The "no-reflow" phenomenon: basic science and clinical correlates

Both animal models of experimental myocardial infarction and clinical studies have provided evidence of impaired microvascular perfusion after reperfusion. Characteristics of no-reflow found in basic science investigations, such as distinct perfusion defects, progressive decrease of resting myocardial flow with ongoing reperfusion and functional vascular alterations are parallelled by clinical observations demonstrating similar features. Treatment strategies of reducing no-reflow after acute myocardial infarction are under investigation. Coronary microembolisation is significantly involved in clinically observed microvascular dysfunction, and new interventional devices provide hope for capturing these emboli before they cause tissue damage. From a practical standpoint, the best way to reduce no-reflow is to reduce infarct size by early reperfusion and adequate pharmacological treatment. However, whether improvement of microvascular perfusion even in zones of irreversibly damaged myocardium - which theoretically might have beneficial effects on ventricular remodelling, infarct healing, and collateral formation - is feasible with pharmacological interventions, remains to be investigated.