Coronary arterial spasm in angina at rest associated with transient ST‐segment changes

Abstract

Summary: In order to clarify the role of coronary arterial spasm in the pathogenesis of angina at rest, coronary arteriography was performed during spontaneous chest pain or following intravenous administration of ergonovine maleate in 40 patients with angina at rest. Coronary vasospasm was demonstrated in 23 patients with ST-segment elevation during chest pain (group I), in 7 with ST-segment depression (group II), and in 4 with both ST-segment depression and elevation (group III).Complete spastic occlusion of the proximal or of the midportion of the left anterior descending artery was always associated with ST-segment elevation in anterior leads. In contrast, transient ST -segment depression in anterior leads was associated with diffuse narrowing of the left anterior descending artery with slow progression of the contrast medium, or complete occlusion of a small branch or of the distal segment of the left anterior descending artery. ST -Segment elevation in inferior leads was associated with complete spastic occlusion or with significant spastic narrowing of the right coronary artery or of the circumflex artery.We conclude that coronary spasm can be demonstrated in a selected cohort of patients with angina at rest associated with transient ST-segment changes. In some cases the site and the severity of the spasm may produce varying degrees of ischemia, thus determining the direction of the ST -segment shift.

Asymptomatic coronary artery spasm with acute pathological ST elevation on routine ECG: Is it common?

“…But there are no case reports of spontaneous ST elevation without chest pain due to coronary spasm. Coronary spasm has always been described with chest pain with or without ECG changes ranging from T wave changes, ST depression and also ST elevation 5. Other causes of chest pain and ST elevation with normal coronary angiography have been described in patients with pericarditis, myocarditis, usage of illicit drugs like cocaine and amphetamines,4 Tatkasubo cardiomyopathy and other forms of cardiomyopathy.…”

Local platelet activation causes vasoconstriction of large epicardial canine coronary arteries in vivo. Thromboxane A2 and serotonin are possible mediators.

“…(Circulation 1989;79:154-166) It is currently believed that the pathophysiology of unstable angina is a primary reduction in coronary blood flow. [1][2][3][4][5][6] In particular, there is a growing body of evidence indicating that in most patients, unstable angina is the consequence of sudden restorations of flow. These alterations in coronary blood flow have been referred to as cyclic flow variations and are caused by transient formation of platelet thrombi at the site of the coronary stenosis and endothelial injury.14-17Subsequent studies from our laboratory have demonstrated that serotonin (5HT) and thromboxane A2 (TXA2) released from activated platelets are two important mediators of cyclic flow variations in this canine model15,17"8 and that the tissue concentration of 5HT and TXA2 is markedly elevated in the coronary artery at the site of the stenosis.…”