First published June 2007, updated February 2022

The ever-increasing burden of heart failure (HF) is a bitter reality worldwide. In the UK between three to 20 per 1000 population are currently suffering from HF1. The number increases to more than 80 per 1000 population above the age of 75. Year on year the number of HF patients rises with at least one new case per 1000 population and an annual increase in new patients of 10 per cent1. Measures to stem the tide of HF must now be put in place and a priority should be to focus on the prevention of new cases.

Risk factors for HF

A number of risk factors2 predispose individuals to developing left ventricular (LV) remodelling and subsequent HF due to LV systolic or diastolic dysfunction. The process may take years3. Myocardial infarction (MI) carries an eight to 10 fold risk of developing HF and its prevention therefore is of critical importance4. Treatment of systemic hypertension, with or without LV hypertrophy, also reduces the incidence of HF, both due to systolic and diastolic dysfunction5. Whereas, the incidence and prevalence of HF in type 2 diabetes is 7.7 per cent and 11.8 per cent respectively6. The other modifiable risk factors for HF include hyperlipidaemia, obesity, alcohol excess, smoking, valve disease and cardiotoxic drugs2,7,8. All of these risk factors need to be treated aggressively2.

Treatment of risk factors

Diabetes patients with one or more risk factors or those with microalbuminuria or smoking habits should be given an angiotensin converting enzyme (ACE) inhibitor2. Hyperlipidaemia should be treated with statins, obesity with weight loss and increase in physical activity, while alcohol excess and smoking should be managed with a change of habit. Cardiotoxic drugs should be used with caution and there should be proper echocardiographic monitoring.

This article will now discuss in further detail some of the various conditions that can lead to HF and review best treatment options.

Asymptomatic LV systolic dysfunction

Studies indicate that the prevalence of asymptomatic LV systolic dysfunction (ALVD) in some populations is from just under eight per cent to 16 per cent9-12 and this rises with age. Patients with ALVD have approximately half the mortality rate (five per cent annual rate) of those with overt symptoms of HF but their risk of death is five to six times that of a normal age matched population2.

In the Study of Left Ventricular Dysfunction (SOLVD)13, patients with untreated ALVD developed overt HF at a 10 per cent annual rate, with a further eight per cent annual risk of death or hospitalisation for HF. An attempt to identify those that have ALVD is therefore required and would allow us to focus on preventing their progression to overt HF. Adopting a low threshold for assessment of LV function in populations at a high risk of cardiovascular disease is likely to reveal such subjects. A general awareness therefore of the need to assess LV function early and more frequently (during a reasonable clinical opportunity) is required in individuals with diabetes, hypertension, hyperlipidaemia, and in those with previous cardiovascular disease.

Treatment

There is good evidence that in such subjects with a high cardiovascular risk early intervention with ACE inhibitors, angiotensin receptor blockers (ARBs), statins or antiplatelet therapy with clopidogrel significantly reduces the occurrence of HF even when LV systolic function is normal14-18.

If asymptomatic LVSD develops, an ACE inhibitor is recommended to prevent progression to HF19. A beta-blocker should also be added if this has occurred after an MI19. Clinical opportunities to assess LV function may include admissions with acute coronary syndromes (ACS); admissions with poorly controlled (or complications of) hypertension, diabetes, gross hyperlipidaemia or alcoholism; and prior to major surgery under a general anaesthetic. Those with a family history of cardiomyopathies may also be considered for early assessment of LV function since relatives of those with idiopathic dilated cardiomyopathy often have asymptomatic LV dilatation and may be at increased risk for developing HF20. In addition, those with a history of alcohol excess or cardiotoxic drug therapy are likely to have ALVD.

LV systolic function after MI

With the development of the MINAP (Myocardial Infarction National Audit Project) database21, recording LV systolic function in all hospitalised ACS patients has become mandatory in the UK. However, there is need to assess LV function early after ACS.

Treatment

Therapies such as the aldosterone antagonist eplerenone have been shown to be effective in such patients post MI. The EPHESUS trial randomised 642 patients three to 14 days after acute MI, if they had signs and symptoms of HF and an LVEF ≤40 per cent, to eplerenone or placebo on top of optimal medical treatment. A significant reduction in overall mortality, death from cardiovascular causes or hospitalisation from CVS causes was seen in the eplerenone group at a mean follow-up of 16 months22.

Much of the benefits occurred early. At 30 days after randomisation23, eplerenone reduced the risk of all-cause mortality by 31 per cent (3.2 per cent versus 4.6 per cent in eplerenone and placebo-treated patients, respectively; p = 0.004) and reduced the risk of CV mortality/CV hospitalisation by 13 per cent (8.6 per cent versus 9.9 per cent in eplerenone and placebo-treated patients, respectively; p = 0.074). Eplerenone also reduced the risk of CV mortality by 32 per cent (p=0.003) and the risk of sudden cardiac death by 37 per cent (p=0.051). In order to commence eplerenone early after MI all such patients must have an early assessment of LV function done, preferably by echocardiography.

Valve disease post MI

Cardiac remodelling following MI is accepted as a determinant of the clinical course of HF. Patients with valve disease or congenital heart disease should be assessed by a specialist and considered for early correction to prevent development of HF18. In view of frequent instances of missed surveillance of valve disease leading to HF, particularly in aortic stenosis and mitral regurgitation, a case for early elective surgery has been made in these situations well before symptoms or LV dysfunction develop24 or current criteria for operating are achieved.

Treatment

All patients with a history of MI should be commenced on an ACE inhibitor and a betablocker to delay progression to HF19. Drug therapy with ACE inhibitors, ARBs, beta-blockers and aldosterone antagonists have all been shown to limit or reverse remodelling if started early in the post infarct stage25,26. Healthy lifestyle choices should be encouraged such as abstinence from smoking, regular exercise, weight reduction and avoiding excess alcohol18.

Other prevention measures

Percutaneous intervention (PCI) for coronary disease has become widely prevalent as a result of advancing technology enabling more complex coronary disease to be tackled. Even the very elderly (eg, >85 year olds) with CHD, who were previously managed with medical treatment, are now being increasingly considered for coronary intervention. The use of techniques that minimise LV systolic dysfunction (such as thrombectomy in primary PCI, distal embolic protection in vein graft intervention) will have a major impact in preventing future HF. Primary PCI intervention for ST elevation MI is already known to prevent and limit LV dysfunction and should be carried out where possible27, and efforts to reduce the transfer time from symptom onset to PCI should be made to further benefit LV function.

Reducing underuse of standard evidence-based therapy for HF, such as beta-blockers and ACE inhibitors will also prevent decompensation of stable HF28,29. There is still apathy amidst physicians to use beta-blockers in HF despite clear evidence and guidelines30,31. Multifaceted interventions are necessary to improve physicians’ adherence to guidelines32. Despite the relative lack of major success of studies using such multifaceted intervention33,34, investigators should continue to explore new types of interventions, physician incentives, and technological advances to try to improve the use of beta-blockers in HF.

Conclusion

Prevention of HF is an important goal. We are currently not doing enough in this regard. Every reasonable opportunity should be utilised to assess LV function in populations at a high risk of HF. This will allow a certain number of asymptomatic LV dysfunction patients to be identified (whether screening for such patients should be performed is a separate debate) and treated with evidence-based therapy to prevent progression to overt HF. All risk factors for HF, particularly CAD and hypertension and diabetes should be treated early and aggressively. All post MI patients should be treated with an ACE inhibitor and a beta-blocker to prevent HF. In addition, early assessment of LV function in post MI patients is required to identify those that would benefit from eplerenone therapy.

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