MJA
MJA InSight
MJA Careers
Research

Chronic heart failure in Australian general practice

Henry Krum, Andrew M Tonkin, Robert Currie, Robert Djundjek and Colin I Johnston
Med J Aust 2001; 174 (9): 439-444.

Henry Krum, Andrew M Tonkin, Robert Currie, Robert Djundjek and Colin I Johnston

MJA 2001; 174: 439-444
For editorial comment, see Horowitz & Stewart; see also Krum

Abstract - Methods - Results - Discussion - Acknowledgements - Reference - Authors' details
- - More articles on Cardiology and cardiac surgery


Abstract

Objectives: To investigate the frequency and general practitioner awareness of patients with chronic heart failure (CHF), and to evaluate a cardiac algorithm and document cardiac investigations performed in establishing this diagnosis.
Design and setting: Between March and August 1998, consecutive patients aged 60 years and older presenting to their GP were assessed. In patients previously diagnosed with CHF, aetiology and diagnostic assessments were documented. In patients with suspected CHF (by a standardised algorithm, based on World Health Organization guidelines), further investigations and GP diagnosis were recorded.
Patients: 80 consecutive patients were assessed by each of 341 GPs throughout Australia, reflecting the Australian metropolitan/rural population mix of 1996. This provided a total of 22 060 evaluable patients.
Main outcome measures: Estimated numbers of patients with CHF in general practice (previously and newly diagnosed); major aetiological factors; use of ancillary diagnostic tests; drugs prescribed.
Results: CHF was diagnosed in 2905 of 22 060 patients (13.2%) (2485 previously diagnosed and 420 newly diagnosed). Major aetiological factors were ischaemic heart disease and hypertension. Echocardiography had been performed in 64% of previously diagnosed patients, but was performed in only 22% of possible CHF patients. Angiotensin-converting enzyme (ACE) inhibitors were prescribed in 58.1% of patients with CHF. Patients with evidence of left ventricular dysfunction were more likely to have received ACE inhibitors.
Conclusions: CHF appears to be very common in the elderly, based on GP diagnosis of the condition. Of 100 patients aged 60 years and over presenting to their GP, two new cases of CHF will be detected using a simple clinical algorithm in conjunction with appropriate diagnostic tests. ACE inhibitors appear to be underutilised.


Chronic heart failure (CHF) is a debilitating condition with high morbidity and mortality, and is a major public health burden. Its prevalence is increasing,1 despite a reduction in age-standardised mortality associated with cardiovascular diseases such as myocardial infarction and stroke.2 Factors implicated in this increased prevalence include the ageing of the population, decreased mortality rates following myocardial infarction, and more frequent diagnosis of CHF after investigations such as echocardiography.3

The epidemiology of CHF in Australia has been assumed to be similar to that in the United States,4-6 the United Kingdom7-10 and Europe.11,12 However, substantive data have been lacking, and the approach taken to diagnosis of patients with suspected CHF in general practice in Australia is also unknown.

Similarly, although international studies have suggested marked underutilisation of angiotensin-converting enzyme (ACE) inhibitors and β-blockers,4-11,13-17 no evaluation of use of drug therapies for CHF in Australia has been reported.

Accordingly, the aims of the Cardiac Awareness Survey and Evaluation (CASE) Study were:

  • to investigate the frequency, awareness, and aetiology of heart failure in general practice in Australia;

  • to document cardiac investigations used by general practitioners in establishing the diagnosis of CHF; and

  • to determine prescribing patterns in the treatment of CHF by Australian GPs.

As the prevalence of heart failure increases steeply with age, the study focused on people aged 60 years and older.


Methods

Recruitment into the CASE study

GPs were recruited solely on the basis of interest in participating in the study. Interest was first ascertained by the local pharmaceutical representative of the study sponsor (see Acknowledgements). The CASE steering committee then sent interested GPs a formal letter of invitation to participate in the study. GPs agreeing to participate attended a local education and information session. These sessions were spread across all Australian States and Territories with a mix of metropolitan, rural and remote regions in an effort to recruit a sample of GPs (and thus patients) representative of their distribution.

Each GP was asked to assess 80 consecutive patients aged 60 years or older for the possibility of heart failure.

