No-reflow: again prevention is better than treatment

Abstract

Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion strategy for treating acute ST-segment elevation myocardial infarction (STEMI). The main goals are to restore epicardial infarct-related artery patency and achieve microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured (necrotic) myocardium.1 Angiographic assessment of myocardial blood flow is reported as thrombolysis in myocardial infarction (TIMI) flow, and although TIMI flow grade relates to outcome, even in the presence of TIMI-3 flow tissue level perfusion can still be disturbed as measured by other indexes such as corrected TIMI frame count (cTFC) or more invasive measures of coronary blood flow. Thus, depending on how it is measured, inadequate tissue level reperfusion can occur in up to 50% of cases. No-reflow is the term used to describe inadequate myocardial perfusion of a given coronary segment without angiographic evidence of mechanical vessel obstruction.2 Despite optimal evidence-based PPCI, myocardial no-reflow can still occur, negating many of the benefits of restoring culprit vessel patency, and is associated with a worse in-hospital and long-term prognosis.2 It is important to outline that no-reflow is only one of the four types of cardiac dysfunction (myocardial stunning, no-reflow, reperfusion arrhythmias, and lethal reperfusion injury) caused by myocardial reperfusion as recently summarized by Yellon and Hausenloy,3 and it refers to the high impedance of microvascular blood flow encountered during opening of the infarct-related coronary artery. In this manuscript, we concentrate on the processes of no-reflow while recognizing the relationships with reperfusion injury and the complexity of each of the interactions involved. The multifactorial nature of no-reflow has been summarized recently into four interacting processes: ischaemic injury, reperfusion injury, distal embolization, and susceptibility of microcirculation to injury ( Figure 1 ).4 Ischaemia–reperfusion (IR) injury is central to the pathophysiology of no-reflow and is associated …