity of myocardial cells. Infusions of

milrinone in patients with heart failure result in increases in stroke volume with

decreases in systemic vascular resistance and pulmonary capillary wedge

pressure. Both positive inotropic and vasodilatory effects work together to

improve hemodynamic pump function.

Milrinone is often selected for use in HF patients secondary to the

reduction in inotropic responsiveness to beta adrenergic agonists such as

dobutamine due to down-regulation of beta adrenergic receptors. Because

milrinone can restore responsiveness of the myocardium to beta stimulation due

to its effect on calcium and cAMP, which are distal to the beta receptor,

milrinone and dobutamine are often given together (Colucci, 1991).

Milrinone infusions have been given to hundreds of patients with chronic

severe heart failure. In one large multicenter trial 48 hour infusions resulted in

improvements in cardiac index for 34% and reductions in pulmonary wedge by

30% with decreases in systemic vascular resistance of 25%. In addition

symptomatic improvement was noted in 40-60% of patients treated (Anderson,

1991).

While inotropic therapy with agents such as dobutamine and/or milrinone

demonstrates some beneficial effects, the logistics of long-term therapy require

intensive home health care and are fairly expensive; from $200 up to







24
$450.00/day (Collins, Skidmore, Melvin & Engel, 1990; Sherman, 1995).

Current use of inotropes is generally for the short in-hospital infusion (24-72

hours) during which time the entire medical management of the patient is

reviewed and adjusted as appropriate, or as final bridge to transplant. The

aggressive tailoring of therapy demonstrates an in improvement of symptoms

and reduce the number of hospitalizations after discharge (Costanzo et al,

1995). Once therapy has been optimized, patients are discharged with detailed

instructions for medical and lifestyle management.

While the focus of inotropic therapy has been on improving central

hemodynamics, improvements in cardiac output, ejection fraction, and left atrial

pressures at rest and with exercise have been shown to not correlate with

improvements in exercise tolerance (Lipkin & Poole-Wilson, 1986;

Higginbotham, Morris, Conn, Coleman, & Cobb, 1983; Franciosa, Ziesche, &

Wilen, 1979; and Szlachcic, Massie, Kramer, Topic, & Tubau, 1985). The

disparity between the rapid hemodynamic improvements seen after

administration of medical therapy such as ace inhibitors and inotropes and the

gradual improvement in exercise performance weeks or months after starting

therapy points to factors other than central hemodynamics that limit or effect

exercise tolerance (Minotti et al, 1991). Impaired skeletal muscle function is felt

by many to be one cause of impaired exercise capacity in patients with HF

(Drexler, Munzel, Riede, & Just, 1991; Hanson, 1994; McKelvie et al, 1995). As

a result many researchers have begun to evaluate the effects of interventions

aimed at improving skeletal muscle function.








25
Role of Exercise Training

The primary intervention evaluated has been exercise training. It has

been demonstrated to be an appropriate intervention to reverse the changes

brought on by deconditioning or adaptations as a result of HF. In spite of this

new knowledge, published exercise training guidelines have listed HF as a

relative contraindication (Fletcher et al, 1992). Prior to our current

understanding, bedrest was considered to be an acceptable form of therapy for

patients with HF (Coats, 1993). This thinking has been updated, with our

knowledge of the detrimental effects of inactivity on normal but more importantly

on chronically ill populations. This is important because the marked decrease in

daily activity levels seen in HF results in deconditioning. Deconditioning is

characterized by muscle atrophy and wasting. Loss of muscle mass leads to

reduction of mitochondrial oxidative enzyme capacity and fiber shifting

regardless of the central hemodynamics (Coyle, Martin, Bloomfield, Lowry, &

Holloszy, 1985; Sullivan et al, 1985; Moore et al, 1987). When deconditioning is

coupled with adaptive mechanisms brought on by HF, impairment of skeletal

muscle metabolism is added to the equation.

Exercise training as a therapeutic intervention in HF can reverse some of

the skeletal muscle changes brought on by deconditioning, and adaptation to a

low flow state. It does not however, appear to result in any significant changes

in left ventricular ejection fraction. The improvements in central hemodynamics

appear to be through increases in efficiency. More work is achieved at a lower







26
heart rate, with increases in both peak cardiac output and peak leg blood flow

(Coats, 1993). Training results in decreases in minute ventilation and reductions

in lactate. The precise effects of the reduction in lactate on exercising muscle is

not known. There is also a decrease in sympathetic tone and increased vagal

tone, indicating a reversal of some of the compensatory mechanisms of HF

(Coats et al, 1992). Skeletal muscle is affected by training through increases in

mitochondrial content, respiratory capacity of muscle fibers and capillary supply.

These improvements can be correlated to increased in peak V02 (Drexler et al,

1992). Katz et al (1997) demonstrated improvements in endothelial-dependent

vasodilation in peripheral resistance vessels after training. After training,

improvements in skeletal muscle metabolism are seen as demonstrated by

reductions in phosphocreatine depletion and an increase in adenosine

diphosphate (ADP) during exercise with better recovery kinetics after eight

weeks of training (Adamopoulos et al, 1993). Exercise training has been shown

to reduce rest plasma catecholamine levels, enhance heart rate variability and

improve baroreflex gain resulting in an increase in vagal tone (Pagani et al,

1988). Minnoti et al (1991) found that exercise training which stimulates training

adaptations can increase exercise performance without altering cardiac function

or exercise blood flow.

Over the past 5-10 years the safety and efficacy of exercise training in HF

patients has been examined. While exercise training in patients in HF has

gained wider acceptance, there are no large scale evaluations of its safety and








27
efficacy. In a review of HF training studies, McKelvie et al (1995) listed nine

randomized and nonrandomized studies with a total of 274 patients. The

difficulty is that there was no consistency in training methodology or assessment

parameters and the number of subjects was small. However, exercise training

appears to be relatively safe for stable HF patients both in supervised or a home

setting.

Exercise training can produce significant improvements in exercise

tolerance and other parameters, even in moderate to severely compromised

participants (Coats, 1993). One of the primary concerns with exercise training

programs in HF is still the safety of home-based programs.

In a randomized trial reported by Coats et al (1992), the safety and

efficacy of a home based bicycle program was reported. Subjects exercised

daily at 50 rpm for 20 minutes with a resistance to keep their heart rate at 60-

80% of max HR. Results showed improvements in exercise time between 2 and

2.6 minutes, peak oxygen uptake by 3.2 ml/min/kg, with improvements in

symptom scores. There were no reports of adverse experiences (ie, death or

myocardial infarction (MI) during the study.

While home-based exercise programs are effective, they generally report

less beneficial effects than a supervised program (Sanderson, 1990). An

alternative is a home-based program with telephone contact with the nurse or

researcher in order to assess compliance and status. Using this model

Sanderson (1990) demonstrated a 96% adherence pattern with a significant







28

improvement in exercise capacity. The issues to utilization of rehabilitation

resources are significant. Lack of third party reimbursement place this option

out of economic feasibility for many patients. The chronicity of HF and the costs

of medications and doctors visits, coupled with frequent hospitalizations make it

difficult to promote compliance with this intervention. Home based programs are

feasible and are cost free. In addition, they encourage daily activity that is not

beyond the scope of every day living. The CDC/ACSM position statement

recommends that everyone increase their daily activity by incorporating normal

aerobic activities into their schedule such as gardening, walking up a flight of

stairs rather than taking the elevator (Pate et al, 1995). While HF patients are in

general deconditioned and somewhat limited, they walk to carry out their daily

activities. Increasing this normal activity can result in improvements in functional

capacity if done in sufficient quantity and with regularity.

Functional Capacity

Functional capacity defined as the level of physical function, is often

measured by standardized tests such as the treadmill exercise test, 6-minute

walk, or other diagnostic methods such as echocardiography, or MUGA to

determine ejection fraction. Physiologically, it is defined as a product of cardiac

output and skeletal muscle arteriovenous oxygen difference (Folta & Metzger,

1989). Functional capacity measured by an exercise test evaluates the

peripheral circulation, pulmonary and skeletal muscle arteriovenous oxygen

difference (A-V02). Although this measure of functional capacity is considered







29
objective it can be affected by patient motivation, environmental conditions,

training, and tester interactions (Francis & Rector, 1994; Clark, Poole-Wilson, &

Coats, 1994). It is even more difficult to correlate performance on an exercise

test to an individuals ability to perform activities of daily living.

The applicability of the maximal exercise test to this HF population as an

accurate reflection of daily exercise tolerance has been questioned (Packer,

1987a). Submaximal, symptom limited tests appear to be more reflective of the

daily activities undertaken by these subjects. Oka et al (1993) demonstrated

that daily physical activities of subjects with HF were low In spite of relatively

high measured exercise capacity (VO2m,). These subjects with HF were more

likely to self-limit their activities to avoid the development of symptoms. Other

methodologies such as shoe-mounted pedometers (Hoodless et al, 1994) and

limb movement sensors (Davies, Jordan, & Lipkin, 1992) have demonstrated the

marked reduction in physical activities of HF patients. Davies et al, (1992)

demonstrated the wide individual and day to day variability in physical activity of

HF patients. An alternative strategy has been the 6 minute walk test. This test

requires the subjects to walk a measured course as many times as they can in 6

minutes without coaching (Guyatt et al, 1985). Dracup et al (1992)

demonstrated a significant correlation between the 6 minute walk, a self-reported

MET level and NYHA class. Bittner et al (1993) demonstrated that the 6 minute

walk results correlated with survival in patients with moderate heart failure. This

testing more closely resembles activities of daily living and is correlated to







30

outcome. The difficulty is that the severity of symptoms in HF patients correlates

poorly with the indices of cardiac function such as ejection fraction and

hemodynamic results, making assessment of function a complex issue (Minotti &

Massie, 1992).

Measurement of symptoms can be through pencil and paper instruments

or during physical examinations and interviews. In HF there is a standardized

classification; the New York Heart Association Classification of Heart Failure

(Criteria Committee, 1964). Patients are asked about their symptoms and

activity status. Based on this self reported information, and clinical examination,

patients they are classified into one of the following categories:

New York Heart Association Classification of Heart Failure

I. Unlimited activity without cardiac symptoms.

II. Ordinary physical activity causes fatigue, dyspnea,

palpitations, or angina pectoris.

III. Marked limitation of activity and symptoms with less-

than-ordinary activity, but no symptoms at rest.

IV. Any physical activity is accompanied by symptoms, and

symptoms may occur at rest.

This classification system has been shown to correlate with mortality (SOLVD

Investigators, 1992).

