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(Circulation. 1995;92:1083.)
© 1995 American Heart Association, Inc.

Articles

Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction

P. Constantinides, MD, PHD

Correspondence to Paris Constantinides, MD, PhD, 430 Chester Rd, Qualicum Beach, BC, V9K 1B9, Canada.

Key Words: Editorials • cells • atherosclerosis • plaque • thrombus

	Introduction

 
In the early 1960s, complete serial section studies through the whole thrombosed segment of occluded coronary arteries of myocardial infarction patients autopsied in St Louis, Mo, showed that all of the occluding thrombi had been caused by fissures of the surface of the underlying atherosclerotic plaques, fissures through which blood sometimes entered the plaque interior before they were sealed by the thrombi.¹ Because essentially similar findings have since been made in Germany,² Great Britain,³ Denmark,⁴ and Russia (A. Vichert, personal communication, 1985) and the same scenario was found to be responsible for cerebral artery thrombosis,⁵ it now seems certain that thrombosis in human atherosclerotic arteries is always triggered by a disruption of their plaque surfaces, even though the size the thrombi achieve and how long they persist probably depends on systemic factors that prevailed at the time of the disruption. In other words, plaque disruptions may occur all the time, but in some persons with high blood coagulability and/or low plasma fibrinolysin activity, they may cause large occlusive thrombi and myocardial infarction, whereas in others they may produce only small nonocclusive thrombi without myocardial necrosis.

Unfortunately, the processes that induce plaque disruption are still unknown. They could be physical stresses or chemical insults emanating from the blood or the plaque interior, insults that disrupt the plaque directly or increase its vulnerability to other factors.

Among the disrupting agents generally considered possible so far are (1) endothelium-injuring processes, (2) factors that damage or kill the myocytes that produce and maintain the . . . [Full Text of this Article]

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