Br Heart J (Supplement) 1994; 72: 87-91

How do changes in lifestyle complement medicaltreatment in heart failure?

J Soler-Soler, G Permanyer-Miralda

Heart failure not only has a poor prognosis butimpairs the quality of life. Research onpharmacological treatments continues to try toimprove the prognosis and symptoms ofpatients with heart failure. However, non-pharmacological measures such as rest anddietary salt restriction have been used to treatheart failure since the time when availabledrug treatment was limited to digitalis or somerudimentary type of diuretic. Despite dramaticadvances in drug treatment, advice onmodifying lifestyle still plays an important partin the treatment of a condition which itselfinfluences lifestyle so much.

Modifications of the lifestyle of patients withheart failure may take three different andsometimes conflicting directions: (a) avoi-dance of harmful habits (excess sodium intake,smoking, alcohol consumption), (b) enhance-ment of wellbeing (limitation of symptomprovoking activity, psychological education fora better acceptance of untreatable limitation),and (c) promotion of favourable changes inneuroautonomic function, muscular status,and peripheral circulation through physicaltraining. The relative emphasis to be laid onthe second or third approaches depends on thepatient's condition and overall prognosis.There are patients who, at best, can hope to befree of only the most severe discomfortwhereas, in others, to achieve a fairly good oreven virtually normal quality of life is arealistic goal.The areas where lifestyle modification has

been advocated for the management of heartfailure include diet; the avoidance of toxichabits; physical activity; and psychologicaladjustment. The evidence on which adviceshould be given is variable in quality andquantity, and clinicians may be left with littlemore than common sense for guidance. As inother "common sense" medical approaches,however, experimental research sometimescontradicts what seems obvious - for example,physical activity.

Servicio deCardiologia, HospitalGeneral UniversitariVail d'Hebron,Barcelona, SpainJ Soler-SolerG Permanyer-MiraldaCorrespondence to:Dr J Soler-Soler,Servicio de Cardiologia,Hospital GeneralUniversitari Vall d'Hebron,Passeig Vall d'Hebron119-129, 08035 Barcelona,Spain.

DietDietary advice in heart failure has traditionallyconcentrated on sodium restriction. Sodiumrestricted diets were introduced at the begin-ning of the century,' based on the knowledgethat in heart failure there is avid sodiumreabsorption by the kidney, and the rationalethat dietary sodium restriction shouldfavourably affect sodium balance. Thus a dietlow in sodium became one of the mainstays oftreatment.2" Well into the 1960s diets with as

low a sodium content as 05 g/day were recom-

mended.3 Progressively, this stringent approach

gave way to a more liberal daily sodium intake(2-3 g/day5 6) on the assumption that sodiumand water retention could be countered byconcomitant judicious diuretic treatmentwithout serious side effects. Despite advancesin drug treatment, moderate to appreciablesodium restriction is still considered one of thecornerstones of the treatment of heart failureby many authorities6 7 and is included incurrent workshop recommendations.8 How-ever, in two recent surveys of doctors' practicein the management of heart failure, one fromthe United States9 and the other from Europe,diet was the first therapeutic measure in onlytwo out of five countries.'0 Some recentreviews on treatment of heart failure do noteven mention dietary sodium restriction."Few modern studies have examined the

effects of a low sodium diet in patients withheart failure,'2 and even then the emphasis ison the neuroendocrine or metabolic ratherthan clinical effect. Severe sodium restrictionactivates the renin-angiotensin system andsympathetic nerve activity.'2 One reason forthe paucity of clinical studies on low sodiumdiet may be the difficulty in carrying out trialswith acceptable measurement of dietarysodium intake outside institutional settings.On the other hand, studies conducted on ametabolic ward may be irrelevant to commonclinical practice. Another powerful reason isthat the effectiveness of a low sodium diet asa general measure might be considered to betoo evident to warrant further investigation.

