Timely delivered coronary revascularization with no residual anatomical stenosis does not always lead
to prompt restoration of anterograde coronary flow and complete myocardial reperfusion. This condition is
known as coronary no-reflow and is associated with major clinical adverse events and poor prognosis. The pathophysiology
of no-reflow phenomenon is still poorly understood. Proposed mechanisms include distal microembolization
of thrombus and plaque debris, ischemic injury, endothelial dysfunction and individual susceptibility to
microvascular dysfunction/obstruction. Older age, diabetes, hypercholesterolemia, prolonged ischemic time,
hemodynamic instability, high thrombus burden, complex angiographic lesions and multivessel disease are frequently
reported to be associated with the no-reflow phenomenon. There is no general consensus on the correct
prevention and management of no-reflow. Non-pharmacological measures such as distal embolic protection devices
and manual thrombus aspiration did not result in improved flow or reduction of infarct size. Current preventive
measures include reduction of time from symptoms onset to reperfusion therapy, and intracoronary administration
of vasodilators such as adenosine, verapamil or nitroprusside.
Keywords: No-reflow, microvascular dysfunction, coronary flow, no-reflow management, distal embolization.
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