GPs were recruited from March 1998, data were collected prospectively and the study was completed in August 1998.

Assessment for CHF

New patients: Patients not previously diagnosed as having CHF were assessed for that possibility using modified World Health Organization criteria (Box 1).18 Alternative conditions that may have contributed to these symptoms and signs were recorded.

In patients suspected of having CHF based on the above criteria, further investigations (chest x-ray [CXR], electrocardiogram [ECG], and echocardiogram) were suggested (but not mandated). GPs were also asked to note any investigations that had been performed in the previous 12 months. For patients who had an echocardiogram, the GP was asked to indicate whether there was evidence of systolic or diastolic ventricular dysfunction (or both) from the echocardiogram report.

At the conclusion of this process, the GPs assessed whether they thought the patient had CHF.

Previously diagnosed patients: For patients who had previously been diagnosed as having CHF by their GP, records were retrospectively analysed for clinical and diagnostic criteria that contributed to that diagnosis. These included use of ECG, CXR and echocardiography, hospital admission for heart failure, and specialist referral for CHF.

Pharmacotherapy

For patients with previously diagnosed CHF, GPs were asked to document current drug therapy specifically prescribed for this condition (name of drug, daily dose, and frequency of administration). For patients with newly diagnosed CHF, GPs were asked whether they instituted pharmacotherapy immediately and what that pharmacotherapy comprised.

A dosage equivalence table of commonly prescribed ACE inhibitors was compiled, and prescribing was divided into low, medium and high doses. To determine prescribing according to decade of life, prescribing was assessed in patients aged 60-69 years (n = 569), 70-79 years (n = 1360), and 80 years and older (n = 976). GP prescribing in patients with echocardiographic evidence of systolic or diastolic left ventricular dysfunction was specifically determined.

Initial pharmacotherapy prescribed for patients diagnosed with CHF as part of the CASE study was evaluated. Because of the cross-sectional nature of the assessment in CASE, most of these patients did not have the opportunity to be up-titrated to target doses of drugs. For this reason, newly diagnosed patients were not included in the analysis of dose of ACE inhibitor prescribed.


Results

Of 523 GPs who originally expressed interest in participating, 341 completed the study. Their geographical distribution (78% metropolitan, 22% rural or remote) was similar to that observed for all Australian GPs (77% metropolitan, 23% rural or remote).

In all, 23 845 patients were entered into the study. Of these, 1785 were excluded from analysis because of patient refusal or missing data, leaving 22 060 who made up the baseline population.

Baseline demographics

The distribution of the CASE patient population by area (capital city, 58.7%; metropolitan, 10.7%; rural, 21.4%; remote, 1.2%; 8% unclassified) was similar to the 1996 Australian population aged 60 years or older.19 However, there were fewer rural patients among the CASE cohort than in the census population.

The total CASE study population comprised 45% men and 55% women; 8612 (39%) were aged 60-69 years (48% men), 9371 (42.5%) were aged 70-79 years (45% men) and 4077 (18.5%) were aged 80 years or older (39% men).

Patients not previously diagnosed with CHF

Box 2 shows the assessment process and results for the 22 060 patients. In the 4807 patients assessed as having possible CHF, at least one further investigation was performed in 2903 (60.4%). To determine whether the CASE audit itself may have prompted further investigation of these patients, the tests were divided into those ordered within the previous 12 months and those ordered subsequent to the CASE audit. Investigations ordered within the 12 months before the CASE audit were ECG in 1953 (40.6%), CXR in 1894 (39.4%), and echocardiogram in 366 patients (7.6%). Investigations subsequent to the CASE clinical assessment were performed in 488 patients who had ECGs (10.2%), 493 who had CXR (10.2%), and 466 who had echocardiograms (9.7%).

The diagnosis of CHF was based on symptoms in 73%, signs in 66%, causative factors in 61%, and investigations in 49% (not mutually exclusive). Presence of at least one symptom and one causative factor had the highest sensitivity for detection of new heart failure (323 of the 420 [76.9%] new cases of heart failure). The sensitivity of the other diagnostic groupings for possible heart failure were > 2 symptoms, 68.6%; > 2 signs, 47.3%; > 1 symptom and > 1 sign, 68.6%; > 1 sign and > 1 causative factor, 66.9%.