If medical therapy for HF does not significantly improve mortality or

morbidity, in most instances, it would not be acceptable. However, in HF with its







31

known high mortality, the improvement of quality of life for the duration of life

expectancy may actually be more significant. Current trends in clinical HF

research, call for assessment of QOL as a secondary outcome measure or in

some cases is combined with mortality as a composite endpoint to assess

therapeutic benefit.

Smptoms associated with HF result in a significant impairment in quality

of life. One of the goals of therapy is for symptom reduction, and improvement in

quality of life. In order for QOL to be affected, treatments have to focused to

specific areas in order to produce tangible improvements for the patients.

Quality of Life

QOL, like HF is a multidimensional concept. The definition of QOL varies

according to the researcher and the population being studied. Wenger (1989)

defined three major components each with several subcomponents; functional

capacity, perceptions, and symptoms and their consequences. Ware (1984)

identified five components; disease, personal functioning, psychological

distress/well-being, general health perceptions, and social role functioning.

According to Grady (1993), these dimensions can be generalized into health,

physical function, psychological function and social interactions.

The assessment of QOL, while very useful in describing the population of

HF, and offering insight to areas of needed therapeutic intervention, has not

been shown to be highly correlated with measures of central performance such

as ejection fraction (Dracup, Walden, Stevenson, & Brecht, 1992; Hawthorne &








32
Hixon, 1994). However, perhaps the perception of a better quality of life is as

important to the patient as actual hemodynamic improvement, in light of the

terminal nature of this disease.

HF is a chronic process that is associated with reduced QOL (Gorkin, et

al, 1993.). Dracup et al (1992) evaluated 134 patients with advanced HF and

found that their reported QOL was significantly compromised. They

demonstrated a wide variability in physical functioning, but overall it was below

normal. They were moderately anxious and hostile, and were moderately to

severely depressed. They concluded that therapy in advanced HF should be

targeted at reducing depression and increasing daily activity levels in addition to

medical management.

Depending on the goals of the research, not all areas of QOL may be

measured when conducting a study. In addition, QOL is not always specifically

pre-defined, but measured as one of many variables and is reported based on

the instruments used. If QOL is to be defined a priori, then the selection of

instruments must be appropriate to the conceptual framework and to the

population being studied. The instruments must be sensitive enough to capture

the dynamic nature of QOL, and in most cases be assessed from the perspective

of the subject who is experiencing the disease.

There are many instruments that have been used in HF subjects. Some

of the most commonly used instruments are the Sickness Impact Profile (SIP)

(Berger, Bobbitt, Carter, & Gilson, 1981), the Psychosocial Adjustment to Illness







33
Scale (PAIS) (Derogatis & Derogatis, 1990), the Profile of Mood States (POMS),

the Multiple Affect Adjective Check List-Revised (MAACL-R) (Zuckerman &

Lubin, 1985), the Spielberger state-trait anxiety inventory, Beck Depression

Inventory (BDI), and the Minnesota Living with Heart Failure Survey (Grady,

1993). Many of these tools measure multiple concepts. The SIP measures

physiological and psychosocial disability in 12 areas, whereas the BDI only

focuses on depression. In order to assess the entire spectrum of QOL, multiple

instruments are often used. The above instruments are frequently used to

identify the psychosocial and mood state domains of QOL.

Summary

HF is a staggering health care problem in the US. It is a complex

syndrome of multiple etiologies, which have effects on the central and peripheral

circulation. Chronic heart failure is characterized by a complex adaptive process

that is delicately balanced through careful medical and lifestyle management.

This balance is often disrupted and results in decompensation and

hospitalization for worsening symptoms. The current treatment of heart failure is

based on the use of digoxin, diuretics and ACE inhibitors in addition to other

medications. Current research has demonstrated that in chronic stable HF

additional interventions such as exercise training can be added to the

pharmacologic, and lifestyle management of the patient to reverse or attenuate

some of the adaptive mechanisms that result from this chronic syndrome,

resulting in improvements in exercise tolerance and reduction in symptoms.







34

What is not known is whether the period immediately after treatment for

decompensation, with its resulting improvements in hemodynamic status, can be

utilized to increase activity levels and prolong the positive effects of medical

optimization.













CHAPTER THREE
METHODS

In this chapter the research methods and materials used in this study are

discussed. Included in this chapter is a description of the research design,

setting of the study, sample selection, and the instrumentation and methods

used for measuring the variables of interest.

Research Design

The purposes of the study were to determine the relationship of medical

optimization on measures of functional capacity, and quality of life at specific

time periods. In addition, to describe the changes which resulted from a home

exercise training program on measures of functional capacity at study entry and

8 weeks. Changes in quality of life were assessed at study entry, 4 and 8

weeks. A quasi-experimental, prospective, randomized, controlled, parallel

group design was used. This convenience sample was recruited from

decompensated heart failure patients admitted for medical optimization

conducted in a large tertiary referral center in the Southeast. The dependent

variables were functional capacity, and quality of life.

Selection of Subjects

All subjects admitted to a large tertiary referral center in the Southeast

with acute exacerbation of HF requiring medical optimization, who met the


35








36

following inclusion, and did not meet any exclusion criteria were approached and

asked to participate in the study. Written informed consent was obtained from

each willing subject. The study protocol was reviewed and approved by the

University of Florida Institutional Review Board.

Inclusion Criteria:

1. Patients with heart failure classified as New York Heart Association
Class Ill-IV.

2. Ejection fraction of 35% or less within the previous 6
months.

3. Age 18 or older.

4. Receiving standard medical therapy for the treatment of heart
failure which may include digoxin, diuretic, and ACE inhibitors, or if
intolerant to ACE inhibitors; losartan, hydralazine/ISDN or
amlodipine.

5. Women of childbearing potential must be using
acceptable forms of birth control, and have a negative
pregnancy test.

Exclusion Criteria:

1. Diagnosed myocardial infarction (MI) within the previous 6 months.

2. Significant peripheral vascular disease.

3. Coronary Artery Bypass Grafting (CABG), Percutaneous
Transluminal Coronary Angioplasty (PTCA) within the previous 6
months.

4. Concomitant illness that would interfere with completion of the
protocol.

5. Patients receiving greater than 12.5mg bid of lopressor or other
beta blocker of equivalent dose








37

Study Protocol

Patients who met the inclusion criteria were asked to participate by

signing a written informed consent. All patients were receiving intravenous

inotropic therapy using either milrinone, dobutamine, dopamine or a

combination. Beginning at hospital admission, medical therapy was optimized

for each patient. The goal was to improve functional capacity and reduce

symptoms of HF by optimizing triple therapy of digoxin, diuretics and ACE

inhibition. Heart rhythm evaluation and patient education took place during the

hospital stay. Patient education and individualized dietary consultation was

standardized and included detailed instructions on medication management,

fluid management, maintenance of daily weight, and general activity instructions.

These interventions were provided by the members of the multi disciplinary heart

failure/transplant team which includes nurse coordinators, social workers,

dieticians, clergy and clinical psychologists.

Medical optimization included IV inotropic infusions. The length of

infusions varied based on clinical indications, and ranged for 36-120 hours. For

most patients, IV infusions were discontinued between 12 midnight and 6 am on

the day of discharge usually within 48 hours after admission. The majority of

patients underwent a clinically indicated right heart catheterization and

hemodynamic parameters were recorded to assess the effects of therapy. Prior

to discharge patients who provided informed consent were randomized, much

like the toss of a coin using a computer generated randomization schedule, to







38

either home exercise intervention or control. They underwent a post-infusion

assessment at study entry which included: 6 minute walk, symptom limited

exercise test (with gas exchange), activity recall, and 2 paper and pencil Quality

of Life assessments. Both groups were given written and oral discharge

instructions (Appendix A). Patients randomized to a home exercise intervention

program were provided with a detailed instruction period prior to discharge which

was reinforced at each follow up visit. This instruction period consisted of

providing patients with an exercise prescription which consisted of a once a day

walking program with duration of walking based on the results of their discharge

exercise test. Patients were instructed at the beginning of each daily walk to

start with a 3-5 minute warm up period of light stretching, followed by walking on

a flat surface for the recommended time period. The range of recommended

duration of walking was 1 to 30 minutes. At the end of each walking period,

patients were instructed to end the activity period with 3-5 minutes of light

stretching.

Prior to discharge, patients in the home intervention group were

instructed on how to fill out daily activity diaries (Appendix B). Diary entries

included preexercise and peak heart rates, exercise time and distance,

perceived exertion, chest pain and shortness of breath scales. Patients in the

home intervention group were contacted by telephone by the investigator at

least once a week to assess their adherence to the exercise intervention, and to

encourage completing the daily diaries. The control group did not fill out daily







39

activity diaries and were not contacted in order to mimic current clinical

management. Both groups completed 7-day Physical Activity Recall surveys at

study entry, 4 and 8 weeks.

After 4 weeks, all patients were contacted by mail or phone and sent a

repeat set of quality of life forms and an activity recall survey. All but one of the

patients in the home exercise intervention group had a home visit, at which time

the investigator obtained the 4 week QOL, and activity recall. In addition, the

patient and investigator walked together for the same duration, intensity, and

location that was being reported in the activity diaries in order to assess ease of

implementation of the home walking program. Patients were asked to return to

clinic at 8 weeks and have a brief physical exam, medication assessment, recall

of activity and to complete QOL forms. In addition patients completed a

symptom limited exercise test with gas exchange, and a 6 minute walk. Study

procedures are illustrated in Figure 3.1.