Excessive sodium retention by the kidneyshas been consistently shown to be a feature ofheart failure'3-'5-possibly an inappropriaterenal response to a fall in cardiac output"-and this is the rationale for sodium restriction.Abnormal handling of sodium is a marker ofeven mild heart failure: Volpe et al recentlyshowed that in patients with left ventriculardysfunction but not in normal subjects atrialnatriuretic factor concentration fails to rise inresponse to a sodium load and sodiumretention occurs. '7 They suggested that theirfindings indirectly supported the usefulness ofsodium restriction. However, noticeabledifferences in avidity for sodium retentionduring a low sodium diet in patients with heartfailure have been found,'2 suggesting thepossibility of different optimal regimens inhaemodynamically similar patients. Inaddition, the effect of diuretic treatment canbe reduced in subjects given a low sodiumdiet,'8 thus raising the issue of the approp-riateness of stringent sodium reduction whendiuretics are given.

In fact, despite the apparently universalconsensus on the desirability of a low sodium

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diet, information on the influence of sodiumrestriction on the long term outcome indifferent clinical settings, with differentconcomitant treatments, and even in differentpatients is not available. One report suggeststhat heart failure due to abnormal leftventricular relaxation in salt sensitive patientswith hypertension might be more dependenton sodium induced volume overload.'9Sodium could be regarded as an actual causeof heart failure in such cases. Even if notdirectly related to diet, research on the relationbetween sodium and heart disease isgrowing.20Emphasis on the need to restrict dietary

sodium in heart failure is justified for doctorson the basis of its effectiveness (even if someaspects deserve further clarification). Althoughdoctors' contribution to changing generaldietary habits in this way is small, there isincreasing evidence for the need to limitsodium intake in the Western population toprevent hypertension, a leading cause of heartfailure.20 21 The detection of salt sensitivesubjects should be relevant in this context.'9 20Thus restricting dietary sodium may be usefulin preventing as well as treating heart failure.A reasonably low sodium intake (about2 g/day) can usually be achieved by the patientwith easily acceptable changes in dietaryhabits.5 7An additional way to facilitate the tailoring

of sodium restriction is to educate patients intothe habit of measuring their diuresis and theirweight. Two other well known practical pointsshould also be kept in mind. Firstly, furtherreductions in sodium intake (down to 05-1 g/day), even if more difficult to carry out,may improve symptoms in severe or refractorycases. Secondly, it is important to preventbinging on salt, which may result in acutesevere decompensation.6 Poor compliance witha low sodium diet has been reported as one ofthe causes for emergency admission to hospitalin patients with chronic heart failure.22 Effortsto keep dietary sodium low, however, shouldnot result in an insufficient energy intakeleading to poor nutritional status. If palatable,salt substitutes can prove to be an alternativeapproach, care being required to ensure thatthey are really sodium free.An issue to be raised is the safety of a low

sodium diet. Uraemia associated with sodiumdepletion was reported as early as 1949.3 Inmany instances, however, it resulted morefrom the injudicious use of diuretics than fromsodium restriction. The occurrence of acuterenal dysfunction, with uraemia and hyper-kalaemia, is a well known complication ofoverzealous treatment of heart failure withdiuretics resulting in excessive sodium andvolume depletion,'5 particularly in vulnerablepatients (such as elderly people or those withprevious renal or arterial disease in whomrenal regulatory mechanisms may beblunted'5). Elderly people may be particularlyprone to poor acceptance and side effects ofmoderate to marked sodium restriction(appetite loss, asthenia, and confusion).23 24The introduction and widespread use of ACE

inhibitors is another potential cause of renaldysfunction.25 ACE inhibitors reduce theefferent glomerular arteriolar tone, which mayresult in renal dysfunction, particularly inpreviously hypertensive patients whose bloodpressure has been appreciably reduced,26 evenwhen they do not have renal artery stenosis.27This problem is not uncommon in patientswith severe acute heart failure who have beenovertreated with diuretics and ACEinhibitors.25 The contribution of low dietarysodium is difficult to assess. Acute volumelosses such as induced by diarrhoea28 mayresult in unduly severe renal dysfunction ifACE inhibitors have blocked the physio-logically protective renin-angiotensin system.

