Heart failure is a common clinical syndrome, often presenting with breathlessness, fatigue and peripheral oedema. It is predominantly a disease of older people. The prevalence is increasing, exceeding 2% of the adult population in developed countries.
The pathophysiology of heart failure is complex. A common feature is salt and water retention, possibly triggered by a relative fall in renal perfusion pressure. Common aetiologies include ischaemic heart disease, hypertension, and valvular heart disease.
The early diagnosis of heart failure relies on a low threshold of suspicion and screening of people at risk before the onset of obvious symptoms or signs. In patients with suspected heart failure, routine investigation with electrocardiography and blood tests for urea and electrolytes, haemoglobin and BNP/NT-proBNP are recommended. Low plasma concentrations of BNP/NT-proBNP exclude most forms of heart failure. Intermediate or high concentrations should prompt referral for echocardiography to identify possible causes of heart failure and the left ventricular ejection fraction (LVEF). Patients can be classified as reduced (<40%) LVEF (HFrEF), normal (>50%) LVEF (HFnEF), or borderline (40–50%) LVEF (HFbEF). Currently HFbEF and HFnEF are managed similarly by current guidelines.
Treatable causes for heart failure (e.g. valvular disease, tachyarrhythmias, thyrotoxicosis, anaemia or hypertension) should be identified and corrected. Patients with heart failure will generally benefit from lifestyle advice (diet, exercise, vaccination). Pharmacological therapy is given to improve symptoms and prognosis. Diuretic therapy is the mainstay for control of congestion and symptoms; it may be life-saving for patients with acute heart failure but its effect on long-term prognosis is unknown. For patients with HFrEF, either angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, or, more recently, angiotensin receptor neprilysin inhibitors, combined with β-blockers and mineralocorticoid receptor antagonists (triple therapy) provide both symptomatic and prognostic benefit. Ivabridine may be added for those in sinus rhythm where the heart rate remains above 70 bpm. Whether digoxin still has a role in contemporary management is uncertain. Cardiac resynchronization therapy is appropriate for symptomatic patients with HFrEF if they are in sinus rhythm and have a broad QRS (>140 ms). Implantable defibrillators provide additional prognostic benefit in selected patients with an ejection fraction below 35%. For patients with HFnEF, treatments directed at comorbid conditions (e.g. hypertension, atrial fibrillation) and congestion (e.g. diuretics and mineralocorticoid receptor antagonists) are appropriate but there is no robust evidence that any treatment can improve prognosis. Heart transplantation or assist devices may be options for highly selected patients with endstage heart failure; many others may benefit from palliative care services. Effective management of chronic heart failure requires a coordinated multidisciplinary team, including heart failure nurse specialists, primary care physicians, and cardiologists.
New treatments have improved the prognosis of heart failure substantially over the past two decades. The annual mortality is now probably less than 5% for patients with HFrEF receiving good contemporary care whose symptoms are stable and controlled. For patients with recurrent or recalcitrant congestion requiring admission to hospital, the prognosis is much worse. In-patient mortality is about 5% for those aged less than 75 years but threefold higher for older patients; mortality in the year after discharge ranges from 20% to 40% depending on age.
Beta-adrenergic receptor blockade and the angiotensin-converting enzyme deletion polymorphism in patients with chronic heart failure