Procedures

Symptom Limited-Graded Exercise Testing with Gas Exchange

Symptom limited-graded exercise testing (SL-GXT) was performed in all

subjects prior to hospital discharge. The exercise protocol consisted of an SL-

GXT using an incremental treadmill (Quinton Instruments, Seattle, WA) exercise







40

Table 3.1 Schedule of Study Protocol Procedures


Procedures Entry Medical Pre-D/C Week Week
Optimization 4 8
History & Physical X
Exam
Physical Exam X X
Medication Titration X
Inotropic Infusion X
Exercise Test with X X
Gas Exchange*
6 Minute Walk* X X
Activity Recall* X X X
NYHA Assessment* X X
Quality of Life X X X
Home Visit X**
* Assessment of functional capacity, ** Home exercise group only.

protocol (Modified-Naughton) Naughton, 1973. The initial workload on the

treadmill was 2.0 mph at 0% grade and progressed every 2 minutes by

increasing the grade by 2 percent until the subject reached voluntary exertion or

became symptomatic with positive hemodynamic or medical indices. Patients

who were not required to undergo testing as part of their transplant evaluation

were scheduled to undergo testing at the Center for Exercise Science using this

methodology. The following criteria recommended by the American College of








41

Sports Medicine (ACSM, 1995) were used for termination of the test:

1. Fatigue,

2. Failure of monitoring equipment,

3. Light-headedness, confusion, ataxia, cyanosis, dyspnea, nausea or
any peripheral circulatory insufficiency,

4a. Onset of grade 2/3 angina pectoris (moderate to severe) with
exercise,

b. Mild angina pectoris with 2 mm of ST segment depression,

5. Symptomatic supraventricular tachycardia,

6. ST segment displacement 4 mm or greater in the absence of angina
pectoris,

7. Ventricular tachycardia (3 or more consecutive premature ventricular
contractions (PVC's),

8. Exercise induced left bundle branch block,

9. Onset of second and/or third degree atrial-ventricular block,

10. R on T PVC's (one),

11. Frequent multi focal PVC's (30% of complexes),

12. Excessive hypotension (greater than 20 mmHg drop in systolic
blood pressure during exercise),

13. Excessive blood pressure rise: systolic blood pressure greater or
equal to 220 or diastolic blood pressure greater or equal to 110 mm
Hg,

14. Inappropriate bradycardia: drop in heart rate greater than 10 beats
per minute with an increase or no change in workload,








42

During the test, expired gases were collected through a low-resistance

two-way valve (Hans Rudolph Inc., Kansas City, MO). Samples of the expired

gases were analyzed using a metabolic cart (Medical Graphics Corporation, St.

Paul, MN). The system was calibrated with standard gases of known gases

before each test. Minute ventilation was determined by an electronic flow meter

on the expired side of the circuit. Volume calibration was performed with a 3-

liter calibration syringe. Analog outputs from each device were continuously

monitored by an on line microcomputer via an analog-to-digital conversion

board. This system provided breath by breath determination of VO2, VCO2 and

ventilation. Subjects were fitted with a headset device, nose clip, and

mouthpiece attached by flexible tubing to the metabolic cart to measure expired

gases.

Heart rate and 12 lead electrocardiogram (ECG) were monitored and

recorded throughout the test using standard lead placement with a Quinton Q

4000 system (Quinton Instruments, Seattle, WA). Blood pressure

measurements, ratings of perceived exertion (RPE), and symptoms of angina

and/or dyspnea were also obtained at the end of each minute throughout the test

using a standard sphygmomanometer, the 15 point Borg perceived exertion

scale, and the 4 point dyspnea and angina scales recommended by the ACSM

(ACSM, 1995).

Subjects requiring testing for transplant evaluation completed a SL-GXT

on an upright Medgraphic bicycle in the pulmonary function lab. Subjects were








43

exercised using a steady ramp protocol which increased 25 watts over each 1

minute period of testing. The subjects were fitted with a headpiece, nose clip

and flexible tubing to capture expired gases. These subjects underwent

identical measurements of breath by breath analysis. Samples of the expired

gases were analyzed using a metabolic cart (Medical Graphics Corporation, St.

Paul, MN). Methods for calibration of the system was the same as that used at

Exercise Science. Heart rate and 12 lead electrocardiogram (ECG) were

monitored and recorded throughout the test using standard lead placement with

a Quinton 3000B system (Quinton Instruments, Seattle, WA). Blood pressure

measurements, ratings of perceived exertion (RPE), and symptoms of angina

and/or dyspnea were also obtained at the end of each minute throughout the test

using a standard sphygmomanometer, the 15 point Borg perceived exertion

scale, and the 4 point dyspnea and angina scales recommended by the ACSM

(ACSM, 1995). Guidelines for terminating the test was also the same at both

facilities. The investigator was present for testing at both locations. Each

subject completed baseline and 8 week testing on the same equipment.

Cardiac Catheterization

Patients who underwent clinically indicated cardiac catheterization to

assess therapeutic effects of treatment, were taken to the catheterization

laboratory on the morning of discharge. Placement of a swan ganz catheter took

place via a jugular vein or femoral vein. Catheters were balanced to air and

calibrated with the data recording system. Right sided pressures; right atrial,







44

right ventricular, pulmonary artery and pulmonary artery wedge pressures were

measured and recorded. Cardiac outputs were obtained using 3-5 injections of

10cc's of normal saline. Temperature gradients were used to calculate the

cardiac output by averaging the derived values. Out of range values were

discarded at the discretion of the physician performing the measurements, and

the remaining values added and divided by the number used.

6 Minute Walk Test

Patients who were capable completed a 6 minute walk test. As

standardized by Guyatt et al (1985), patients were taken by wheelchair to a

premeasured hallway, free of traffic. Patients were given standardized

instructions to walk back and forth from two identified marks in the hallway until

time was called. Patients were advised they could stop and begin again, slow

their pace or do whatever was necessary to complete the entire 6 minutes. No

encouragement was provided during the test. Distances were then recorded at

the end of the 6 minute period. Due to extreme fatigue, two patients were not

able to complete this phase of the baseline physiological testing.

Quality of Life Assessments

Quality of life assessments were obtained using the Multiple Affect

Adjective Check List-Revised (MAACL-R) and the Psychosocial Adjustment to

Illness Scale-Self Report (PAIS-SR). Subjects were given instructions on how to

respond to these paper and pencil tests. Forms were left with the patient and

retrieved later in the day so that patients could complete them in privacy.








45

The MAACL-R is a paper and pencil tool that is used to measure affect;

state and trait. It's clinical use has been in areas where changes in affect are to

be determined. The tool is 132 item adjective check list that measures anxiety,

depression, hostility, positive affect, sensation seeking scales. In addition to

these affect scores it measures a negative affect, dysphoria which is the

combination of anxiety depression and hostility and a positive affect score which

combines sensation seeking and positive affect. Normative data was

established in 1491 subjects, which represented sexual, racial, regional,

educational, and income distribution in the US. The scales are standardized

separately for males and females in order to remove sex bias on the raw scores.

Measures of internal reliability range from alphas of .49 to .95 for the state form

and .50 to .95 for the trait form. Retest reliabilities have been determined for

periods up to 8 weeks with the trait form and range from an alpha of .39 to .64.

Convergent, discriminant and diagnostic validity have been reported

(Zuckerman & Lubin, 1985). The tool requires subjects to check off all

adjectives that they feel are pertinent at the time of testing or in general. The

number of items checked are then grouped and counted according to the affect

associated with the response. These raw scores are taken and converted to

standard T scores which are broken down by sex and total number of responses

checked.

The PAIS-SR is a self report tool designed to assess the quality of a

patient's psychosocial adjustment to a current medical illness or its residual








46

effects. The areas of adjustment to illness are reported in seven primary

domains; health care orientation, vocational environment, domestic environment,

sexual relationships, extended family relationships, social environment and

psychological distress. It is a 46 item scale rated on a 4 point (0-3) scale of

adjustment. Higher scores indicate worse adjustment. The instructions ask that

the subject consider their responses within the time frame of how they have felt

over the recent 30 days. This tool can be used to assess any medical condition

which has an identifiable psychosocial component, and which is of sufficient

severity to have an impact on the quality of life of the patient.

Reliability and validity testing of this tool have been reported (Derogatis &

Derogatis, 1990). Reliability coefficients for the PAIS-SR based on cardiac,

cancer and renal dialysis patients ranged from .47 to.93 demonstrating relatively

high internal consistency. Inter rater reliabilities have been reported at .86 and

.83 for two cancer populations. Construct validity has been established. The

most extensive use of the PAIS-SR has been in measuring adjustment to illness

in cardiac patients. Folks et al, (1988) demonstrated high predictive validity for

the PAIS in predicting clinical depression post surgery. In addition it has been

used to document changes in adjustments over a 6-12 month period after

transplant (Freeman et al, 1988).

Subjects were assessed at baseline, 4 and 8 weeks using the PAIS-SR.

Raw scores were converted to T scores to calculate the total domain score. The








47

cardiac patients as the reference group. Patients in the reference group were

predominantly male (92%), white (98%) and age 53.7 years.

7-Day Physical Activity Recall

Assessment of baseline and follow up physical activity levels were

recorded using the 7-day Physical Activity Recall (PAR) questionnaire. This

questionnaire was initially used as a determination of eligibility for the Activity

Counseling Trial (ACT). Each assessment of activity was conducted by the

investigator to maintain consistency.

Patients were randomized prior being taken to complete the SL-GXT to

either home exercise intervention or control group. Patients who were

randomized to the control group were given general discharge instructions for

management of HF and were requested to complete two quality of life

assessments by mail. On their scheduled return visit at 8 weeks they were

asked to complete another set of forms.

Home Exercise Intervention

Patients randomized to home exercise intervention group received a

standard written prescription for a progressive home-walk program based on the

results of the discharge exercise test. Educational needs of patients were

assessed during hospitalization, and every attempt was made to include family

members in this education process. The exercise prescriptions were

individualized into specific guidelines for frequency, intensity, duration, mode

and progression. Patients were instructed to begin and end with a 3-5 minute







48

warm-up and cool down periods of light stretching. For patients who were the

most decompensated, interval training using 1-5 minutes of low level walking

broken up by 1-2 minute rest periods were recommended. Frequency was 1-2

times per day, 5 days per week. The intensity of the activity was based on the

Borg Perceived exertion scale which was demonstrated during the predischarge

exercise test. A target of 11-14 ("Light" to "Somewhat Hard") was used to guide

exercise sessions and to determine the need to increase the duration or intensity

of the exercise. Symptoms of angina or shortness of breath served as a guide to

terminate the walking. Patients were familiarized with how to score their

symptoms using the Angina and Dyspnea Scales. Each patient was provided

with a written copy for use at home (Appendix D).

Angina Dyspnea

1+ light, barely noticeable 1+ mild, noticeable to patient

2+ moderate, bothersome 2+ mild, noticeable to tester

3+ severe, very uncomfortable 3+ moderate but can continue

4+ most severe pain ever 4+ severe, patient can't continue



Patients were advised to stop activity if they experienced greater than 2+

on either scale. Return demonstration by the patient on how to score perceived

exertion, chest pain and/or dyspnea was performed. The initial

recommendations for duration of walking for the patients in the home exercise

intervention group varied from 1-30 minutes based on the total exercise time and







49

peak oxygen consumption values obtained from the symptom limited exercise

test completed at study entry. Due to the acuity of the patients, the initial

recommendations were based primarily on symptomatology, not on intensity or

based on a percentage of maximum VO2. Patients were asked to record their

daily activities on a provided daily activity form. They were asked to attempt to

walk 5 days a week maximum or 3 days a week minimum. Based on individual

tolerance, duration of each exercise session was gradually increased. The

intensity target was a perceived exertion of 11-14.

