Editorial Comment Pathogenetic Mechanisms Coronary Artery Spasm*

Coronary artery spasm was first proposed as a cause of spontaneous, recurring angina1 attacks over a century ago (1). Because this brilliant clinical intuition could not be demonstrated at postmortem study, it fell into progressive disrepute until, in the early 1950s coronary artery spasm was considered “the resort of the diagnostically destitute” (2). In 1959, the notion of coronary artery spasm was bravely resurrected with clinjcal acumen by Prinzmetal et al. (3), and it became a proved hypothesis in the mid-1970s (4). Dynamic coronary artery stenoses caused by increased coronary tone, thrombosis or their combination are now recognized components of stable and unstable ischemic syndromes (5-g). Yet coronary artery spasm, as most typically observed in variant angina, appears to be a rare condition with some rather unique features: it is usually localized to a segment of epicardia] coronary artery and causes transmural myocardial ischemia typically manifested by ST segment elevation, as documented during continuous electrocardiographic (ECG) monitoring. Coronary spasm tends to be transient and is usually promptly relieved by immediate administration of nitrates. In variant angina, it is usually episodic; patients may experience a waxing and waning of the disease for weeks, months and even years as spasm occurs spontaneously. Coronary spasm can be reproduced by ergot derivatives and by hyperventilation. Many variations of this classical clinical picture can be encountered, and it would be unwise to consider any single pathogenetic mechanism responsible for the whole spectrum of ischemic syndromes related to abnormal coronary vasoconstriction. The present study. In this issue of the Journal, Hoshio et al. (9) conclude that “a coronary vasomotion disorder, which involves increased basal coronary artery tone and hyperreactivity to vasoconstrictive stimuli, not only at a