Mechanisms of transient myocardial ischemia.

The second Pisa Conference nine years ago established the frequency of transient reduction of coronary flow, as a cause of angina. Understanding of mechanisms remains very incomplete and there is great overlap between different clinical syndromes. The following facts appear established: Episodes of spontaneous ischemia are frequently asymptomatic and may occur even in patients with classic stable angina of effort: Large coronary arteries exhibit tone; they do not take part in autoregulation: In the presence of advanced organic obstruction, large coronary artery tone may be sufficiently increased by physiological alpha-adrenergic stimulation to provoke ischemia. The following deductions seem justifiable: Clinically, increased large coronary tone can be suspected as a cause of ischemia when there is a background of severe organic coronary narrowing with effort angina, when rest attacks occur in association with stimuli such as cold or isometric stress and when their frequency can be reduced by alpha blockade: Spasm, as distinct from physiological increase in tone, can be suspected when there is minimal organic disease, an absence of effort angina and when attacks are unrelated to stress: The mechanism of spasm is unknown; it may be associated with intimal trauma and probably is more frequent in the presence of early atherosclerotic change: Spasm may be simulated by pseudo-spasm where a physiological increase in tone may cause marked luminal narrowing at a site of still pliable quite mild intimal proliferation; it may be suspected when apparent localised spasm is associated with diffuse acute narrowing of all coronary arteries. Apart from the smooth muscle, acute luminal narrowing with rest angina can result from coronary thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)