Possible false negative diagnoses: Of the 4807 patients who met diagnostic criteria for suspected CHF, 466 underwent echocardiography after the CASE audit (when systolic, diastolic or no dysfunction was specifically noted). Of these 466 patients, 108 had an echocardiographic report of left ventricular systolic or diastolic dysfunction. However, despite this objective evidence of ventricular dysfunction, GPs diagnosed CHF for only 77 of these 108 patients.

Possible false positive diagnoses: Of the 420 patients newly diagnosed as having CHF, 162 underwent echocardiography. Nineteen of these 162 patients (11.7%) had no evidence of left ventricular systolic or diastolic dysfunction on this test, yet were still classified as having CHF by their GP.

Patients previously diagnosed as having CHF

CHF had been previously diagnosed in 2485 of the baseline population of 22 060 (11.3%). Both electrocardiograms and CXRs had been performed in 96% of the patients previously diagnosed as having heart failure, and 64% had had echocardiography performed. For these patients, in the previous 12 months:

  • 1640 patients (66%) had been referred to a specialist;

  • 1744 patients (70%) had either not been admitted to hospital with CHF or their hospitalisation status was unknown; and

  • of the 741 patients admitted for CHF, 459 (62%) had one admission, 165 (22%) had two admissions, and 58 (8%) had three admissions. Six patients (1%) had been admitted 10 or more times for CHF.

CHF patients in the CASE study

At the end of the study, 2905 of the 22 060 baseline population (13.2%) were considered to have CHF: 2485 (11.2%) with a previous diagnosis, and 420 (1.9%) with a new diagnosis. The prevalence of CHF in these patients was closely related to age group (Box 3).

The cardiovascular diagnoses that may be contributing to CHF in these patients are summarised in Box 4. Hypertension and ischaemic heart disease were major comorbidities and potential aetiological factors in both the new and previously diagnosed cohorts.

Pharmacotherapy

Specific CHF pharmacotherapy for the 2905 patients with CHF is summarised in Box 5. Most patients were receiving diuretics and ACE inhibitors. Alternatives to ACE inhibitors in patients who can not tolerate this medication include nitrates and hydralazine (prescribed for 0.6%) and/or angiotensin II receptor antagonists (prescribed for 4.3%).

β-Blockers were prescribed for 12% of patients. Less than 50% of β-blocker prescribing was of the non-selective, vasodilating β-blocker carvedilol, approved for CHF in Australia.

The dose of ACE inhibitor was determined in patients previously diagnosed as having CHF (Box 6). Based on our dosage equivalence table, prescribed doses were low in 60%, medium in 31%, and high in 9% of patients.

Prescribing according to echocardiographic findings: Pharmacotherapy prescribed for CHF according to left ventricular (LV) systolic (found in 932 patients) or diastolic (found in 376 patients) dysfunction is summarised in Box 5. The presence of LV dysfunction on echocardiography resulted in higher prescribing of ACE inhibitors than in the overall patient cohort. However, the frequency of ACE inhibitor prescribing was not different between the systolic and diastolic LV dysfunction groups. Furthermore, there were very few differences among other agents in these groups according to systolic or diastolic LV dysfunction.

Prescribing according to decade of life: Prescribing of drug therapy specifically for CHF according to decade of life is summarised in Box 5. ACE inhibitor prescribing was unaltered in the very elderly (≥ 80 years). Prescribing of β-blocker demonstrated an age-dependent decrease, whereas prescribing of digoxin and diuretics (thiazide and loop) demonstrated an age-dependent increase.

Prescribing in patients with newly diagnosed CHF: Use of pharmacotherapy among newly diagnosed CHF patients was less than that observed in patients with previously diagnosed CHF. In particular, only 51% of newly diagnosed patients were prescribed ACE inhibitors, 37% diuretics, 17% received calcium-channel blockers, 10% digoxin and 8% β-blockers.