Avoidance of harmful habitsIn view of the deleterious effects of smokingon the cardiovascular system and respiratoryfunction, it is obvious that patients with heartfailure should not smoke. It is also commonpractice to forbid alcohol consumptionbecause it may acutely depress ventricularperformance.29 In addition, cessation ofexcessive intake may result in improvement ofdepressed systolic function.30 In cases of heartfailure clearly not associated with alcoholabuse, however, the psychological conse-quences of depriving patients of the pleasureof a modest amount of alcohol probablyoutweigh the questionable long term benefitsof abstinence, especially in countries wheremoderate wine drinking during meals is awidespread habit.

Physical activityThe promotion of physical activity is thegreatest recent change advocated for thetreatment of heart failure. Classically, rest wasemphasised as it seemed obvious that, as theheart was unable to meet the body's needs,these should be kept to a minimum todecrease cardiac work. As early as the 1960s,however, recommendations3 for prolongedbed rest were already being questioned4 5 andresumption of moderate symptom free activitywas encouraged after compensation had beenreached. Research suggested that excessiverest might be harmful by causing musculardeconditioning, whereas exercise programmesresulted in fewer symptoms during everydayactivities. Controlled exercise programmeswere considered beneficial to the myocardialand muscular circulation, particularly inpatients with coronary disease.5 Now exerciseis being recommended as a therapeuticintervention for heart failure, at least inselected patients. Some of the features ofrecent studies on physical exercise in heartfailure are relevant to the present discussion.

(1) As mentioned, active physical trainingmay be beneficial in cardiac failure. Traininghas been consistently shown to improvesymptoms, exercise capacity, and peak oxygenuptake and to reduce ventilatory drive duringsubmaximal and maximal exercise.31-35 Nocomplications-for example, exercise induced

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arrhythmia-were recorded in these selectedpopulations of patients. Information on longterm outcome is lacking, but there is specu-lation that physical training may result inimproved survival,36 as one of the variablesshown to predict mortality (low exercisecapacity37) can be reversed, and that theenhanced survival with vasodilator treatmentmay, in part, be mediated by the improvedexercise capacity and physical activity broughtabout by such drugs.36 Therefore, rest is nolonger considered appropriate treatment forheart failure in compensated cases.35 38

(2) Such studies contribute to a betterunderstanding of some of the clinical andpathophysiological features of heart failure. Inthe above mentioned studies, no improvementin systolic function was found aftertraining." 3 Rather, improved performancewas associated with evidence of improvedoxygen delivery to peripheral tissues, reducedarteriovenous difference in lactate concen-trations, and increased lactate utilisation.3'Evidence that muscle enzymatic andhistological abnormalities occur in heartfailure, either from deconditioning alone orfrom heart failure itself,36 is well known.39 40Training seems to improve muscle functionand reverse the impaired oxidative capacity ofmuscle in heart failure.4' Most importantly, inone study a significant shift towards reducedsympathetic and enhanced vagal activitiesachieved by training was shown by powerspectral analysis of RR interval variability andnoradrenaline kinetics.35 This improvement inabnormal sympathovagal balance mayimprove circulatory function and reducearrhythmias and sudden death.

(3) These studies have also shed light on thedifferences between maximal exercise testing(measuring aerobic capacity and thus overallcardiopulmonary function) and submaximalexercise,31 38 42 which is more similar to thesituation encountered during everydayactivities. Training studies have helped explainsome apparent discrepancies such as whypatients with good aerobic capacity experienceexcessive fatigue after exercise.42

Patients with heart failure should beencouraged to exercise regularly within theircapabilities. The time may have come forroutinely prescribing formal exercise trainingto patients with compensated heart failure,although the resources required to do thissafely and effectively must not be under-estimated. The available studies suggest thatcontrolled physical training programmesimprove symptoms and exercise capacity,implying that a more active lifestyle can beadopted. However, the safety and benefit ofuncontrolled vigorous activity has not beendetermined.Some considerations regarding the exercise

studies should be kept in mind:(1) The populations from which the study

patients were drawn were not preciselycharacterised and, as a rule, the clinicalfeatures of the study patients were notextensively reported.

