Microvascular alterations after temporary coronary artery occlusion: the no-reflow phenomenon.

Abstract

In experimental models of temporary coronary artery occlusion, tissue perfusion at the microvascular level remains incomplete even after patency of the infarct-related epicardial coronary artery is established, and distinct perfusion defects develop within the risk zone. This no-reflow phenomenon can be regarded as a basic cardiac response to ischemia-reperfusion. Perfusion defects observed in the clinical realm after reperfusion therapy for myocardial infarction may substantially be related to this mechanism in addition to microembolization and activation of platelets, as suggested in several recent studies. A major determinant of the amount of no-reflow seems to be infarct size itself. Reperfusion-related expansion of no-reflow zones occurs within the first hours after the reopening of the coronary artery with a parallel reduction of regional myocardial flow, resulting in a potential therapeutic window. With various cardioprotective interventions, a close correlation between the size of the anatomic no-reflow and necrosis is a reproducible feature, which suggests a causal link between both entities of ischemic cardiac damage. Although vasodilating interventions failed to uncouple no-reflow zones from necrosis, the steps in the causal chain between microvascular and myocardial damage remain to be identified. On a long-term basis, tissue perfusion after ischemia-reperfusion remains markedly compromised for at least 4 weeks. Recent morphometric cardiac analyses suggested that the level of tissue perfusion after 4 weeks is a significant predictor of various indices of infarct healing, such as scar thickness, and infarct expansion index. As a consequence, improving tissue perfusion might concomitantly improve the healing process, which may provide the pathoanatomic basis for prognostic implications of no-reflow.