MECHANISMS OF ANGINA-PECTORIS IN SYNDROME-X

Syndrome X defines a group of patients who present with typical, usually exertional angina pectoris and a normal coronary arteriogram. They often have a positive exercise test, but direct signs of ischemia are detectable in only a minority of patients. A reduced coronary vasodilative response to dipyridamole or pacing is observed in such patients with or without a positive electrocardiographic exercise test. It is proposed that patients with syndrome X have a patchily distributed abnormal constriction of coronary prearteriolar vessels not involved in metabolic autoregulation of flow. An increased resistance of prearteriolar vessels can explain the reduced coronary vasodilative response observed in these patients, even when arterioles dilate maximally. Distal to the most constricted arterioles a localized compensatory increase of adenosine concentration can cause angina even in the absence of ischemia because adenosine is an algogenic substance. Ischemia can develop when myocardial metabolic demand exceeds blood supply or when metabolic or pharmacologic arteriolar vasodilation causes excessive reduction of pressure at the origin of the arterioles and possibly prearteriolar collapse. The more severe and confluent is the patchy prearteriolar constriction, the more detectable become the signs of myocardial ischemia. The proposed abnormal prearteriolar constriction could be caused by lack of endothelium-derived relaxing factor flow-mediated vasodilation, by abnormal nervous stimuli or by a combination of these two mechanisms. However, the causes of abnormal coronary prearteriolar constriction are not necessarily the same in all patients.