(2) The studies do not permit assessment of

whether the effects of training apply equally tocoronary artery disease and to other types ofheart disease.

(3) The results of exercise training in heartfailure due to diastolic dysfunction have notbeen addressed.

(4) Although the need to categorise patientsby their haemodynamic features to predict theoutcome of exercise training is recognised,42-44no specific criteria have been established forselection. Scalvini et al have suggested thatoxygen uptake of less than 16 ml/kg/min at thepeak workload of exercise testing couldidentify a severe subgroup less likely to benefitfrom training. 34 Such findings should befurther evaluated-as well as the value ofsimple clinical variables-as guidelines forentering a training programme. Clinicalcontraindications to training should also bekept in mind.43

(5) A standard exercise protocol foradequate evaluation and discrimination of allpatients with heart failure is considered bysome experts not to be available44; in addition,the issue of whether some type of isometrictraining is advisable for these patients has notbeen addressed as all published studies dealwith dynamic aerobic exercise.45

(6) As previously stated, no long terminformation about patients undergoingtraining is available; adverse long term effectsof exercise have not yet been ruled out.

(7) Studies have been performed inspecialised institutions and sophisticatedlaboratories, with a particular emphasis onphysiological measurements (although,remarkably, in the study by Coats et al thetraining programme was performed at thepatients' home and not directly supervised35).Adequate information from communitysettings and less selected populations would bedesirable.The research on exercise programmes

suggests that more liberal counsellingregarding vocational rehabilitation, return towork, recreational activity, and sexual habits iswarranted in patients with heart failure. Untilmore information is available clinicians shouldadvise patients individually on how muchexercise they should take. Resumption of anactive lifestyle may improve the psychologicaloutlook. Some decisions for example, thoseregarding returning to work-require clinicaljudgment of the functional status of patients,their psychological demands (or economicneeds), and the activity under consideration.

Psychological adjustmentWhen patients have been systematicallyassessed in quality of life studies, emotionaldistress, anxiety, depression, and psychosocialmaladjustment are prevalent in heartfailure.4649 Improvement has been reported inresponse to treatment for heart failure,47 butoccasional patients may benefit frompsychiatric care. Exercise training may improvethe psychological outlook and self confidenceof patients.35 Psychological adjustment to thelifestyle imposed by the disease usually

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requires the patient, the family, and the healthcare professionals to be fully informed.50The need for supportive care is increasingly

recognised, as is the case with patients aftercardiac surgery or myocardial infarction.50 Therole of nursing staff may be important inhelping patients to participate in a normaldaily life, improve their psychosocialadjustment, and comply with medicaladvice.'51 Nursing staff may also help familymembers to cope.'5' More research isrequired on these types of intervention, bothin hospital and in the community.

Measurement of quality oflifeTo assess the effects of modifying lifestyle weshould know how to measure them.47-49 52 53One goal is to have objective evaluations ofhow and how much heart failure influencespatients' lives and of how patients cope withdisease. These evaluations may be useful asbaseline and outcome measures and shouldprovide a framework to determine the impactof any change on patients' quality of life.Although there have been advances in the

measurement of quality of life in heart failureduring recent years, methodological problemsremain, and it is premature to advocate its usefor clinical purposes in individual patients.The achievement in quality of life measure-ment in heart failure can be summarised asfollows: (a) general profiles of populationswith heart failure in terms of quality of lifehave been developed46 47 54; (b) the validity ofthe measuring instruments has beentested48 49 54 and correlated with clinicaloutcome47 49 54; and (c) the need to includequality of life studies as outcome measures inclinical trials such as SOLVD has beenrecognised.48 49 55 56Problems in measuring the quality of life of

