Abstract

Total coronary occlusion by thrombus is the cause of transmural acute myocardial infarction (AMI) in at least 90 % of cases, but patency may be reestablished spontaneous1y.l These total occlusions occur mostly at the site of preexisting coronary artery stenosis, which need not be severe.2, 3 The extent of myocardial damage depends on (1) the rapidity of occlusion, (2) the duration of the occlusion, (3) collateral flow, and (4) the coronary vascular and myocardial response to acute ischemia.4 Coronary thrombosis is the most common initial step in a more complex occlusion process involving anatomic and functional mechanisms. The purpose of this review is to describe the existing experimental and clinical methods available to assess platelet and neutrophil function in acute coronary arterial thrombosis. A better understanding of the functional and anatomic microvascular and myocardial changes should help in the management of evolving and recurrent myocardial infarction and its complications, in particular the so-called “no-reflow phenomenon.”

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