Discussion

We undertook a clinical algorithm approach to the possible diagnosis of CHF. By identifying possible CHF based on the grouping of symptoms, signs and causative factors, we demonstrated an 8.7% rate of identification of CHF (420 of 4807 patients). Although this approach resulted in a relatively low rate of successful diagnosis of CHF, the algorithm used was entirely clinical with a very simple screening process. Our results suggest that, of 100 patients aged 60 years or older presenting to a GP, two will have previously undetected CHF that can be simply diagnosed by attention to clinical symptoms and signs in conjunction with appropriate diagnostic tests.

Prevalence of CHF

We found somewhat higher rates of CHF patients (13.2%) than in earlier general practice based studies.4,7-9 Specifically, reported prevalence of CHF among patients aged 65 years or older in UK general practice ranged from 2.8%9 to 8.0%.7 The higher rate in the CASE study may reflect the differing methods by which the diagnosis of CHF was made (eg, patient file review,4,9 morbidity registry8), greater use of objective testing (ie, echocardiography in our patient cohort), or our study being a more representative sample of the true CHF population than previous geographically restricted studies performed in the US or UK.

In contrast to the above assessments of CHF frequency, population studies where echocardiographic ventricular dysfunction was the main criterion for diagnosis detected fewer CHF patients within these age groups than in the CASE study.10,12

Numbers of CHF patients in the CASE Study increased dramatically with each decade of life — more than 20% of patients aged 80 years or older were diagnosed with CHF. Given the ageing of the population, these findings have important implications for resource allocation.

Aetiology

The aetiology of CHF was as expected, with a major contribution from ischaemic heart disease and previous myocardial infarction, as well as hypertension. Hypertension was a major contributor to CHF in the Framingham study,20,21 but less so in analysis of the Studies of Left Ventricular Dysfunction (SOLVD)22 and other, more recent data.23 The major contribution of hypertension in the CASE cohort may reflect the advanced age of the population studied, in which hypertension is a frequent comorbidity.

Investigations

Use of ECG and CXR was high, and echocardiography was used in more than half the patients. The lower use of echocardiography (despite recommendations by major organisations such as WHO)18 may reflect lack of full knowledge of the sensitivity and specificity of this diagnostic test, concerns regarding expense, and difficulty with access.

Pharmacotherapy

Use of ACE inhibitors: ACE inhibitor prescribing by Australian GPs ranges from 51%-71% of CHF patients, depending on the specific population studied. Prescribing of ACE inhibitor was more likely in patients in whom ventricular dysfunction had been objectively documented. These findings are consistent with international studies, in which prescribing of ACE inhibitors ranges from 10% to 60%.5,6,8-10,14-17

ACE inhibitors reduce morbidity and mortality across the entire spectrum of CHF severity, including in patients with asymptomatic systolic left ventricular dysfunction.24-26 Therefore, all patients with systolic left ventricular dysfunction should be receiving ACE inhibitors unless contraindicated or intolerant. Lack of compliance with these prescribing recommendations may relate to contraindications to ACE inhibitor therapy (ie, bilateral renal artery stenosis) or observed side effects such as hyperkalaemia or cough. Furthermore, ACE inhibitors are not of proven benefit in patients with diastolic CHF. Definitive diastolic dysfunction on echocardiography comprised only a small percentage in the CASE study, although the true percentage is undoubtedly considerably higher. Potential alternatives to ACE inhibitors in patients who are ACE intolerant or have contraindications include angiotensin II receptor antagonists and hydralazine (the latter as part of the hydralazine/nitrate combination). However, only 4.3% of patients were taking angiotensin II receptor antagonists and 0.6% were taking hydralazine. Our findings suggest that, despite the definitive data supporting the use of ACE inhibitors in CHF, these agents are still being underutilised.

Dose of ACE inhibitors: Submaximal doses of ACE inhibitors were prescribed for those patients who are taking these drugs. The major clinical trials conducted in patients with CHF (SOLVD,24 CONSENSUS25) and LV dysfunction post-MI (SAVE27) used much higher doses (150 mg of captopril or 20-40 mg of enalapril) than the median and mean doses prescribed in this study. Doses prescribed by Australian GPs were generally lower than both the target and achieved ACE inhibitor doses used in these major trials.