patients with heart disease have been recog-nised for years.52 57 In view of the insufficiencyof simple activity scales such as that of theNew York Heart Association or similarclassifications,58 59 the development of bettermeasuring instruments is required. The idealinstrument should be a valid, reproducible,and sensitive to change measure of symptoms,activity, and emotional and psychologicalstatus.52 Several questionnaires and analoguescales have been devised for thispurpose.49 56 6062 Some of them, such as theMinnesota living with heart failurequestionnaire, have been validated in morethan one large clinical trial,49 5 whereasothers, such as the chronic heart failurequestionnaire,61 are included as outcomemeasure instruments in trials now under way.Despite the initial reports on validation andreliability, further experience is requiredbefore these measures can be widely accepted.A recent substudy of the SOLVD trialincluded no less than nine quality of lifeinstruments to be administered to eachpatient.48 Obviously, such a complexprocedure is irrelevant for routine clinicalpractice. Even for clinical research, a simpler,less cumbersome method is desirable.

1 Michaelson CR. Congestive heart failure. St Louis, Missouri:CV Mosby, 1983:354-99.

2 Blumgart HL, Zoll PM. The clinical management ofcongestive heart failure. Circulation 1960;21:218-28.

3 Wood P. Diseases of the heart and circulation. London: Eyreand Spottiswoode, 1968:325-46.

4 Benack RT. Congestive heart failure. Springfield, ILL:Charles C Thomas, 1966:54-86.

5 Myerson RM, Pastor BH. Congestive heart failure. St Louis,MI: CV Mosby, 1967:90-136.

6 Cohn JN. Current therapy of the failing heart. Circulation1988;78: 1099-107.

7 Smith RW, Braunwald E, Kelly RA. The management ofheart failure. In: Braunwald E, ed. Heart disease. Atextbook of cardiovascular medicine. Philadelphia:Saunders, 1992:468.

8 Expert Group on Treatment of Heart Failure. Recommen-dations from the group. In: Workshop: pharmacologicaltreatment of heart failure. Uppsala: Medical ProductsAgency, 1993:193-206.

9 HlatzkyMA, Fleg JL, Hinton PC, et al. Physician practicein the management of heart failure. J7 Am Coll Cardiol1986;8:966-70.

10 Olshausen KV, Erbel R, Perkins CM, Brogard JM.Diagnosis and treatment of heart failure in differenteuropean countries: a young AEMIE quesionnaire. AnnMed Interne (Paris) 1986;137:226-8.

11 Packer M. Treatment of chronic heart failure. Lancet1992;340:92-5.

12 Cody RJ, Covit AB, Schaer GL, Laragh JH, Sealey JE,Feldschuh J. Sodium and water balance in congestiveheart failure. J Clin Invest 1986;77: 1441-52.

13 Packer M. Pathophysiology of chronic heart failure. Lancet1992;340:88-92.

14 Harris P. Role of arterial pressure in the oedema of heartdisease. Lancet 1988;i:1036-8.

15 Badr KF, Ichikawa I. Prerenal failure: a deleterious shiftfrom renal compensation to decompensation. N Engl JMed 1988;319:623-9.

16 Cleland JGF, Dargie HJ. Heart failure, renal function andangiotensin converting enzyme inhibitors. Kidney Int1987;31(suppl 20):S220-80.

17 Volpe M, Tritto C, DeLuca N, et al. Abnormalities ofsodium handling and of cardiovascular adaptationsduring high salt diet in patients with mild heart failure.Circulation 1993;88: 1620-7.

18 Good J, Frost G, Meek J, Oakley C, Cleland J. Sodiumrestriction impairs a frusemide-induced diuresis inpatients with heart failure [abstract]. Eur Heart J1992;13(suppl):217.

19 Sullivan JM, Ratts TE, Taylor JC, et al. Hemodynamiceffects of sodium in man: a preliminary report.Hypertension 1980;2:506-14.

20 Soberman JE, Sullivan JM. New thinking about sodiumand the heart. Current Opinion in Cardiology 1993;8:728-36.

21 Rose G. The strategy of preventive medicine. Oxford: OxfordUniversity Press, 1992.

22 Wagdi P, Vuilliuomenet A, Kaufmann U, Richter M, Bertel0. Ungenugende Behandlungdisziplin, Patienten-information und Medikamentenverschreibung alsUrsachen fur die Notfallhospitalisation bei chronischherzinsuffizienten Patienten. Schweiz Med Wochenschr1993;123:108-12.

