Primary percutaneous coronary intervention (PCI) represents the reperfusion strategy of choice for patients presenting with ST-segment elevation myocardial infarction. However, despite the restoration of epicardial flow, primary PCI may not determine an effective reperfusion of myocardial tissue due to the occurrence of microvascular obstruction. This phenomenon also known as “no-reflow” may occur in 30-60% of patients treated with primary PCI. Of importance, no-reflow attenuates the benefit of reperfusion therapy and is associated with a poor clinical outcome in terms of adverse ventricular remodeling, heart failure and mortality. The pathophysiology of no-reflow is complex and multiple players may be involved. Indeed, distal embolization, ischemia-reperfusion injury and an individual predisposition to microvascular dysfunction synergically interact to determine the occurrence of no-reflow. In this review, we will analyze the pathophysiological mechanisms, the diagnostic tools and the main therapeutic targets of no-reflow, with particular attention to the most recent acquisitions in this field.
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