There are a number of reasons why the recommended target doses may not be achieved in general practice. First, patients may not tolerate the highest dosage because of hypotension, particularly if up-titration is rapid. Second, because these agents improve symptomatology, patients may become asymptomatic at lower doses of drug and the need to go to higher doses not be entertained in an asymptomatic patient. Finally, until recently, there has been no clear evidence that higher doses offer substantial clinical benefits over and above the use of ACE inhibitors at lower doses. The ATLAS study28 demonstrated a reduction in the combined endpoint of death/heart failure related hospitalisation with lisinopril 32.5-35 mg daily compared with lisinopril 2.5-5 mg daily. Mortality alone was reduced by 8% in the high-dose lisinopril subgroup. Although this reduction is modest, it does suggest that an attempt should be made to maximise ACE inhibitor dosage in every patient.

β-Blockers: Prescribing of β-blockers was low, despite overwhelming evidence supporting the benefits of these agents in patients with New York Heart Association (NYHA) Class II-III symptoms.29-31 However, much of this evidence has only been published subsequent to the completion of the CASE study.30,31

Prescribing of the β-blocker vasodilator carvedilol occurred in fewer than half the patients receiving β-blockers. As carvedilol is the only β-blocker approved in Australia for CHF, this suggests that much of the prescribing of β-blockers for the CASE cohort was for indications other than CHF (eg, ischaemic heart disease and hypertension). As GPs in Australia are not permitted to prescribe carvedilol, our observed rate of use of β-blockers reflects specialist prescribing.

Factors affecting prescribing: In patients with a definitive diagnosis of ventricular dysfunction by echocardiography, prescribing of ACE inhibitor therapy was higher than for the overall CASE CHF cohort. This may reflect more confidence with the cause of patient symptomatology as being related to CHF. Alternatively, it may be that a GP who is more likely to perform echocardiography to diagnose CHF is also more likely to prescribe best-practice pharmacotherapy.

It was also noteworthy that the difference in overall prescribing for systolic versus diastolic dysfunction in these patients appeared similar, although many of the agents (eg, ACE inhibitors) are not of proven benefit in diastolic CHF. Furthermore, some drugs, such as non-dihydropyridine calcium-channel blockers, are relatively contraindicated in patients with systolic heart failure, yet prescribing rates were similar for the entire patient cohort. Conversely, these agents may be of particular benefit in diastolic heart failure, but again prescribing rates appeared similar to the entire patient cohort.

There was no reduction in prescribing of ACE inhibitor with each decade of life, suggesting that GPs supported the use of these agents in CHF management in the very elderly (≥ 80 years). Very few data exist to support the use of ACE inhibitors in this group of patients, although studies are currently being conducted. In contrast, β-blocker use declined with each decade of life, suggesting less comfort in prescribing these agents for older patients. Increased digoxin and diuretic use with advanced age may reflect the need to increasingly prescribe these agents for comorbidities such as atrial fibrillation and oedema of other causes.

Study limitations

The CASE study had a number of potentially significant limitations.

  • Selection of GPs was not random, but was based on interest in undertaking the study. This could introduce significant bias, and therefore we have not classified our evaluation as a prevalence or incidence study. Nevertheless, every effort was undertaken to ensure a representative distribution of general practices according to State, regional area and metropolitan versus rural practice.

  • The study has also demonstrated the difficulty in making a clinical diagnosis of CHF. Diagnosis of CHF was left to the clinical judgement and decision of the GP. We noted a significant false positive and negative rate using documented left ventricular dysfunction on echocardiogram as the "gold standard" of CHF in conjunction with relevant signs, symptoms and causative factors. This is a limitation of many surveys of this type, in which the diagnosis is made based on subjective clinical criteria.4,9

  • A further limitation may have been the algorithm used to assist the GP in making the diagnosis. This clinical algorithm approach has not been used previously in the diagnosis of CHF. Therefore, the possibility exists of patients being wrongly assigned as having CHF using this approach. This is particularly true as echocardiography was not mandated for all patients. Nevertheless, this algorithm did yield an extra two new CHF patients for every 100 patients aged 60 years and older studied in this way.



