Pathophysiology, Diagnosis, and Management of Coronary No-Reflow Phenomenon

Abstract

Coronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but they have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

Prediction of no-reflow phenomenon in patients after primary percutaneous coronary intervention by using optical coherence tomographyA systematic review and meta analysis

“…Coronary no-re ow phenomenon is a mechanism of ongoing myocardial injury, following successful revascularization of an infarct-related coronary artery. This phenomenon occurs at a high rate after PCI and is an independent predictor of poor clinical outcome, potentially leading to heart failure, increased mortality, and malignant arrhythmias 10,11 . The pathogenesis of no-re ow is not fully understood, and multiple factors are associated with the pathogenesis of no-re ow, including atherosclerotic thromboembolism, ischemic injury, reperfusion injury, and increased susceptibility of coronary microcirculation to injury.…”

“…Plaque rupture is associated with a higher incidence of TCFA and large lipid burden, and may be of particular importance in patients presenting with no re ow phenomenon after PCI 20 . Plaque rupture is a major contributor in the setting of thrombosis during an acute myocardial infarction 21 .PCI of the culprit vessel is attempted in the presence of heavy thrombus burden, resulting in further embolization of thrombus into the distal microvasculature 10 . Our study com red that frequency of thrombus was higher in the no re ow group (OR=3.53, 95% CI: 1.76 to 7.09, p=0.0004).…”