Many theories have been developed to explain the pathogenesis of unstable angina, but so far none has adequately explained all the known facts about this disease. Most patients with unstable angina have atheromatous deposits in their coronary arteries, and progressive stenosis caused by large atheromatous plaques was once thought to be responsible for the development of ischaemic symptoms. However, a study comparing the coronary arteries of patients who had a history of chronic stable angina for at least two years with those who had a history of unstable angina failed to support this hypothesis.1 The study found that the severity of atheroma varies greatly between individuals and that patients with uncomplicated chronic stable angina tended to have more severe atheroma than patients who have unstable angina as the first clinical manifestation of ischaemic heart disease.

An alternative theory that has gained wide acceptance attributes unstable angina to the sudden fissure or rupture of an atherosclerotic plaque. This exposes the highly thrombogenic endothelium to the circulation, and a platelet rich thrombus rapidly develops over the site of plaque rupture. The thrombus obstructs but usually does not fully occlude the vessel. Blood flow may be occasionally reduced causing distal ischaemia but the myocardium remains viable. Although thrombosis undoubtedly has a central role in unstable angina, recent studies indicate that other mechanisms also play a part in some patients. It is therefore appropriate to reconsider the evidence concerning the aetiology of this condition.