Acknowledgements

The CASE study was supported by the National Heart Foundation of Australia and the Royal Australasian College of General Practitioners.
The CASE Management Committee wish to thank all 341 GPs who participated in the CASE study and Servier Laboratories, Australia, who provided input into the study design as well as financial and logistical assistance in the conduct of the study. Servier Laboratories were not involved in the analysis of data. In addition, the Committee acknowledges the expert statistical assistance provided by Dr Chris Reid and Mr Stephen Lim (Baker Medical Research Institute, Prahran, VIC).


References

  1. Bonneaux L, Barendregt J, Meeter K, et al. Estimating clinical morbidity due to ischemic heart disease and congestive heart failure: the future risk of heart failure. Am J Public Health 1994; 84: 20-28.
  2. Waters A-M, Bennett S. Mortality from cardiovascular disease in Australia. Cardiovascular Disease Series No. 3. Canberra: Australian Institute of Health and Welfare, 1995.
  3. McGovern PG, Pankow JS, Shahar E, et al. Recent trends in acute coronary heart disease. Mortality, morbidity, medical care and risk factors. N Engl J Med 1996; 334: 884-890.
  4. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993; 22: 6A-13A.
  5. Gardin JM, Siscovick D, AntonCulver H, et al. Sex, age and disease affect echocardiographic left ventricular mass and systolic function in the free-living elderly: the Cardiovascular Health Study. Circulation 1995; 91: 1739-1748.
  6. Lauer MS, Evans JC, Levy D. Prognostic implications of subclinical left ventricular dilatation and systolic dysfunction in men free of overt cardiovascular disease (the Framingham Heart Study). Am J Cardiol 1992; 70: 1180-1184.
  7. Mair FS, Crowley TS, Bundred P. Prevalence, aetiology and management of heart failure in general practice. Br J Gen Pract 1996; 46: 77-79.
  8. Morbidity statistics from general practice. 4th National Survey, 1991-92. Royal College of General Practitioners, Office of Population Census and Survey and Department of Health and Social Security. London: HMSO, 1995.
  9. Parameshwar J, Shackell MM, Richardson A, et al. Prevalence of heart failure in three general practices in west London. Br J Gen Pract 1992; 42: 287-289.
  10. McDonagh TA, Morrison CE, Lawrence A, et al. Symptomatic and asymptomatic left-ventricular systolic dysfunction in an urban population. Lancet 1997; 350: 829-833.
  11. Ambrosio GB, Riva LM, Casiglia E. Prevalence, clinical features and prognosis of congestive heart failure (CHF) in the elderly. A survey from a population in Veneto region. Acta Cardiologica 1994; 49: 324-325.
  12. Mosterd A, Bruijne de MC, Hoes AW, et al. Usefulness of echocardiography in detecting left ventricular systolic dysfunction in population based studies (The Rotterdam Study). Am J Cardiol 1997; 79: 103-104.
  13. Hillis GS, Trent RJ, Winton P, et al. Angiotensin-converting enzyme inhibitors in the management of congestive heart failure: are we ignoring the evidence? Q J M 1995; 89: 145-150.
  14. Mosterd A, Hoes AW, de Bruijne MC, et al. Prevalence of heart failure and (a) symptomatic left ventricular dysfunction in the general population. The Rotterdam Study. Eur Heart J 2001; in press.
  15. Bart BA, Gattis WA, Diem SJ, O'Connor CM. Reasons for underuse of angiotensin-converting enzyme inhibitors in patients with heart failure and left ventricular dysfunction. Am J Cardiol 1997; 79: 1118-1120.
  16. Newman J, Ahmed O, Hyngstrom T, et al. Heart failure treatment with angiotensin converting enzyme inhibitors in hospitalized Medicare patients in 10 large states. Arch Int Med 1997; 157: 1103-1108.
  17. Stafford RS, Saglam D, Blumenthal D. National patterns of angiotensin converting enzyme inhibitor use in congestive heart failure. Arch Intern Med 1997; 157: 2460-2464.
  18. World Health Organization/Council on Geriatric Cardiology Task Force on Heart Failure Education. Concise guide to the management of heart failure. Geneva: WHO/CGC, 1997; 6-9. Available at <http://www.who.int/ncd/cvd/concguid.pdf>.
  19. Rural, remote and metropolitan areas classification. 1991 Census Edition. Canberra: AGPS, 1994.
  20. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham Study. N Engl J Med 1971; 285: 1441-1446.
  21. Kannel WB, Belanger JA. Epidemiology of heart failure. Am Heart J 1991; 121: 951-956.
  22. Bangdiwala SI, Weiner DH, Bourassa MG, et al. Studies of Left Ventricular Dysfunction (SOLVD) Registry: rationale, design, methods and description of baseline characteristics. Am J Cardiol 1992; 70: 347-353.
  23. Teerlink JR, Goldhaber SZ, Pfeffer MA. An overview of contemporary etiologies of congestive heart failure. Am Heart J 1991; 121: 1852-1853.
  24. The SOLVD Investigators. Effect of Enalapril on survival in patients with reduced left ventricular ejection fraction and congestive heart failure. N Engl J Med 1991; 325: 293-302.
  25. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1987; 3161: 1429-1435.
  26. Nicklas JM, Pitt B, Timmis G, et al. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992; 327: 685-691.
  27. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the Survival and Ventricular Enlargement Trial. N Engl J Med 1992; 327: 821-828.
  28. Packer M, Poole-Wilson PA, Armstrong PW, et al. Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. ATLAS Study Group. Circulation 1999; 100: 2312-2318.
  29. Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med 1996; 334: 1349-1355.
  30. CIBIS II investigators and committees. The cardiac insufficiency bisoprolol study II (CIBIS II): a randomised trial. Lancet 1999; 353: 9-13.
  31. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet 1999; 353: 2001-2007.