Data Analysis

Descriptive statistics were performed on baseline characteristics.

Student-t tests were used for repeated measures of functional capacity and

quality of life. Repeated measures ANOVA were used for measures of

functional capacity and quality of life to assess for interaction, and to examine

within group differences.

Summary

This chapter presented the research design, criteria for selection of

subjects, study protocol and procedures for this study. The data analysis

methods were presented.













CHAPTER FOUR
ANALYSIS OF DATA


This chapter presents a description of the recruitment process and the

demographic and physiological characteristics of the sample. This chapter also

presents the results of the statistical analyses of these data with respect to the

research hypotheses.

Recruitment Procedures

A convenience sample of 24 patients who had been admitted for medical

therapy optimization at a tertiary referral center in the Southeast were

approached and agreed to participate in the study. All patients were

approached after admission to the hospital and prior to the discontinuation of

their inotropic therapy. Patients signed a written informed consent and were

randomized by a computer generated randomization schedule to either home

intervention or control. Patients were then scheduled for baseline testing which

included assessments of functional capacity as measured by symptom limited

exercise testing with gas exchange, activity recall, and 6 minute walk test.

Quality of life was assessed by two paper and pencil questionnaires; the PAIS-

SR, and the MAACL-R.





50








51

Method of exercise testing with gas exchange was determined based on

clinical indications. Since some patients were undergoing transplant evaluation,

they required exercise testing with gas exchange to be completed by the

pulmonary function department which conducted bicycle exercise tests with gas

exchange (n= 1), patients not clinically required to perform an V02 test were

scheduled for an exercise treadmill with gas exchange at the Center for Exercise

Science on campus (n=12). Each patient conducted the repeated exercise test

with gas exchange on the same equipment, using the same protocol as used at

baseline. In addition to protocol required testing, all but 4 patients underwent

predischarge right heart catheterization to assess hemodynamic status after

medical optimization and inotropic therapy.

Characteristics of the Sample

Of 24 randomized patients who signed an informed consent, one patient

was never randomized due to inability to complete assessments at study entry.

The baseline characteristics for the remaining 23 randomized patients, 13

in the home intervention group and 10 in the control group, are presented in

Table 4.1. Statistical testing using Student t tests demonstrated that there were

no statistically significant differences between the two groups for any of the

demographic variables. The ages of the 10 control patients ranged from 21 to

58 years (2 45.3, 11.4), while the ages of the 13 home intervention group

ranged from 39 to 63 years (x 52.4, 8.2). There were no statistically significant

difference in the mean ages (t=-1.738, p = 0.0968), although there was a trend







52
Table 4.1 Characteristics at Study Entry for 23 Patients

Variables Home Intervention Control
(n=13) (n=10)
X SD X SD
Age (yrs) 52.4 8.2 45.3 11.4
Weight (kg) 85.4 + 12.8 91.6 + 12.8
Duration of HF (months) 43.5 48.3 48.7 45.7
LVEF (%) 19.0 + 7.3 21.0 8.1
Male Gender (n) % (9) 70% (9) 90%
Etiology of HF (n) %
Ischemic (5) 38% (3) 30%
Idiopathic (5) 39% (5) 50%
Hypertensive (0) 0% (1)10%
Valvular (2)15% (0) 0%
Viral (1) 8% (1) 0%
NYHA Class
III (5) 38% (7) 70%
IV (8) 62% (3) 30%
Previous Inotropic Infusion (5) 38% (3) 30%
Myocardial Infarction (5) 38% (3) 30%
Coronary Bypass Surgery (4) 31% (3) 30%
Hypertension (4) 31% (4) 40%
Diabetes Mellitus (3) 23% (1) 10%
History of Smoking (7) 54% (4) 40%
Current Medical Therapy
Digoxin (11)85% (9) 90%
ACE Inhibitors (11) 85% (9) 90%
Diuretics (13)100% (9) 90%
Anticoagulants (4) 31% (4) 40%
Nitrates (3) 23% (3) 30%
Beta-blockers (5) 38% (2) 20%
Values are: mean S.D.; HF=Heart Failure; LVEF=left ventricular ejection
fraction; NYHA=New York Heart Association







53
with the control group being slightly younger. Males made up 90% (n=9) of the

control group and 69% (n=9) of the home intervention group. Ninety percent

(n=9) of the control group was married, compared to 85% (n=11) of the home

intervention group. The etiology of heart failure was ischemic heart disease in

30% (n=3) and idiopathic in 50% (n=5) of the control group. In the home

intervention group ischemic heart disease was the etiology in 38% (n=5) and

idiopathic in 38% (n=5). The etiology of the remaining patients were classified

as hypertensive, valvular or viral. The ejection fraction in the control group

ranged from 10 to 40% (x 21 8.1), compared to 10 to 35% (T 19 7.3, t=0.557,

p=0.5834) in the home intervention group. The duration of heart failure for each

group was widely variable between patients, however, the means were similar.

The duration of heart failure for patients in the control group ranged from 1

month to 120 months (x 48.7, 45.7). In the home intervention group the

duration of heart failure ranged from 4 to 168 months (x 43.5, 48.3; t=0.259,

p=0.7975).

At study entry all patients were classified either Class III or IV according

to the NYHA system. In the control group the NYHA classification was class IV

in 30% (n=3), and 61% (n=8) of the home intervention group. Using Chi Square

analysis, there were no statistically significant differences between the groups

(X2 =2.253, p=0.13). Medical therapy on admission was not different between

the two groups. The majority of patients (greater than 75%) were on what is

considered to be standard therapy; digoxin, diuretics and ACE inhibitors.








54

After entry patients were then randomized to home intervention or control

and completed study required psychosocial assessments of quality of life, and

functional capacity. Assessments of functional capacity were exercise testing

with gas exchange, 6 minute walk test, and completing an activity recall

questionnaire. Due to the close proximity of testing, 2 patients were not able to

complete the study entry six minute walk test due to fatigue.

Patients Withdrawn from Study

Based on the results of the right heart catheterization and/or the exercise

test with gas exchange, 4 patients; 3 in the home intervention group and one in

the control group were not discharged from the hospital and were not considered

in the final analyses. These patients were placed back on inotropic therapy and

listed status I for heart transplantation. Of these 4 patients, two patients in the

home intervention group began the walking program while in the hospital but

were transplanted before the 8 week assessment. Anecdotally, these two

patients reported that they felt the walking program prior to transplantation

resulted in them being stronger immediately after the transplant. The third

patient in the intervention group was placed on a ventricular assist device and

was never able to walk. The one patient in the control group was transplanted

within 3 days of completing the baseline assessments.

Two patients in the home intervention group died before completing 8

weeks of participation. One patient died of worsening heart failure and

dehydration two weeks after discharge. The patient had been rehospitalized at








55

another facility 3 days after discharge and never began the intervention. The

second patient died suddenly 4 weeks after discharge while sitting in a chair at

home. Prior to this event, the patient had been feeling well and was walking one

mile a day without symptoms. Two patients in the control group did not return for

8 week testing due to personal reasons and could not be rescheduled within a

reasonable time period. As a result, the final analyses of data was completed on

15 patients who had baseline and 8 week assessments (8 in the home

intervention group and 7 in the control group). Sample characteristics of the 15

patients are shown in Table 4.2.

There are no statistically significant differences between the two groups.

The mean age was 45.6 years for the control group versus 49.6 years for the

home intervention group (t=-0.762, p= 0.459). Males accounted for 85% (n=6) of

the control group and 75% (n=6) of the home intervention group (X2 =0.268,

p=0.605). Married patients accounted for 86% (n=6) of the control patients and

87% (n=7) of the home intervention patients. Etiology of heart failure was

primarily idiopathic in the control group, 43% (n=3); and ischemic heart disease

50% (n=4) respectively in the home intervention group. There were no

differences between the groups (X2 =3.616, p=0.460). NYHA Class III, defined

as marked limitations of activity and symptoms with less-than ordinary activity,

but no symptoms at rest, accounted for 71 % (n=5) of the control group and 63%

(n=5). Class IV, defined as any physical activity is accompanied by symptoms,

and symptoms may occur at rest, occurred in 29% (n=2) of the control group,







56

Table 4.2 Characteristics of 15 Patients
Variables Home Intervention Control
(n=8) (n=7)
Age (yrs) 49.6 7.5 45.6 12.8
Weight (kg) 88.9 9.9 92.5 15.1
Duration of HF (months) 57.0 54.5 41.4 46.6
LVEF (%) 20 8.9 20 9.6
Male Gender (n) % (6) 75% (6) 86%
Etiology of HF
Ischemic 50% 29%
Idiopathic 38% 43%
Hypertensive 0% 14%
Valvular 12% 0%
Viral 0% 14%
NYHA Class
III (5) 63% (5) 71%
IV (3) 37% (2) 29%
History of Inotropic
Infusion (2) 25% (2) 29%
Myocardial Infarction (4) 50% (2) 29%
Coronary Bypass Surgery (3) 37% (2) 29%
Hypertension (3) 38% (2) 29%
Diabetes Mellitus (3) 37% (1) 14%
History of Smoking (7) 88*% (2) 29%
Current Medical Therapy
Digoxin (6) 75% (7)100%
ACE Inhibitors (6) 75% (7)100%
Diuretics (8) 00% (7)100%
Anticoagulants (2) 25% (3) 43%
Nitrates (3) 37% (2) 29%
Beta-blockers (4) 50% (1) 14%
Values are mean S.D.; HF=Heart Failure; LVEF=left ventricular ejection
fraction; NYHA=New York Heart Association; *p<0.05








57
and 37% (n=3) of the home intervention group (X2=0.134, p=0.714). Medical

therapy on admission to the hospital was similar between both groups. Past

medical history was not different between the two groups with the exception of

history of smoking. Only 28% (n=2) of the control group reported a history of

smoking compared to 87% (n=7) of the home intervention group (X2 =5.402,

p=0.020).

