Experimental induction of spasm, sudden progression of organic stenosis and intramural hemorrhage in the epicardial coronary arteries

Recurrent ST-segment elevations in a patient without significant coronary disease

“…It is also shown in an animal study that coronary artery spasm itself induces endothelial damage (ie, intramural hemorrhage of abrupt onset) [22,24]. Furthermore, the cyclic blood flow reductions in the coronary artery are shown at the site of vascular damage in a canine model and appear to result from alternating platelet aggregation and cyclic release of platelet-derived vasoactive products [22,25]. These facts are capable of playing important roles in the unstable character of coronary artery spasm.…”

“…It has been shown that coronary artery spasm enhances platelet aggregation in the coronary circulation and that the spasm itself induces the release of a potent vasoconstrictor, platelet-derived growth factor, further aggravating the spasm [23]. It is also shown in an animal study that coronary artery spasm itself induces endothelial damage (ie, intramural hemorrhage of abrupt onset) [22,24]. Furthermore, the cyclic blood flow reductions in the coronary artery are shown at the site of vascular damage in a canine model and appear to result from alternating platelet aggregation and cyclic release of platelet-derived vasoactive products [22,25].…”

“…There is the notion that unstable angina is a consequence of platelet activation and vasoconstriction at sites of coronary endothelial injury [22]. It has been shown that coronary artery spasm enhances platelet aggregation in the coronary circulation and that the spasm itself induces the release of a potent vasoconstrictor, platelet-derived growth factor, further aggravating the spasm [23].…”

“…Most coronary artery spasms occur at the site of organic stenosis associated with atherosclerosis [22,26] ST-segment elevation in coronary artery spasm is considered to appear in leads that reflect the area of the heart corresponding to the coronary artery involved with the spasm. In this patient, ST-segment elevations were identified in lead II during the first to the fourth episodes and in leads II, III, and aVF during the fifth to the seventh episodes, which suggested that the right coronary artery was involved in the coronary artery spasm.…”

Coronary Artery Spasm: Part I Clinical Aspect

“…Furthermore, the progression of coronary atherosclerosis may ensue as a consequence of acute vascular injury. The authors have developed a porcine model of coronary artery spasm (Shimokawa et al 1983;Nakamura 1991), demonstrating that agonist-induced spasm could cause structural changes of endothelial cells ("squeezing") and promoted adhesion of leukocytes at the spastic site (Nagasawa et al 1989). In addition, intra-plaque hemorrhage was induced by repetitive spasm, leading to the rapid progression of coronary atherosclerosis and the development of AMI (Nagasawa et al 1989;Kuga et al 1993a).…”