23 Berkman M, Tran M. Le sujetage, le regime sans sel et lesdiuretiques. Semaine des H6pitaux (Paris) 1978;54:1167-70.

24 Belmin J. Low sodium diet and congestive heart failure inthe elderly. JAm Geriatr Soc 1992;40:298-9.

25 Cleland JGF. Adverse reactions and drug interactions withACE inhibitors. In: Cleland JGF, ed. The clinician's guideto ACE inhibition. Edinburgh: Churchill Livingstone,1993:179-97.

26 Toto RD, Mitchell HC, Lee HC, Milam C, Pettinger WA.Reversible renal insufficiency due to angiotensinconverting enzyme inhibitors in hypertensive nephro-sclerosis. Ann Intern Med 1991;115:513-9.

27 Bridoux F, Hazzan M, Pallot JL, et al. Acute renal failureafter the use of angiotensin-converting-enzyme inhibitorsin patients without renal artery stenosis. Nephrol DialTransplant 1992;7: 100-4.

28 McMurray J, Matthews DM. Effect of diarrhoea in apatient taking captopril. Lancet 1985;i:581.

29 Horwitz LD, Atkins JM. Acute effects of ethanol on leftventricular performance. Circulation 1974;49: 124-8.

30 Pavan D, Nicolosi GL, Lestuzzi C, Burelli C, Zardo F,Zanuttini D. Normalization of variables of left ventricularfunction in patients with alcoholic cardiomyopathy aftercessation of excessive alcohol intake: an echo-cardiographic study. Eur Heart J 1987;8:535-40.

31 Sullivan MJ, Higginbotham MB, Cobb FR. Exercisetraining in patients with severe left ventricular dys-function: hemodynamic and metabolic effects. Circulation1988;78:506-15.

32 Sullivan MJ, Higginbotham MB, Cobb FR. Exercisetraining in patients with chronic heart failure delaysventilatory anaerobic threshold and improves sub-maximal exercise performance. Circulation 1989;79:324-9.

33 Koch M, Douard H, Broustet JP. The benefit of gradedexercise in chronic heart failure. Chest 1992;101 (suppl):23 1-5S.

34 Scalvini S, Marangoni S, Volterrani M, Schena M, QuadriA, Levi GF. Physical rehabilitation in coronary patients

S 90

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ber 1994. Dow

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How do changes in lifestyle complement medical treatment in heart failure?

who have suffered from episodes of cardiac failure.Cardiology 1992;80:417-23.

35 Coats AJS, Adampoulos S, Radaelli A, et al. Controlledtrial of physical training in chronic heart failure: exerciseperformance, hemodynamics, ventilation, and autonomicfunction. Circulation 1992;85:2119-31.

36 Minotti JR, Massie BM. Exercise training in heart failurepatients. Does reversing the peripheral abnormalitiesprotect the heart? Circulation 1992;85:2323-5.

37 Szlachcic J, Massie BM, Kramer BL, Topic N, Tubau J.Correlates and prognostic implication of exercise inchronic congestive heart failure. Am J Cardiol 1985;55:1037-42.

38 Shabetai R. Beneficial effects of exercise training incompensated heart failure. Circulation 1988;78:775-6.

39 Lipkin DP, Jones DA, Round JM, Poole-Wilson PA.Abnormalities of skeletal muscle in patients with chronicheart failure. Int J Cardiol 1988;18:187-95.

40 Schaufelberger M. Skeletal muscle metabolism and theeffect of physical training in congestive heart failure. In:Workshop: pharmacological treatment of heart failure.Uppsala: Medical Products Agency, 1993:161-74.

41 Adamopoulos S, Coats AJS, Brunotte F, et al. Physicaltraining improves skeletal muscle metabolism in patientswith chronic heart failure. J Am Coil Cardiol 1993;21:1101-6.

