2005, Volume 12, Issue 03, pages 161-244

Major advances have been made in the management of heart failure (HF) over recent years. Modern day pharmacotherapy and device-based therapy have brought about significant improvements in prognosis and a reduction in morbidity.

The review by Vazir and colleagues in this issue of the journal (see pages 219–23) comes as a timely and practical update on the implications, diagnosis and treatment of sleep-disordered breathing (SDB) in congestive heart failure (CHF).

The Department of Health has supported the standards and targets set in the National Service Framework (NSF) for coronary heart disease (CHD) with a programme of investment and reorganisation.

In the previous article, Dr Sarah Jarvis provides a useful perspective on the management of heart failure in primary care. Recent reports from the Department of Health and the Healthcare Commission have highlighted the lack of progress in implementing evidence-based practice in heart failure. It is essential that primary and secondary care work together to improve the situation.

Increasing rates of coronary heart disease and the increasing longevity of the UK population mean that the number of cases of heart failure seen in general practice is rising rapidly. Simultaneously, this disease area has been recognised by the National Institute for Clinical Excellence, which has published guidelines for its management, and it has been made a target for remuneration under the new General Medical Services contract. This, together with the latest clinical trial evidence, has dramatically changed how heart failure is managed in primary care. Considering these recommendations and the latest clinical trial evidence, a logical management plan for heart failure is suggested.

The management of heart failure has altered greatly and good outcomes are dependent on an accurate, specific diagnosis and modern therapy. In 50% of cases, heart failure is diagnosed in hospital, with high readmission rates. There is evidence of variations in the diagnosis and management practices between specialists and hospitals, compromising uniformly high standards. In turn, this is likely to affect the quality of ongoing management in primary care. This qualitative study explores specialists’ attitudes and practices in the diagnosis and management of heart failure with a view to identifying barriers to provision of uniformly high standards of care.

Coronary artery spasm is an uncommon presentation of angina and may be associated with other vasospastic diseases such as Raynaud’s disease. It is widely accepted that local imbalance of production and removal of nitric oxide (NO) and other endothelium-derived factors is generally responsible for the arterial spasm in variant angina. Very rarely, diffuse spasm can herald ventricular arrhythmias due to sudden reduction in perfusion.

Hypokalaemia and hyperkalaemia are common complications of heart failure and its treatment: either may increase markedly the risk of arrhythmias and sudden cardiac death. Hypokalaemia predominates in the early stages of heart failure. The risk of hyperkalaemia increases as renal function declines, usually in the context of advancing heart failure. For patients with heart failure, serum potassium levels of between 4.5–5.5 mmol/L are recommended. Monitoring of serum potassium is essential, with more frequent monitoring in patients with moderate renal failure, relatively high serum potassium, or in those at high risk of renal impairment, e.g. elderly or diabetic patients. Hypokalaemia can be ameliorated by a potassium-sparing diuretic or an aldosterone receptor antagonist; increasing dietary potassium intake or taking potassium supplements is less effective. Doses of loop or thiazide diuretics should be optimised. Hyperkalaemia is more often seen in advanced heart failure. Restriction of dietary potassium and withdrawal of potassium supplements are standard. Temporary discontinuation of angiotensin-converting enzyme inhibitor and/or aldosterone receptor antagonist therapy may be appropriate but attempts should be made to reintroduce these. Excessive diuretic therapy should be avoided. With routine potassium monitoring and pre-emptive intervention included in heart failure protocols, the risks to patients can be minimised.

Sleep-disordered breathing (SDB) is common in patients with congestive heart failure (CHF). SDB appears to be associated with accelerated progression of heart failure. However, it is seldom recognised in cardiology clinics, especially as CHF patients with SDB rarely report symptoms specific to SDB, such as excessive day-time sleepiness. The term SDB incorporates both central sleep apnoea (CSA) and obstructive sleep apnoea (OSA). CSA is thought to be a consequence of heart failure, whereas OSA is thought to be associated with hypertension and excessive sympathetic nerve activation, which may exacerbate failure of the heart through haemodynamic and mechanical mechanisms. The treatment of SDB is likely to be an important complementary step in the management of heart failure, particularly OSA, where treatment with continuous positive airway pressure is well established and significant improvements in left ventricular ejection fraction plus quality of life have been reported. The treatment of CSA remains unclear and requires further research. This review will examine the prevalence, diagnosis, pathophysiology, clinical features and treatment of SDB in patients with CHF.

Aldosterone is intimately linked to the pathophysiology of heart failure, and high levels of aldosterone are associated with worse prognosis. Many non-renal effects of aldosterone contribute to the congestive heart failure syndrome, including endothelial dysfunction, reactive myocardial fibrosis and cardiac remodelling. The precise mechanism by which aldosterone stimulates myocardial collagen accumulation and fibrosis is not yet fully understood. It may largely occur secondary to aldosterone-related endothelial dysfunction and inflammation, since endothelial dysfunction can lead to micro-thrombus formation and tissue micro-infarction, which repairs itself by fibrosis. Other contributory effects may include a direct impact of aldosterone on the collagen synthesis pathway. In the RALES study, spironolactone in conjunction with an angiotensin-converting enzyme (ACE) inhibitor was found to reduce mortality in chronic moderate-to-severe heart failure; the EPHESUS study more recently reported significant reductions in death and hospitalisation when eplerenone was added to ACE inhibitor and beta blocker therapy in patients with clinical evidence of heart failure following acute myocardial infarction. Clinicians should now consider routinely adding an aldosterone receptor antagonist to standard therapy of patients with left ventricular dysfunction and heart failure in order to reduce cardiac morbidity and mortality.

Improvements in the management of acute myocardial infarction together with population ageing have contributed to a growing burden of heart failure. Around half of new cases of heart failure in patients aged less than 75 years are due to coronary artery disease; many of these patients develop heart failure in the context of acute myocardial infarction. Left ventricular systolic dysfunction is the single most common cause of heart failure after myocardial infarction. Of the estimated 65,000 new cases of heart failure in the UK each year, it is likely that around 15,000 occur in the context of acute myocardial infarction. Ventricular remodelling generally occurs in the early period after myocardial infarction, and early identification offers the potential to modify this process and reduce the risk of heart failure. Clear guidelines should be built into the myocardial infarction care pathway to ensure an integrated approach from hospital and community services.