Hemodynamic Characteristics of 12 Patients

All but 3 patients underwent right heart catheterization to assess their

response to medical optimization and inotropic infusions. Hemodynamic

characteristics for those patients are presented in Table 4.3

Table 4.3 Post Medical Optimization Hemodynamics
Variables Home Intervention Control
(n=5) (n=7)
X SD X SD
Heart Rate (bpm) 88 12.7 92 14.3
Systolic Blood Pressure (mmHg) 107 10.2 108 + 10.9
Diastolic Blood Pressure (mmHg) 65 4.4 69 + 10.4
RA Pressure (mmHg) 8.6 4.1 4.6 1.9
RV Systolic Pressure (mmHg) 38 + 7.5 50 16.3
RV Diastolic Pressure (mmHg) 5 + 1.9 9 4.1
PA Systolic Pressure (mmHg) 38 + 7.5 50 16.3
PA Diastolic Pressure (mmHg) 16 5.7 24 + 11.5
Mean PA Pressure (mmHg) 23 8.9 33 12.5
Pulmonary Artery Wedge (mmHg) 14 7.2 27 13.8
Cardiac Output (L/min) 4.16 1.6 3.84 0.7
Values are mean SD; RA=right atrial; RV=right ventricular; PA=pulmonary
artery;








58

(n=12; 7 control, 5 home intervention). Statistical analyses using student t tests

indicated no statistically significant differences between the two groups.

There were trend toward worse hemodynamic values in the control patients.

The mean right atrial pressure in the control group was 8.6 4.1 compared to

4.6 1.9 in the intervention group (t=2.000, p=0.0733), mean right ventricular

diastolic pressure and mean pulmonary artery wedge pressures were similarly

different (9 4.1 vs 5 1.9; t=2.000, p=0.0733; and 27 13.8 vs 14 7.2,

t=1.998, p=0.0736). All remaining variables were not significantly different.

Pulmonary artery pressures were elevated in both control and intervention

groups (50/24 compared to 38/16). Cardiac output measurements were below

normal values of 5.0 L/min reflective of the compromised central hemodynamics.

Functional Capacity

Symptom limited-graded exercise testing with Gas Exchange

Maximal oxygen uptake was measured in all patients by open-circuit

spirometry during maximal or symptom limited exercise testing at study entry and

after 8 weeks of intervention. Baseline VO2max ranged from 6.0 to 21.5 ml.kg-

1.min-1 for both groups. There were no statistically significant differences

between the two groups at study entry. Baseline VO2m,, for the control group

was 12.4 3.21 compared to 13.5 5.1 (t= 0.493, p=0.6296). After 8 weeks of

intervention there were improvements in both groups, however these differences

were not statistically significant between groups. The control group increased to

a mean of 14.93 5.4 ml.kg1.min-1 while the home intervention group increased








59
to 13.8 4.02 ml.kg-'.min-1 ( t= 0.4428, p=0.6658). In order to examine within

and between group differences for VO2m, at study entry and 8 weeks, multi

variate repeated measures ANOVA was performed. There

Table 4.4 Cardiopulmonary Responses before and after Home Intervention
Home Control
Intervention (n=7)
(n=8)
Variable Entry 8 Weeks Entry 8 Weeks
Exercise Time (secs) 320 100 396 175 383 203 388 280
HRprex beats.min-1 88 13 83 13 92 14 89 11
HRpak beats.min-1 124 24 131 24 130 18 134 30

HReserve beats 37 46* 39 42
SBPprex mmHg 107 10 122 24 108 11 108 19
DBPrex mmHg 65 + 4 68 12 69 10 67 12
SBPpk mmHg 130 17 152 28 126 14 119 22
DBPpeak mmHg 75 + 9 74 12 77 13 70 10

VO2peak m.kg-1.min-' 13.5 5.1 13.8 4.0 12.4 3.2 14.93 5.4
RERpeak 1.08 0.1 1.06 0.2 1.04 0.1 1.07 0.1
RPE,k 13 1.7 13 3.2 13 2.2 14 1.3
Values are mean SD; PREX=pre-exercise; PEAK=peak exercise; HR=heart
rate; SBP=systolic blood pressure; DBP=diastolic blood pressure; V02= oxygen
consumption per minute; RER=respiratory exchange ratio; RPE=perceived
exertion, *p<0.05


was no statistically significant change in VO2m, within patients (t=1.473, p=

0.200) and no interaction was between groups (t=0.7082, p=0.4165). When the

entire sample was combined, there were no statistically significant improvements

in maximal oxygen uptake from study entry to 8 weeks.








60

Exercise Time

Exercise time at study entry for the sample ranged from 120 to 688

seconds (2 to 11 minutes). Mean values at study entry were higher for the

control group, 383 203 seconds compared to 320 100 seconds, but these

differences were not significant (t=0.777, p=0.450). After 8 weeks both the

control and home intervention groups improved, 2% and 24% respectively.

These changes were not statistically significant (t=-0.066, p=0.9482). Table 4.4

demonstrates the cardiopulmonary responses of both groups on entry into the

study and 8 weeks later. When total exercise time was analyzed for the entire

sample, there were no statistically significant improvements over the 8 weeks of

the study.

Measures of perceived exertion and respiratory exchange ratio were

similar for both groups indicating a similar level of effort and perceived exertion.

Using paired student t tests there were not statistically significant differences

between the two groups. Within group analysis revealed no statistically

significant differences in any variable for the control group from baseline to 8

weeks. In the home intervention group there were trends towards significance in

measures of resting systolic blood pressure (t= 4.348, p= 0.0034), peak heart

rate (p=0.0604) and peak systolic blood pressure (t=2.303, p=0.0608). In

addition there was a statistically significant difference in baseline and 8 week








61

Table 4.5 Analyses of Cardiopulmonary Variables of Home Intervention Group
Variable Mean Std Dev T p value
Exercise Time (secs) 76.00 200.30 1.07 0.3188
HRprex beats.min-' -4.75 11.37 -1.18 0.2761
HRpak beats.min-1 6.25 7.90 2.23 0.0604

HRrerve beats 9.75 6.34 4.34 0.00348*
SBPprex mmHg 14.87 17.90 2.35 0.0511
DBPprex mmHg 3.25 9.31 0.98 0.3566
SBPpeak mmHg 17.71 20.34 2.30 0.0608
DBPpak mmHg -1.42 12.14 -0.31 0.7663

VO2peak ml.kg-l.min-' 1.31 5.27 0.70 0.5039
RERpeak -0.01 0.14 -0.24 0.8150
RPE,,k 0.20 3.19 0.14 0.8954
* p<0.05


values for heart rate reserve (peak heart rate minus baseline heart rate). This

increased from a mean of 37 to 46 bpm (t= 4.348, p= 0.0034). These analyses

are illustrated in Table 4.5.

6 Minute Walk

Six minute walk distances at entry were 129.7 meters for the home

intervention group versus 203.8 for the control group. At 8 weeks the home

intervention group walked 142.5 meters versus 236.8 for the control group.

There were no statistically significant differences between groups at entry

(t=0.8563, p=0.4102) or 8 weeks (t=0.6359, p=0.5472). Although there were

increases in both groups from baseline to 8 weeks these changes were not







62

statistically significant. The sample size was variable at each testing due to the

close proximity of testing with the symptom limited exercise test with gas

exchange. At entry 7 home intervention patients and 6 control patients were

able to attempt the walk. At 8 weeks, 6 intervention and 4 control patients were

able to complete the testing.

Home Intervention

The home intervention program selected was generally a low intensity

program individualized to each individual patient. The basic exercise was

walking. The patients were instructed to walk, after a 5 minute warm up period

for periods ranging from 1 to 15 minutes, based on their discharge exercise test.

Patients were instructed to attempt to walk daily if possible but at a minimum of 3

days per week. They were asked to use the Borg perceived exertion scale to

guide the intensity of the exercise with a goal of 11 to 13. Patients were given a

daily diary and asked to record their baseline heart rate, peak heart rate. At

peak exercise they were asked to rate their chest pain (if present), shortness of

breath and level of perceived exertion. Diaries were collected at 4 and 8 weeks.

Patients were considered 100% compliant if they reported activity 3 days a

week. One patient in the home training group did not keep a diary and was

considered completely non-compliant with the protocol intervention. One patient

was partially non-compliant due to healing foot ulcer which impeded regular

exercise until the last 2 weeks of the study.

Home visits were scheduled and took place with the investigator visiting








63
all but one of the home intervention patients. All patients lived in areas that

allowed for walking. Some environments were more conducive to walking than

others. For example some neighborhoods had more tree cover and shade,

allowing patients more opportunities to walk in the hotter months, during which

time the majority of this data was collected. Several patients elected to expand

their exercise beyond walking on a flat surface. One patient combined walking

with swimming laps. Swimming laps was accomplished by using a float board

and only using their legs. Attempts at swimming using both arms and legs

resulted in increased angina. One patient utilized a bicycle, and the third used a

self propelled treadmill. Table 4.6 summarizes the exercise periods for each

individual in the home intervention group. The duration of exercise ranged from

0 to 60 minutes, with a mean of 13.5 minutes. Of the 8 patients who completed

Table 4.6 Characteristics of and Adherence to Home Intervention by Patient
Patient Exercise Duration Reported % Compliance
Number (minutes) Exercise Periods (3 days/week)
Mean (range, SD) (8 weeks)
1 4.3 (2-10, 1.5) 58 241%

2 5.1 (0-10, 4.8) 47 195%
3 0 0 0%
4 6.9 (0-60, + 12.9) 31 129%
5 16.7 (10-20, 4.8) 11 45%
6 30 (30-30, 0) 36 150%

7 26.8 (20-40, + 4.8) 42 175%
8 18.7 (0-31, 7.4) 30 75%








64
8 weeks of intervention, 62% (n=5) were 100% compliant with a 3 day a week

program as indicated by at least 24 activity periods reported in 8 weeks. Table

4.6 illustrates individual intervention activities and patient compliance.

Assessment of New York Heart Association

At study entry all patients had their HF classified according to New York

Heart Association by the admitting physician. All patients were either class III or

class IV. At the 8 week visit, there was a shift towards improved functional

classification in both groups. Table 4.7 illustrates the change in overall

percentages.

Table 4.7 Changes in NYHA Classification over 8 weeks
Control Home Control Home
Baseline Intervention 8 Weeks Intervention
(n) % Baseline (n) % 8 Weeks
(n) % (n) %
Class I 0 0 0 0
Class II 0 0 (3) 43% (3) 38%
Class III (5) 71% (5) 63% (4) 57% (4) 50%
Class IV (2) 29% (3) 37% 0 (1) 12%



Activity Recall Questionnaire

The 7-Day Physical Activity Recall was used to determine self-reported

activity levels in both groups at study entry, 4 and 8 weeks. The reported hours

of activity are then used to calculate energy expenditures per day and hour.

