Derrick Garwood, Freelance Medical Writer and Editor

There is a widespread belief that heart failure is the sudden stopping of the heart as a result of sudden fright. Not so! It is the inability of the heart to pump sufficient blood, which usually develops over a period of time, and different symptoms are produced by the different sides of the heart. When the left ventricle fails to pump adequately, blood 'backs up' and fluid accumulates in the lungs, causing congestion, shortness of breath and reduced plasma oxygen levels, leading to fatigue. Deficiency of the right ventricle increases pressure in the venous vessels and fluid is forced out into the body tissues, producing oedema, particularly in the legs and feet. For those who prefer the multi-media approach, there is an interactive module with a simple explanation here.

The left ventricle pumps only a proportion of the blood it contains. This is known as the ejection fraction and is a measure of the heart's efficiency. In a healthy heart the ejection fraction is 55% or more, but if the cardiac muscle becomes weakened or the heart becomes enlarged, much lower values may result. Where ventricular contraction is reduced, the condition is termed systolic heart failure. By contrast, in diastolic heart failure the reduced volume of blood pumped at each beat (the stroke volume) is caused by impaired relaxation of the ventricle, and the incomplete filling which results. The pathological mechanisms involved are described in great detail on the emedicine site, which also includes an awesomely long list of causes of heart failure and some sobering statistics. In the USA, the estimated 5-year mortality rate is 50% and the condition accounts for some $23 billion of inpatient treatment plus $40 billion of outpatient treatment. A study published earlier this month calculated the annual incidence in the US to be 219 cases per 100,000 population (250 for women and 194 for men), confirming it to be a considerable burden to the health of the community.

Diagnosis is made upon the basis of the patient's medical history, a physical examination and the results of a range of tests, particularly the B-type natriuretic peptide (BNP) test. BNP is released from the ventricles when heart failure develops and its concentration in the blood is proportional to the severity of the condition. The test is quick (15 minutes) and inexpensive, and in one study accurately detected heart failure in 83% of cases. Further details of the diagnostic tests on this page can be found by clicking on the underlined headings.

Drug treatment primarily involves diuretics, ACE (angiotensin-converting enzyme) inhibitors, b-blockers and digitalis; most patients are treated with drugs from at least two of these classes. The types of diuretic commonly used are loop, thiazide and potassium-sparing agents. Loop diuretics act by inhibiting the re-absorption of chloride, sodium, potassium and hydrogen ions by the ascending loop of Henle in the kidney. Thiazides inhibit sodium and chloride re-absorption more distally; compared with loop diuretics they induce less urine formation but a greater loss of sodium and potassium. Potassium-sparing drugs generally retain magnesium as well, but are often combined with agents from the other two classes, as their diuretic action is weak. This site has very comprehensive information on the effective use of these drugs in heart failure and the phenomenon of diuretic resistance – a slightly briefer account can be found here.

ACE inhibitors block the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor) and reduce the degradation of bradykinin (a potent vasodilator). The effect is to lower arteriolar resistance and to increase venous capacitance, cardiac output and stroke volume. Although the benefits of these agents are well established, a 2004 US study found that they are under-used in heart failure and almost a third of sufferers face an increased risk of death as a consequence.

Traditionally, b-blockers were avoided in heart failure, but a 1998 meta-analysis of 18 placebo-controlled trials demonstrated that these compounds reduced total mortality by 32%, sudden deaths by 41% and hospitalisation by 37% . There are short term risks associated with their use, but complications can usually be avoided by starting treatment with an extremely low dose and then increasing it very slowly.

Digoxin does not reduce mortality; it is used to relieve persistent symptoms in patients who are already receiving drugs that reduce the risk of death, such as ACE inhibitors. Its primary effect is to increase the force of myocardial contraction whilst decreasing oxygen consumption, but it also affects the contractile function of vascular smooth muscle and the activity of the autonomic nervous system.

In the last few days, it has been reported that patients with diastolic heart failure (about 40% of cases) appear to fare better if they take statins to lower their cholesterol levels. Mortality was reduced by 22%, possibly as a result of the beneficial effect of these drugs on coronary artery disease. Other exciting discoveries are that genetic mutation could contribute to heart failure, by disrupting the calcium cycle that effects cardiac contraction, and that stem cells can be converted to heart muscle cells using vitamin C. One new physical device that has undergone trials and is awaiting approval is an individually-tailored mesh 'sock' which fits closely around a failing heart to prevent it becoming enlarged and weakening further. At least the patient shouldn't get cold!

This tour was submitted by Derrick Garwood, a Freelance Medical Writer and Editor

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