Heart failure – from pathophysiology to therapy
Authors: Swedberg K. 
Published: November 2003

Swedberg K et al. (Department of Medicine, Östra University Hospital, Göteborg, Sweden). Heart failure – from pathophysiology to therapy (Minisymposium). J Intern Med 1996; 239: 305–43.

Population studies, together with data from clinical records, reveal a range of estimated heart failure prevalence of 1–10%. Estimated incidence rates vary around 1% per annum. In community studies, the five‐year mortality is between 50–60%, while in patients requiring hospital admission, the annual mortality is 10–20% in those with mild–moderate symptoms and as high as 40–60% in severe heart failure.

Many definitions of heart failure have been formulated. Making a diagnosis is a complex process. Heart failure is not a diagnosis or even one syndrome, but is a cluster of syndromes. The diagnosis is therefore only part of the assessment process. Essential parts for the diagnosis include symptomatology, objective evidence of important cardiac dysfunction and evaluation of the response to therapy. The cardinal symptom is exertional breathlessness. At present, echocardiography remains the most useful tool for confirming cardiac dysfunction, but determination of atrial natriuretic peptide or magnetic resonance imaging may supersede it. Heart failure has been viewed primarily as an oedematous disorder, in which fluid retention occurs because the heart cannot pump adequate quantities of blood to the kidneys. This model led to the utilization of diuretics for heart failure, but it failed to recognize that heart failure is a chronic progressive disorder that impairs both the quality and quantity of life, even when oedema is adequately controlled.

A new model has been developed in which the development and progression of heart failure is viewed as resulting from the interplay of haemodynamic and neurohormonal mechanisms. Both mechanisms support the inotropic state of the heart following an injury to the myocardium, but when sustained for long periods, these mechanisms act to enhance ventricular wall stress, and, thereby, impair ventricular performance. As the heart failure evolves, endogenous mechanisms that are normally activated to control wall stress become exhausted, and peripheral vasoconstriction and sodium retention develop. Unopposed activation of haemodynamic stresses and neurohormonal systems leads to further destruction of myocardium and progression of the underlying disease. The acceptance of this haemodynamic–neurohormonal model has led to the development of vasodilators and neurohormonal antagonists which have been shown to be useful alone  – or added to diuretics – in the treatment of heart failure.

Non‐pharmacological therapy includes counselling of life style and, for patients with moderate heart failure, light exercise. Within the last decade, pharmacological therapy was improved considerably. Asymptomatic patients with left ventricular dysfunction benefit from acetylsalicylic acid (ASA) and beta‐blockers. In patients with progressive dilatation of the left ventricle and with an established left ventricular dysfunction treatment with angiotensin‐converting enzyme (ACE) inhibitors has beneficial effects on mortality and morbidity.

In symptomatic patients and those with clear systolic left ventricular dysfunction in addition to digitalis and diuretics, ACE inhibitors are clearly indicated in addition to ASA. Beta‐blockers may be added but the true benefit is not established. The initiation of both ACE inhibitors and beta‐blockers should be careful and the dose titrated slowly. Antiarrhythmic class I agents should be avoided unless clear indications are present, e.g. life‐threatening arrhythmias. Amiodarone might be considered as an alternative.

The prognosis for patients with heart failure remains serious and the search for even better therapies should continue.