The results are shown in Table 4.8. There were no statistical differences in

either group at any time period. The overall means show increases in activity in








65

both groups over the first 4 weeks. The home intervention group continued to

demonstrate increases in activity levels at 8 weeks, whereas the control group

had a slight reduction in activity level. Due to the small sample size and wide

range of variability these improvements are not statistically significant. In

addition to the recall of hours and type of activity (light, moderate, heavy), a

more global subjective comparison of the previous weeks level of activity was

also assessed using this tool. There appears to be a perception of improved

activity level in the home intervention group with 50% of patients responding

reporting more activity at 4 and 8 weeks compared to only 14% of the control

group reporting more activity. On entry, 71% of the control reported less activity

in the week prior to hospitalization, this decreased but at 4 and 8 weeks 43% of

Table 4.8 Activity Recall at Entry, 4 and 8 Weeks
Home Intervention Control
Variables Entry 4 8 Entry 4 8
_Weeks Weeks Weeks Weeks
Kcal/kg/day 34.55 34.58 37.98 35.66 37.38 35.74
3.2 2.0 8.4 5.9 4.9 5.8
Kcal/day 2936 3014 3226 3264 3504 3431
+537 499 740 1053 1115 1353
Kcal/hr 122.3 125.6 134.4 136 146 142.9
22.4 20.8 30.8 43.9 46.5 56.4
Recall
More 13% 50% 50% 0% 14% 14%
Less 38% 13% 25% 71% 43% 43%
Same 38% 25% 13% 39% 14% 43%








66
the group still reported less activity at each assessment period compared to 13%

and 25% of the patients in the home intervention group. These changes were

not statistically significant but indicate some subjective improvements in the

home intervention group.

Self-Reported Quality of Life

Quality of Life was assessed on entry in to the study, 4 and 8 weeks using

two paper and pencil instruments. The scores are shown in Table 4.9 and 4.10

and 4.11. The MAACL-Revised instrument measured anxiety, depression,

hostility, positive affect, sensation seeking. Dysphoria is measure of negative

affect and is a combination of the scores of anxiety, depression and hostility.

PASS is a measure of positive affect which combines the scores of positive

affect and sensation seeking Table 4.9 represents trait (how you generally

feel) responses for the MAACL-R. These values are presented only on entry

into the study, as they generally do not change over time. Table 4.10 illustrates

state (how you feel today) responses which were assessed at baseline, 4 and 8

weeks to look for changes in affect in response to the intervention. Responses

were converted to T scores using a standardized scale to account for known

differences between men and women in number of items checked.

There were no differences in baseline state or trait characteristics

between the two groups. After 4 and 8 weeks of intervention, there were no

statistically significant differences between the two groups for any variable

tested.







67

Table 4.9 MAACL-R Traits at Study Entry
Home Intervention Control
Variables Entry Entry
Anxiety 47.4 8.9 58.3 24.9
Depression 47.1 8.9 52.9 20.4
Hostility 43.7 1.7 53.0 20.5
Positive Affect 49.4 6.6 46.7 14.1
Sensation Seek 49.4 11.8 43.1 17.9
Dysphoria* 44.3 4.6 55.3 21.7
PASS* 52.7 7.8 46.4 11.2
Values are mean SD; *Dysphoria=Anxiety+Hostility+Depression;
*PASS=Positive Affect+Sensation Seeking


In addition to the MAACL-R, the PAIS-SR was given. The PAIS-SR

measures psychosocial adjustment to illness and includes seven primary

domains. Health care orientation (HCO), vocational environment (VOC),

domestic environment (DOM), sexual relationships (SEX), extended family

relationships (EFAM), social environment (SOC), psychological distress (PSY)

and a total score. There were no statistical differences between the two groups

at baseline. These results are shown in Table 4.8. At study entry, 4 and 8

weeks there were no statistical differences between the two groups for any

variable tested. Scores were reported as T scores which are a standardized








68

Table 4.10 MAACL-R State Responses at Entry, 4 and 8 Weeks
Home Intervention Controls
Variables Entry 4 8 Entry 4 8
Weeks Weeks Weeks Weeks
Anxiety 54.6 50.3 58.7 57.1 50.7 58.0
18.8 13.9 24.9 24.6 16.3 26.6
Depression 59.7 49.4 59.0 44.9 44.0 51.6
27.0 13.4 26.1 2.5 3.7 19.4
Hostility 55.9 46.1 44.3 43.3 43.0 44.7
22.5 6.6 4.0 3.1 3.7 6.8
Positive 54.3 63.7 50.7 60.1 54.1 54.7
Affect 15.3 27.2 14.9 10.3 7.2 9.9
Sensation 49.3 52.6 44.6 50.7 49.0 50.6
Seek 5.5 11.8 10.3 8.5 4.2 6.2
Dysphoria* 59.3 47.7 55.9 50.0 45.7 49.3
28.1 14.2 25.1 17 11.2 22.3
PASS* 53.4 58.1 51.0 58.3 54.4 55.0
14.1 19.5 16.2 10.3 7.3 9.9
Values are mean SD; *Dysphoria=Anxiety+Hostility+Depression;
*PASS=Positive Affect+Sensation Seeking


score based on a mean score for the reference group of 50%. A higher score

means poorer adjustment to the illness. There was a change in scores towards

better overall psychosocial adaptation to chronic illness in the control group

when compared to the home intervention group. However, analysis of variance

did not demonstrate a statistically significant change within patients (F=0.85,

p=0.49). In addition, there were no significant interactions of main effect or time.

These results are limited by the sample size and variability within groups.








69

Table 4.11 PAIS-SR Responses at Entry, 4 and 8 Weeks
Home Intervention Controls
Variable Entry 4 8 Entry 4 8
Weeks Weeks __Weeks Weeks
HCO 52.3 50.3 53.0 49.5 47.7 49.3
15.5 11.4 13.9 10.6 4.7 5.3
VOC 41.9 48.0 44.5 49.6 39.9 + 43.7
12.9 8.9 13.7 11.2 8.2 7.0
DOM 47.0 50.7 49.7 44.8 44.3 36.9
11.4 9.4 11.8 10.5 4.9 16.9
SEX 46.1 45.0 49.2 48.7 44.1 + 44.9
9.5 8.4 10.8 8.3 6.4 7.7
EFAM 49.7 52.6 56.7 49.7 48.6 52.1
9.1 10.1 9.9 6.9 3.8 6.4
SOC 50.9 46.7 52.8 50.3 49.0 48.0
7.8 9.2 6.3 10.3 9.6 7.5
PSY 51.1 47.6 47.8 50.2 46.9 46.9
10.8 10.5 11.6 10.8 6.6 11.6
TOT 338 341 354 343 320 + 316
61.5 54.4 68.3 54.4 25.1 44.0
HCO=Health care orientation, VOC=vocational environment, DOM=domestic
environment, SEX=sexual relationships, EFAM=extended family relationships,
SOC=social environment, PSY=psychological distress


Analyses of Data in Relation to the Hypotheses

Hypothesis 1

Hypothesis 1 stated that patients with decompensated HF who undergo

optimization of medical therapy combined with inotropic therapy will result in an

increase in exercise time and peak oxygen consumption, and improvement of

quality of life after 8 weeks. The results did not support this hypothesis. The








70
data demonstrated no statistically significant improvements for the entire sample

from study entry to the end of 8 weeks for total exercise time, oxygen

consumption or quality of life.

Hypothesis 2

Hypothesis 2 stated that HF patients discharged after medication

optimization who participated in the home intervention program would

demonstrate significant improvements in total exercise time and peak oxygen

consumption at 8 weeks when compared to controls.

The mean exercise time at baseline was 382 seconds in the control group

with a range of 180 to 680 seconds 203 seconds. After 8 weeks the mean

exercise time was 388 seconds with a range of 0 to 780 seconds 280 seconds.

In the home intervention group the baseline mean exercise time was 319

seconds with a range of 120 to 420 seconds 99.7 seconds. After 8 weeks, the

mean exercise time was 395 seconds with a range of 195 to 720 seconds 175

seconds. Although there was an approximately 24% increase in exercise time

(76 seconds) in the home training group after 8 weeks, it was not statistically

significant ( t=0.066, p=0.9482). The relative change in exercise time in the

control group at 8 weeks was less, only 2% (6 seconds). Using paired student t-

tests there were no differences between the groups at baseline or 8 weeks, or

within groups from baseline to 8 weeks. There were trends towards significance

in several exercise variables in the home intervention group. There was a trend

to an increase in resting systolic blood pressure, mean difference of 14.87








71

17.9 mm Hg (t= 4.348, p= 0.0034); peak heart rate, mean difference of 6.25

7.9 beats per minute (t = 2.24, p = 0.0604); peak systolic blood pressure, with a

mean difference of 17.71 20.3 mm Hg (t = 2.3, p =0.0608) after 8 weeks of

intervention. The measure of heart rate reserve, (peak heart rate minus resting

heart rate) was significantly higher in the home intervention group, 37 beats at

baseline with an increase to 46 after 8 weeks, compared to a baseline of 39

beats to a post-intervention value of 42 in the control group ((t= 4.348, p=

0.0034)

The data for peak oxygen consumption also did not support the

hypothesis that there would be significantly better improvements in the home

intervention group. In the control group, mean VO2mx increased from 12.4 3.2

ml-kg-'-min-' to 14.9 5.4 ml-kg-1-min-1 an approximately 20% increase. In the

home intervention group, mean VO2mx increased from 13.5 5.1 ml-kg'-min-~ to

13.82 4.0 ml-kg-*min-.an approximately 2% increase. Although there were

overall improvements in each group, repeated measures t-test procedures

revealed that these changes were not significantly different.

Evaluation of respiratory exchange ratio (RER) demonstrated that both

groups achieved values greater than 1.0 indicating close to maximal effort.

While the means for both groups indicate that there were improvements in both

groups with regard to VO2mx, there was such a wide range of variability between

patients that anticipated improvements while seen are obscured by the level of

variability.







72

Hypothesis 3

Hypothesis 4 stated that home exercise in HF patients discharged after

inotropic infusions and medical optimization will result in significant

improvements in their quality of life when compared to controls at 4 and 8 weeks.