42 Dubach P, Froelicher VF. Cardiac rehabilitation for heartfailure patients. Cardiology 1989;76:368-73.

43 Rossi P. Physical training in patients with congestive heartfailure. Chest 1992;101(suppl):350-3S.

44 Working Group on Rehabilitation of the European Societyof Cardiology. Chronic heart failure. Eur Heart J1992;13(suppl. C):42-4.

45 Coats AJS. Exercise rehabilitation in chronic heart failure.J7Am Coll Cardiol 1993;22(suppl A):172-7A.

46 Dracup K, Walden JA, Stevenson L, Bracht ML. Quality oflife in patients with advanced heart failure. Journal ofHeart and Lung Transplantation 1992;11:273-9.

47 Mayou R, Blackwood R, Bryant B, Garnham J. Cardiacfailure: symptoms and functional status. J Psychosom Res199 1;35:399-407.

48 Gorkin L, Norvell NK, Rosen RC, et al. Assessment ofquality of life as observed from the baseline data of thestudies of left ventricular dysfunction (SOLVD) trialquality-of-life substudy. Am J Cardiol 1993;71: 1069-73.

49 Rector TS, Cohn JN. Assessment of patient outcome withthe Minnesota living with heart failure questionnaire:reliability and validity during a randomized, double-blind, placebo-controlled trial of pimobendan. Am HeartJ 1992;124:1017-25.

50 Mumford E, Schlesinger HJ, Glass GV. The effects ofpsychological intervention on recovery from surgery andheart attacks: an analysis of the literature. Am J7 PublicHealth 1982;72:141-51.

51 Rideout E. Chronic heart failure and quality of life: theimpact of nursing. Canadian Jrournal of CardiovascularNursing 1992;3:4-8.

52 Guyatt GH. Methodological problems in clinical trials inheart failure. J Chron Dis 1984;38:353-63.

53 Feinstein AR, Fisher MB, Pigeon JG. Changes in dyspnea-fatigue ratings as indicators of quality of life in thetreatment of congestive heart failure. Am J Cardiol1989;64:50-5.

54 Stewart AL, Greenfield S, Hays RD, et al. Functional statusand well-being of patients with chronic conditions.Results from the Medical Outcomes Study. JAMA1989;262:907-13.

55 Rector TS, Kubo SH, Cohn JN. Validity of the Minnesotaliving with heart failure questionnaire as a measure oftherapeutic response to enalapril or placebo. Am JCardiol 1993;71:1 106-7.

56 Tandon PK, Stander H, Schwarz RP. Analysis of quality oflife data from a randomized, placebo-controlled heart-failure trial. J Clin Epidemiol 1989;42:955-62.

57 Bulpitt CH, Fletcher AE. Measurement of the qualityof life in congestive heart failure. Influence of drugtherapy. Cardiovascular Drugs and Therapeutics 1988;2:419-24.

58 Permanyer-Miralda G, Alonso J, Ant6 JM, Alijarde-Guimera M, Soler-Soler J. Comparison of perceivedhealth status and conventional functional evaluation instable patients with coronary artery disease. J ClinEpidemiol 1991 ;44:779-86.

59 Cox J, Naylor D. The Canadian Cardiovascular Societygrading scale for angina pectoris: is it time forrefinements? Ann Intern Med 1992;117:677-83.

60 Cowley AJ, Stainer K, Wynne RD, Rowley JM, HamptonJR. Symptomatic assessment of patients with heartfailure: double-blind comparison of increasing doses ofdiuretics and captopril in moderate heart failure. Lancet1986;i:770-2.

61 Guyatt GH, Nogradi S, Halcrow S, Singer J, Sullivan MJJ,Fallen EL. Development and testing of a new measure ofhealth status for clinical trials in heart failure. J GenIntern Med 1989;4:101-7.

62 Rector TS, Johnson G, Dunkman WB, et al. Evaluation bypatients with heart failure of the effects of enalaprilcompared with hydralazine plus isosorbide dinitrate onquality of life. V-HeFT II. Circulation 1993;87(supplVI):VI-71-7.

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