heart failure

heart failure The characteristic symptoms of heart failure are recognizable in writings at least as far back as the twelfth century, when the health problems of Alexius I ( Comnenus), the Byzantine emperor, were documented by his physician. The ‘failure’ is manifest in the heart not providing sufficient output of blood to meet the ‘demands’ of the body. A useful term here is ‘exercise intolerance’. A typical heart failure patient will have become accustomed to an inexorable decline in physical vigour. Activities such as climbing stairs, carrying a heavy load (perhaps a suitcase), even walking, far less running, and other such ‘exercises’ usually considered to be within the normal range become increasingly difficult or impossible. One key associated symptom is breathlessness, another is oedema (the accumulation of fluid in the tissues) for example in the ankles. Both symptoms reflect raised pressure in the veins ultimately caused by the insufficient pumping action of the heart. The seriousness of heart failure is such that, at the time of writing, about half of the patients affected die within five years of the initial diagnosis. Of these fatalities, about half will suffer a major heart attack, the remainder will suffer a steady decline of heart function until pump failure itself proves fatal. Against this gloomy scenario, new discoveries about the underlying causes, the development of new drugs to slow down, halt, and ultimately reverse the harmful aspects, and an increasing awareness of the value of lifestyle and dietary change promise to improve the prospects for the heart failure patient in the twenty-first century — even if too late for the Emperor Alexius.

The most common single cause in modern Western society, accounting for about half of the cases, is a heart attack. By killing one region, the attack leaves heart function compromised. Until the later decades of the twentieth century a very major cause was undiagnosed and untreated high blood pressure — the heart in this instance must work harder and harder to force blood into the arteries where the pressure is too high, and eventually ‘tires’. Although long-term high blood pressure is still a contributor to heart failure, modern drugs have helped to reduce its significance. A range of other causes include the various heart valve malfunctions, certain infections, congenital structural abnormalities, genetically-determined disorders, and drug abuse. There is clear evidence that the factors that increase the likelihood of heart attack also contribute to the severity of the ensuing heart failure. These factors include high blood cholesterol, atheromatous vascular disease, sedentary lifestyle, and smoking. In third-World countries, infections such as the insect-transmitted trypanosomal Chagas' disease are among the main causes of heart failure. Even amongst economically advanced nations there are wide differences in the incidence of heart failure between, say, Japan (very low) and Western Europe and the US (high); nation-specific combinations of dietary and genetic factors are thus the target of much research into underlying causes. There is widespread agreement that taking regular exercise not only strengthens the heart and improves its own circulation (particularly by improving collateral blood supplies) but also that exercise is a very useful part of any rehabilitation regime designed to prevent the development of heart failure after a heart attack.

Heart failure refers to a characteristic pattern of features caused by an abnormality of the heart. It is a complex clinical syndrome resulting from the entanglement of cause and effect, of symptoms and compensatory changes. Several body systems and organs are involved, especially the lungs, kidneys, and blood vessels, their associated hormonal systems, as well as the heart itself. It is increasingly clear that many and varied patterns of disturbance to each of these systems can result in convergence into the full repertoire of malfunctions which together are termed heart failure.

In normal circumstances, the ‘challenge’ to the heart posed by ‘demand’ for increased blood supply is most obvious during exercise, however mild. The physiological challenge is similar when the heart is unable, by virtue of disease, to meet even normal requirements. In either case, homeostatic mechanisms operate which promote the maintenance of two parameters of heart function: blood pressure and blood flow. An example of these compensatory processes is one promoting retention of water and salts by hormonal influences on the kidneys. This will increase blood volume and tend to keep up both blood pressure and cardiac output (the volume pumped). Unfortunately, in heart failure, the compensatory mechanisms prove clearly ineffective; they actually contribute to the symptoms observed (e.g. breathlessness and ankle swelling) and become important factors in the gradual worsening of the condition. The use of diuretic drugs (which stimulate kidney function and reverse fluid retention) is widespread in the treatment of heart failure. The heart itself generally responds to an abnormal workload by increased growth (hypertrophy), but the nature of the growth is abnormal in subtle ways, unlike the hypertrophy associated with general physical fitness which is positively beneficial. It is now known, for example, that a hypertrophied failing heart both contracts and relaxes more slowly, and is more prone to life-threatening electrical abnormalities.

David J. Miller, and Niall G. MacFarlane

See also heart; heart attack.