The data did not support this hypothesis. There were no statistically significant

differences between the two groups at 4 or 8 weeks. As reported there were no

statistically significant differences in multiple measures of quality of life, either at

baseline, 4, or 8 weeks. Examining the State MAACL-R scores indicates that

the control group had less depression and hostility, and better overall positive

affect at baseline than the home intervention group. However, the wide range of

variability makes any conclusions difficult. The PAIS-SR demonstrated similar

levels of adjustment to the domains at baseline for both the control and home

intervention groups. Over time it appears that the control group continues

towards better adjustment than the home intervention group, but due to the wide

range of variability and small sample size and resulting lack of statistical

significance definitive conclusions are not appropriate.

Summary

This chapter presented the data obtained during the study.

Characteristics of the patients including demographic and cardiovascular

variables were presented. Results of the data analyses were presented for each

hypothesis tested.

There were no statistically significant changes in measures of functional








73

capacity; total exercise time, VO2pek, distance walked in 6 minutes. There were

trends towards differences in several cardiopulmonary variables; systolic blood

pressure preexercise and at peak exercise, peak heart rate in the home

intervention group from study entry to 8 weeks. There was a statistically

significant increase in heart rate reserve.

There were no statistically changes in measures of quality of life at entry,

4 or 8 weeks in measures of trait or state affect or adaptations to chronic illness.













CHAPTER FIVE
CONCLUSIONS, DISCUSSION, AND RECOMMENDATIONS


This chapter presents conclusions and a discussion of the findings.

These findings are compared to current knowledge and research on medical

optimization and exercise with decompensated heart failure patients.

Conclusions are derived from these data, recommendations for future research,

and implications for nursing practice are presented.

The purposes of this research was to describe the effect of a home

exercise intervention on 15 patients with decompensated HFafter receiving

medical optimization. The variables chosen to describe the effect are: measures

of functional capacity and quality of life. An experimental design was chosen to

study the effect of this home exercise intervention. There were 8 patients in the

intervention group and 7 in the control group.

Measures of functional capacity were total exercise time, maximal oxygen

uptake (VO2,pak) measured by gas exchange during exercise, six minute walk,

NYHA classification on entrance into the study and 8 weeks later. Changes in

quality of life as a result of the home exercise intervention were assessed using

the MAACL-R and PAIS-SR. These tools were administered on entrance into

the study, at 4 and 8 weeks.



74








75

It was hypothesized that there would be significant improvements in

selected measures of functional capacity and self reported quality of life for both

groups at 8 weeks. It was also hypothesized that greater improvements in

functional capacity would occur in the intervention group due to the effects of

increased activity. This study also sought to determine if implementation of the

home exercise intervention was feasible and safe.

Initially 24 patients admitted for medical optimization met the inclusion

and exclusion criteria and gave written informed consent. Using a computer

generated randomization schedule, these 24 patients were assigned to home

exercise intervention or a control group. Of the 24 randomized patients, nine

patients were unable to complete the study. One patient was unable to complete

testing at study entry, or to return for follow-up. After completion of study entry

testing, four patients; three in the intervention group and one in the control group

were restarted on inotropic therapy, not discharged from the hospital and

underwent heart transplantation within the next 8 weeks. Two patients in the

exercise group died prior to the 8 week testing. Of these two, one did not begin

the intervention. The patient was rehospitalized three days after discharge and

died one week later in an outside hospital. The second patient died suddenly

while at home sitting in a chair. Prior to that event, this patient had reported

feeling much better and had been walking one mile 3-5 days a week without any

increase in symptoms. Two patients in the control group did not return for 8

week testing because of personal schedule conflicts and could not be








76
rescheduled. The final sample consisted of 15 patients (eight in the intervention

group and seven in the control group) who were able to complete 8 weeks of

intervention and/or follow-up and return for repeat testing.

Conclusions

It was hypothesized that medical optimization in patients with

decompensated HF would result in an increase in functional capacity after 8

weeks. There were no statistically significant differences in measures of

functional capacity (total exercise time, VO2peak, 6 minute walk distance) from

baseline to 8 weeks for the entire sample. This hypothesis was not supported by

the data. There was a shift towards Class II and III from III and IV at 8 weeks in

both groups. This change was not statistically significant.

In addition to the effects of medical optimization, it was hypothesized that

the home exercise intervention would result in significant improvement in

functional capacity at 8 weeks when compared to the control group. With the

exception of heart rate reserve, there were no statistically significant differences

in cardiopulmonary responses to exercise (total exercise time, VO2pak, or 6

minute walk distance after 8 weeks of intervention between the two groups.

This hypothesis was not supported by the data. There were increases in

exercise time (24% and 2%), and VO2peak, (2% and 20%), and 6 minute walk

distance (10% and 16%), in the home exercise and control groups respectively,

these changes were not statistically significant.








77
In addition to assessing measures of functional capacity, it was

hypothesized that the home exercise intervention would result in significant

improvement in quality of life when compared to controls at 4 and 8 weeks. This

hypothesis was not supported by the data. There were no statistically significant

differences between groups at study entry, 4 or 8 weeks.

In addition it was hypothesized that implementation of this home exercise

intervention in patients with decompensated HF who have been discharged after

medical optimization appears to be feasible and safe. The data support this

hypothesis. Although the sample is small and there were two deaths in the

home intervention group, these deaths were not related directly to the

intervention. One patient died without beginning the intervention, the second

death occurred suddenly and not was not associated with the prescribed home

intervention.

The program was easily implemented within the context of each patient's

home environment. The program was individualized based on resources. Some

patients were able to vary their walking with other activities such as swimming,

or biking. Or in some cases, patients were able to increase their ability to walk

by using a treadmill indoors to avoid the heat of the summer. The majority of

patients (75%) were compliant with the program, exercising a minimum of 3 days

per week. There were no financial limitations that led to the inability of the

interventions implementation.







78

Discussion of the Findings

The characteristics of the two groups at study entry were similar. There

were no statistically significant differences in any demographic or cardiovascular

history variable with the exception of history of smoking. In the home exercise

group there was a higher percentage (88% vs 29%, p=0.0034) of patients

reporting a history of having ever smoked when compared to controls.

Importantly, there were no significant differences in cardiovascular history

variables. The duration of HF, ejection fraction, NYHA classification, history of

inotropic therapy and current medical therapy were not different.

Post medical optimization assessment of hemodynamic responses to

therapy for the patients completing 8 weeks of the study had trends towards

differences between the two groups, with the control group having higher right

heart pressures. However, these differences did not correlate to lower study

entry measures of functional capacity. This assessment was not required as

part of the study and three of the home exercise patients were not studied,

however it does provide better characterization of the hemodynamic status of the

majority of patients at hospital discharge.

In the home exercise group there were trends towards significant

differences in right atrial pressure, right ventricular diastolic pressure, and

pulmonary artery wedge. Although the data indicates improved hemodynamic

function in the intervention group when compared to the control group, these

changes did not translate to significant differences in baseline measures of








79

functional capacity; specifically, total exercise time, or VO2ak, or 6 minute walk

distance between the two groups. In fact, the control group with worse

hemodynamic measures had generally higher baseline values for total exercise

time, 6 minute walk and slightly lower values for VO2pak.

Functional Capacity

There were no significant differences in cardiopulmonary responses to

exercise at baseline between the two groups. The baseline measure of VO2m,

12.4 and 13.5 ml.kg combined with the mean ejection fraction of 21%, and NYHA

classification of III and IV reflects the severity of disease in the patients that

were studied, in spite of optimization of medical therapy. The EF, and VO2mx

values are similar to the patient characteristics reported in other research

studies which have evaluated home exercise training in HF patients (Coats,

Adamopoulos, Radaelli, et al, 1992; Coats et al, 1993). Research into the

effects of exercise training in patients with HF has been conducted primarily in

stabilized NYHA Class II and III patients and has been found to be efficacious

(Adamopoulos et al, 1993; Coats, 1993; Hanson, 1994; McKelvie et al, 1995).

More recent exercise training studies have been conducted in stabilized Class IV

severe HF patients (Demopoulos, Bijou et al, 1997; Meyer, Samek et al, 1997),

which is the population examined in this study. Although the classification of HF

is similar to more recent reports, this study evaluated the implementation of a

home exercise intervention immediately upon discharge after medical

optimization, making this study unique. While the hypothesis of feasibility and








80

safety was confirmed, the small sample size at 8 weeks and the wide range of

variability of individual data make conclusions about efficacy of the intervention

impossible. In addition to the small sample size and variability, full effects of

medical optimization may not have been fully appreciated until greater than 8

weeks or later after therapy adjustments, particularly with the known

pharmacologic effects of inotropic therapy and ACE inhibition (Liang et al, 1984;

Drexler et al, 1989).

Although the program is feasible, the intensity of the home exercise

training program, which was low, may have contributed to the lack of efficacy.

The program was designed to be implemented in a relatively unstable

population, and was kept at a level of daily activity to reduce potential health

risks for the patients. This low intensity may have resulted in a lack of significant

training effect. Although there were improvements in total exercise time in the

home intervention group, this change was not statistically significant. However,

the percentage increases are consistent with those seen in other studies of

conventional training. Coats et al, (1992) reported an 18% increase in VO2peak

after 8 weeks of training. Sullivan et al (1988) reported a 23% increase, and

Hambrecht et al (1997) reported 31% increase after 24 weeks. It has also been

demonstrated in research by Demopoulos et al, (1997) and Belardinelli et al,

(1995) that training programs using low work load corresponding to less than

50% of peak VO2 can achieve significant training effects. The small sample








81
size, and wide variability in the intensity, duration and frequency of training may

explain the lack of effect seen in this study.

Although patients in the exercise group were generally compliant with the

program, the intervention rarely resulted in peak heart rates over 100 bpm. In

addition, the home setting without close supervision may have limited the

exercise group from pushing themselves to higher levels of exertion for fear of

the development of chest pain, or severe shortness of breath.

The severity of illness in these patients was one factor in the selection of

a protocol with such low intensity. In this severely ill population it is not

anticipated that they will achieve full return to preHF condition, the goal of any

therapy is to optimize within the limits of the system. Attaining some level of

mastery over simple activities of daily living is a primary goal, not the ability to

complete a maximal exercise test. This parallels the ACSM/CDC

recommendations for increased activity levels in normally healthy but sedentary

people, which can result in improvements in long-term outcomes (Pate et al,

1995). Anecdotal comments from exercise patients were that they felt better

after exercising.

In addition to the intensity of the program, at least one clinical factor

directly affects the baseline status and impact of an exercise intervention.

