Why the study?
Despite successful revascularization, myocardial underperfusion (no-reflow) can persist and confers a worse prognosis, with complicated multifactorial pathogenesis warranting description of its mechanisms and predictors.
The no-reflow phenomenon in STEMI is multifactorial, and identifying its specific pathogenetic components and predictors in individual patients may guide personalized treatment.
May guide personalized no-reflow prevention in STEMI; extends mechanistic models of its pathogenesis.
Despite successful and timely revascularization of the infarct-related artery, myocardial tissue remains underperfused in some patients. This condition is known as the no-reflow phenomenon, which is associated with a worse prognosis. The first part of the systematic review on no-reflow focuses on description of the no-reflow pathogenesis and predictors. This phenomenon has a complicated, multifactorial pathogenesis, including distal embolization, ischemic injury, reperfusion injury, and a component of individual predisposition. Meanwhile, this phenomenon undergoes spontaneous regression in some patients. Several studies have demonstrated the role of definite biomarkers and clinical indexes as risk predictors for no-reflow. The significance of each pathogenetic component of no-reflow is suggested to be different in different patients, which may warrant an individualized approach in the treatment.
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Zhuravlev et al. (2021) studied this question.
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