(Received 24 Dec 1999, accepted 28 Oct 2000)



Authors' details

Alfred Hospital, Melbourne, VIC.
Henry Krum, PhD, FRACP, Associate Professor, Clinical Pharmacology Unit, Department of Epidemiology and Preventive Medicine, and Department of Medicine, Monash University.

National Heart Foundation of Australia, Melbourne, VIC.
Andrew M Tonkin, MD, FRACP, Director, Health, Medical and Scientific Affairs.

North East Valley Division of General Practice, Melbourne, VIC.
Robert Currie, MB BS, FRACGP, Director.

Servier Laboratories, Melbourne, VIC.
Robert Djundjek, BSc, Manager, Scientific Projects.

Austin and Repatriation Medical Centre, Melbourne, VIC.
Colin I Johnston, MD, FRACP, Professor and Head, Department of Medicine, University of Melbourne.

Reprints will not be available from the authors.
Correspondence: Professor C I Johnston, Baker Medical Research Institute, Prahran, VIC 3181.


Make a comment



 

 

1: Modified World Health Organization18 criteria for assessment of possible chronic heart failure

Symptoms: Dyspnoea, chronic fatigue, oedema, and exercise intolerance.

Signs: Third or fourth heart sounds, heart murmur, cardiomegaly, pulmonary crackles, raised jugular venous pressure, and dependent oedema.

Causative factors: Angina, previous myocardial infarction, hypertension, valvular heart disease/rheumatic fever, and cardiomyopathy.

Patients were considered to have possible CHF if they had:

            > 2 symptoms,
> 2 signs,
> 1 symptom and > 1 sign, or
> 1 symptom and > 1 causative factor.
Back to text
 
Box 2
Back to text
 
Box 3
Back to text
 
4: Cardiovascular comorbidities that may be contributing to chronic heart failure
     
  Percentage of patients
 
  New CHF Previous CHF

Hypertension 69.1% 63.6%
Angina 44.2% 53.4%
Previous MI 28.1% 39.3%
Valve disease 15.2% 23.0%
Cardiomyopathy 5.2% 11.8%

MI = myocardial infarction.
Back to text
 
5: Percentage (95% CI) of patients with chronic heart failure prescribed each class of drug, by evidence of left ventricular dysfunction, and by age group
       
    Left ventricular dysfunction*
  All patients
  (n = 2905) Systolic (n = 932) Diastolic (n = 376)

