Heart failure in older people: the epidemic we had to have

Despite these gains, recent evaluations indicate that the prevalence of heart disease in most communities is rising steadily, and that this is reflected in costs of hospitalisation if not in mortality data.¹ This rise suggests that the strategies directed at reducing risk of ischaemic heart disease (such as cessation of smoking and lowering of serum cholesterol level) should be regarded as means of postponing disease onset rather than as "vaccines" against eventual ischaemia. Therapies such as thrombolytic agents³ and coronary angioplasty⁴ for patients with acute myocardial infarction, and β-adrenoceptor antagonists⁵ and angiotensin-converting enzyme (ACE) inhibitors⁶ for those with symptomatic heart failure, have led to increased survival rates, and thus more individuals with chronic heart disease. In addition, in older people, increasing rates of atrial fibrillation and aortic stenosis also contribute to cardiac disability.

The Cardiac Awareness Survey and Evaluation (CASE) Study examined the current contributions of general practitioners to the diagnosis and management of chronic heart failure (CHF) in patients over the age of 60 years. The results, published in this issue of the Journal,⁷ shed considerable light on the magnitude of this emerging problem in Australia.

One of the most complex questions in cardiology is the diagnosis of CHF. In the vast majority of controlled clinical trials to date, the diagnosis of CHF has been predicated on objective evidence of left ventricular systolic dysfunction, documented by echocardiography or radionuclide ventriculography. Most intervention studies have only included patients with severe systolic dysfunction, in order to maximise the frequency of end-points. Yet, this is just the tip of the CHF iceberg in the general population. For patients with predominantly diastolic, or mild degrees of systolic, left ventricular (LV) dysfunction, estimation of LV ejection fraction alone provides little diagnostic information, and the diagnosis of CHF becomes somewhat arbitrary. This was so in some patients in the CASE study: it is clear that GPs do not use echocardiography widely to assess patients with possible CHF. This blurring around the edges of the diagnosis (especially in patients with mild dysfunction) is regrettable, but there is no easy solution. Conversely, however, it is impossible to exclude from the CASE study design a number of patients with LV dysfunction but minimal symptoms, a group which may benefit from appropriate pharmacotherapy. Overall, one recommendation from the CASE study, which resulted in new diagnosis of CHF in 2% of the study population, is that widespread access to echocardiography by GPs for people older than 60 years is likely to be cost effective.

The major stimulus to the diagnosis of CHF is the institution of appropriate therapy. It is here that the CASE study is most revealing. There have been dramatic advances in the management of CHF in the past 15 years, resulting in considerable improvement in outcomes for this patient population,⁸ although there is clearly scope for further reductions in both morbidity and mortality.⁹ ACE inhibitors (preferably in the largest tolerated dose),⁶ spironolactone¹⁰ and β-adrenoceptor antagonists⁵ all reduce mortality and morbidity in patients with LV systolic dysfunction. There is also evidence for the use of angiotensin-receptor antagonists or hydralazine/nitrates in patients intolerant of ACE inhibitors. Digoxin, in patients in sinus rhythm, has no major effect on mortality but slightly reduces hospitalisation risk.¹¹ Conversely, some agents, notably calcium antagonists¹² and the COX-1 (and possibly the COX-2)¹³ inhibitors, should be used with caution in patients with CHF, and the role of diuretic therapy is probably limited to the prevention of peripheral and/or pulmonary oedema.

It is therefore an important finding of the CASE study that, even in the hands of an "interested" cohort of GPs, ACE inhibitors were used in little more than half of the patients, and usually with low-dose regimens. In contrast, use of diuretics and digoxin was surprisingly high. This makes it clear that in Australia, as in other countries,¹⁴ CHF is largely under-treated, and the price we pay is increased risk of deterioration, hospitalisation and death. It is possible, although not specifically examined by the CASE study, that the prescribing habits of GPs are directed towards agents which are likely to produce rapid relief of symptoms rather than agents with prognostic benefits.

The epidemic of CHF in older people has its counterpart in an explosion of recent relevant clinical trial information. The HOPE study results suggest that all patients at high risk of ischaemia should be considered for treatment with ACE inhibitors, irrespective of the presence or absence of CHF.¹⁵ The data on the beneficial effect of spironolactone are quite recent, as are some of the β-adrenoceptor antagonist data. It is also clear that community-based outreach services for CHF patients may improve outcomes.¹⁶ Identification of and optimal therapy for these patients constitutes a major challenge for the new millennium.

John D Horowitz
Professor of Cardiology
University of Adelaide, and Director Cardiology Unit
North Western Adelaide Health Service, Adelaide, SA

Simon Stewart
Ralph Reader Postdoctoral Fellow
Department of Public Health
University of Glasgow, Glasgow, UK

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