Duration of HF determines the current level of deconditioning in any given

patient. In more chronically ill patients the level of compensatory adaptations

that have occurred over time will be higher, and resulting changes in skeletal








82

muscle metabolism and kinetics will be greater. Current data suggests that

exercise training programs increase VO, and exercise capacity by improving

skeletal muscle performance (Hambrecht et al, 1997). With more chronically ill

patients it is anticipated that there is more opportunity to effect peripheral

changes. And that in severely ill patients more significant changes may be seen

with more modest training programs. In this group of patients although the

mean duration was 41 months there were several patients who had a duration of

HF of less than one year which could correlate with better general physical

health at study entry, requiring higher intensity exercise to promote changes in

fitness and skeletal muscle function.

This study allowed for any etiology of HF, and important differences may

exist in the time sequence of adaptive mechanisms that are activated, in a

idiopathic versus chronic ischemic cardiomyopathy patients. It has been

reported that patients with ischemic cardiomyopathy as the etiology of their HF

have a higher mortality rate than other etiologies (Costanzo et al, 1995).

The 6 minute walk was assessed based on its simplicity and known

correlation to outcome (Bittner et al, 1993). There were no significant

differences between the two groups at baseline or at 8 weeks. However, the

sample size at each testing period was not consistent. Due to the close

proximity of testing (within 8 hours) at baseline (VO2peak testing, heart

catheterization, 6 minute walk) and at repeat testing (VO2max, 6 minute walk)

within 3 hours, several patients would not, or could not complete the 6 minute








83
walk due to fatigue, low blood pressure or angina. Examination of the total

distance walked indicates improvement in both groups although not statistically

significant. The baseline values for the home exercise group appear to be much

less than the control group in spite of similar levels of activity prior to

hospitalization. Again, small sample size and large variability, make

interpretation of this data difficult.

Quality of Life

Both tools used for measurement of quality of life, the MAACL-R which

measures changes in affect over time and the PAIS-SR which measures

adjustment to illness did not show statistically significant changes over time.

Although there were no clinically significant changes over time in adjustment to

illness, patients were able to adapt to the home exercise intervention as

evidenced by the 75% compliance, demonstrating a positive or effective

adaptation as illustrated by Roy.

The assessment of these variables is also confounded by the time frame

of the illness during which this study was targeted. The majority of patients were

admitted and being evaluated for eligibility for heart transplantation. The

psychological impact of the diagnosis and status of transplant eligibility may

have confounded the data. Several patients were informed during this study that

they were not eligible for transplantation. Others were selected and listed,

giving them a potentially better therapeutic outcome than those not selected.

Although many studies have demonstrated improvements in QOL associated








84
with various interventions in HF(SOLVD Investigators, 1993; Freeman et

al,1988), others have not (Rector et al, 1993). A larger sample size would help

to further answer this question.

Summary

The results of this study suggest that a home exercise training program,

consisting primarily of walking, in severely ill HF patients is safe and feasible. It

demonstrated that this did not require special equipment or expense but could

be adapted to their individual situations. The majority (75%) of patients in the

intervention group were 100% compliant with a 3 days a week program. The

institution of a home exercise program appeared to result in some improvements

in functional capacity although modest they were not statistically significant. The

improvements in exercise time and VO2m,, were below those seen for most

exercise programs evaluated in the literature (Coats et al, 1992; Adamopoulos et

al, 1993; Stratton et al, 1994), but the intensity of this program was well below

those previously evaluated. There was a shift in NYHA classification from III and

IV, to II, III and IV for both groups possibly related to the effects of medical

optimization.

This study was not able to demonstrate any changes in measures of

affect or adjustment to illness over the 8 weeks of the study. The confounding

features of the hospitalization for an acute exacerbation of HF, transplant

evaluation process may have led to the inability of the tools to assess the effects

of exercise training within that milleau.








85

The small sample size, variability of the patients recruited affect the ability

to make any conclusions, and limit the generalizability of the findings. The lack

of homogeneity of the etiology of HF, appears to have increased the variability of

the data, further confounding its interpretation.

Recommendations

In this study the effects of medical optimization and 8 weeks of home

exercise training on functional capacity, QOL were measured in 23 patients with

severe Class III, IV HF. The following are specific recommendations for future

nursing research based on the findings of this study:

This study design, with minor modifications should be replicated with a

larger number of patients to provide more power to the statistical analyses. The

inclusion criteria should be modified to focus the sample in specific etiology

groups ie ischemic, idiopathic, and viral with sufficient sample size in each group

to make definitive conclusions and limit variability. Careful examination of the

age criteria should be undertaken to limit variability. Due to the severity of

illness in these patients, the number of assessments should be limited.

Functional capacity using one measure such as VO2, rather than multiple

measures, would insure more complete data. Quality of life should be measured

with one tool to simplify testing

The training program should be longer in duration, 16 weeks in order to

be able to discriminate potential changes in function related to the delayed

effects of pharmacologic therapy from the effects of exercise intervention. The








86
exercise intervention should be modified to incorporate the walking program as

the early transition from hospital to home for the first 8 weeks, and then to

increase the intensity for the next 8 weeks in order to assist the patients in

achieving a higher level of function through a more rigorous training program.

The modification of the exercise intervention could involve a combination

of home exercise with periodic supervised sessions at a fitness center, or more

home visits conducted by home health personnel who were knowledgeable of

the principles of exercise training. In addition, the monitoring of the program

could be enhanced by more frequent contact by the investigator. This study had

contact once a week. Increasing this to 2-3 times per week could potentially

improve compliance. Assessment of compliance could also be better evaluated

using pedometers or other direct measures of physical activity other than diaries.

Use of more sophisticated equipment for home monitoring could also be

examined.

Implications for Nursing Practice

Strong data exists regarding the cost effectiveness of nurse managed HF

clinics. They significantly reduce costs by reducing rehospitalization rates

(Cintron, Bigas, Linares, Aranda & Hernandez, 1983; J. Brass-Mynderse, 1996).

These clinics generally provide complete management recommendations for

patients with HF. The effects of exercise training in HF patients has clearly

demonstrated the beneficial effects in the majority of patients (McKelvie et al,

1995). These recommendations offer the nurse practitioner the opportunity to







87

further improve the functional capacity of patients with HF by prescribing

exercise prescriptions to assist patients in optimizing their function. This study

offers some insight into possible treatment recommendations even for the newly

discharged patient.

In addition, the knowledge gained by the nurse practitioner can be taught

to other health care providers specifically those who provide home health

support. A comprehensive outpatient program that incorporates exercise as

intervention along with standard medical management could result in further

improvements in patients level of functioning. Nurse practitioners offer a unique

perspective to patients of promoting wellness and patient education, to insure

that patients are knowledgable about their disease and take an active role in

their therapies.













APPENDIX A
EXERCISE INSTRUCTIONS


Your exercise program will be a gradual program tailored specifically for you. In
order to get the best results it is necessary to be consistent in your exercise.
There will be some days when your heart condition will not allow you to exercise,
do not get discouraged we expect this to happen occasionally. If you have
concerns about exercising, please give me a call at 352-846-0610.

Take your pulse prior to exercising and record on your exercise diary.

Start with light STRETCHING 5-10 minutes

Begin your walk, on level ground for XX minutes.
If necessary, stop and rest for 1-2 minutes in order to continue.

At the end of your walk take your pulse within 15 seconds, record on your
exercise diary.

End with light STRETCHING 5-10 minutes

Your Target Heart Rate should be XX-XX. Do not exercise beyond
this heart rate.

STOP if you reach a 2+ on either the chest pain or shortness of breath scales
shown below. We are working toward a target of perceived effort of 11-14 (Light
to Somewhat Hard)

Chest Pain Shortness of Breath

1+ Light, barely noticeable 1+ mild, noticeable to you
2+ Moderate, bothersome 2+ mild, noticeable to others
3+ Severe, very uncomfortable 3+ moderate, but could continue
4+ Most severe pain ever 4+ severe, you can't continue




88













89


APPENDIX B
LIFESTYLE MANAGEMENT INSTRUCTIONS


It is very important for you to monitor your heart condition. You are the most
knowledgeable person about how you are feeling. The goal is to keep your
condition under good control.

Your Medications:
Must be taken consistently. Do not let yourself run out of
medications. Do not stop them on your own without calling your
doctor. If expense is an issue, please bring this up immediately so
we can work with you, it is much more expensive to come to the
hospital.

Fluid Restrictions
You must watch your fluid intake!!! You should try and
keep your intake to 2 liters a day which is 8 large glasses
of fluid a day. Watch for beverages that contain Sodium.

Salt Restriction
No added salt in your diet. READ ALL Labels. Try to avoid
anything with sodium. You will be more successful if you stick to
fresh fruits and vegtables, almost all processed foods have sodium.
WEIGH yourself daily. If you notice more than a 2-3 pound fluctuation
you may be retaining fluid. If so, examine what you have eaten and drunk
in the past several days. If you have increased your fluids and salt intake,
STOP at once. If there is no improvement in a day or so please call so
that they can adjust your medications.














90

APPENDIX C
ACTIVITY DIARY

/ / / / / I / /I/_I

Baseline Baseline Baseline Baseline Baseline
Heart Rate Heart Rate Heart Rate Heart Rate HeartRate


Peak Peak Peak Peak Peak
Exercise Exercise Exercise Exercise Exercise
Heart Rate Heart Rate Heart Rate Heart Rate HeartRate


Exercise Exercise Exercise Exercise Exercise
Time (min) Time (min) Time (min) Time (min) Time(min)


Exercise Exercise Exercise Exercise Exercise
Distance Distance Distance Distance Distance


Chest Pain Chest Pain Chest Pain Chest Pain ChestPain
Scale Scale Scale Scale Scale


Shortness of Shortness of Shortness of Shortness of Shortnes
Breath Breath Breath Breath ofBreath
Scale Scale Scale Scale Scale


Exertion Exertion Exertion Exertion Exertion
Scale Scale Scale Scale Scale


Rate the Rate the Rate the Rate the Rate the
Day Day Day Day Day


Daily Wt Daily Wt Daily Wt Daily Wt Daily Wt













91

APPENDIX D
SCALES FOR ACTIVITY DIARY


Chest Pain Shortness of Breath

1+ Light, barely noticeable 1+ Mild, noticeable to you
2+ Moderate, bothersome 2+ Mild, noticeable to others
3+ Severe, very uncomfortable 3+ Moderate, but could continue
4+ Most severe pain ever 4+ Severe, you can't continue


Perceived Exertion Scale' Rate the Day
6 No exertion at all 1 Good
2
7 Extremely Light 3 Fair
4
5 Poor
8
9 Very Light
10
11 Light

12
13 Somewhat Hard

14
15 Hard
16
17 Very Hard

18
19 Extremely Hard

20 Maximal Exertion