Diuretics (thiazide, loop) 63.3 (62.4-64.2) 60.3 (58.7-61.9) 62.2 (59.7-64.7)
ACE inhibitor 58.1 (57.2-59.0) 70.7 (69.2-72.2) 70.5 (68.1-72.9)
Digoxin 31.3 (30.4-32.2) 35.0 (33.4-36.6) 33.2 (30.8-35.6)
beta-Blocker 11.8 (11.2-12.4) 13.9 (12.8-15.0) 17.8 (15.8-19.8)
CCB-DHP 10.1 (9.5-10.7) 11.1 (10.1-12.1) 12.0 (10.3-13.7)
CCB-NDHP 10.0 (9.4-10.6) 10.3 (9.3-11.3) 11.2 (9.6-12.8)
Aspirin 10.3 (9.7-10.8) 9.3 (8.3-10.3) 9.6 (8.1-11.1)
Warfarin 7.7 (7.2-8.2) 8.2 (7.3-9.1) 8.8 (7.3-10.3)
Spironolactone 8.1 (7.6-8.6) 6.9 (6.1-7.7) 1.0 (0.5-1.5)
Hydralazine 0.6 (0.5-0.7) 0.2 (0.1-0.3) 0.0 (0.0-0.0)
AIIA 4.3 (3.9-4.7) 6.4 (5.6-7.2) 7.7 (6.3-9.1)
Age group (years)

60-69 (n = 569) 70-79 (n = 1360) ≥80 (n = 976)

Diuretics (thiazide, loop) 57.1 (55.0-59.2) 62.1 (60.8-63.4) 68.4 (66.9-69.9)
ACE inhibitor 58.7 (56.6-60.8) 58.0 (56.7-59.3) 58.1 (56.5-59.7)
Digoxin 24.8 (23.0-26.6) 29.9 (28.7-31.1) 37.2 (35.7-38.7)
beta-Blocker 14.1 (12.6-15.6) 13.2 (12.3-14.1) 8.4 (7.5-9.3)
CCB-DHP 9.5 (8.3-10.7) 11.0 (10.2-11.8) 9.0 (8.1-9.9)
CCB-NDHP 10.2 (8.9-11.5) 11.0 (10.2-11.8) 11.2 (10.2-12.2)
Aspirin 10.0 (8.7-11.3) 11.4 (10.5-12.3) 8.9 (8.0-9.8)
Warfarin 9.5 (8.3-10.7) 8.8 (8.0-9.6) 5.0 (4.3-5.7)
Spironolactone 6.7 (5.7-7.7) 8.8 (8.0-9.6) 8.0 (7.1-8.9)
Hydralazine 1.1 (0.7-1.5) 0.6 (0.4-0.8) 0.3 (0.1-0.5)
AIIA 3.5 (2.7-4.3) 5.4 (4.8-6.0) 3.4 (2.8-4.0)

* According to echocardiography. ACE = angiotensin-converting enzyme. CCB-DHP = calcium-channel blocker - dihydropyridine. CCB-NDHP = calcium-channel blocker - non-dihydropyridine. AIIA = angiotensin II receptor antagonist.
Back to text
 
6: Dosage equivalence table for angiotensin-converting enzyme (ACE) inhibitors, and median and mean doses prescribed for patients with diagnosed chronic heart failure
         
  Dosage equivalence (mg)

  Low Medium High  

Captopril ≤ 50 ≤ 100 ≤ 150  
Enalapril ≤ 10 ≤ 20 ≤ 40  
Perindopril ≤ 2 ≤ 4 ≤ 8  
Lisinopril ≤ 10 ≤ 20 ≤ 40  
Ramipril ≤ 5 ≤ 10 ≤ 20  
Fosinopril ≤ 10 ≤ 20 ≤ 40  
Trandolopril ≤ 2 ≤ 4 ≤ 8  
Quinapril ≤ 10 ≤ 20 ≤ 40  
 
Dose (mg)
  Media Mean SD n
Captopril 50 67.5 44.1 383
Enalapril 10 15.6 12.0 308
Perindopril 4 3.6 2.2 223
Lisinopril 10 12.6 9.7 218
Ramipril 5 5.1 4.3 98
Fosinopril 10 14.3 7.1 81
Trandolopril 1 1.9 1.8 76
Quinapril 10 11.6 9.1 74
Back to text
Henry Krum
Andrew M Tonkin
Robert Currie
Robert Djundjek
Colin I Johnston