Abstract

No-reflow, i.e., the lack of distal myocardial perfusion to fully recover following recanalization of an acutely occluded coronary artery, is not only a mere consequence of ischemic injury, as substantial microvascular alterations may also develop subsequently, after initial restoration of perfusion. Since part of perfusion impairment is secondary to events set in motion by reperfusion, this gives way to the possibility of preventing it through adequate interventions. Duration and severity of ischemia influence the occurrence of reperfusion-mediated no-reflow, since severity of ischemic injury sets the stage for events which actually unfold after restoration of blood flow. Proposed mechanisms of no-reflow are impaired vasodilation, intravascular thrombosis, and accumulation of neutrophils in the microvasculature, orchestrated by activation of vascular endothelium. Experimental studies have unraveled much of mechanisms of noreflow, and delineated possible ways of intervention. Despite successful experimental data, in the clinical setting results have been much less encouraging, and no drug can be currently recommended for routine use to prevent or treat microvascular injury and no-reflow in patients. Reperfusion-mediated impairment of microcirculation in postischemic hearts remains a challenges for investigators and clinicians alike. Large multicenter studies, specifically aimed at evaluating the effects of the more promising interventions (adenosine, nicorandil, statins, ACE inhibitors or angiotensin II receptor blockers) need to be designed and performed, to test the effect of these promising interventions on microvascular alterations during postischemic reflow, and their ability to improve tissue perfusion, myocardial function and prognosis in patients with acute myocardial infarction.

Keywords: No reflow, reperfusion injury, reactive oxidant species, nitric oxide, neutrophils.