No-reflow phenomenon in acute myocardial infarction: Relieve pressure from the procedure and focus attention to the patient

Re-opening of the culprit epicardial coronary artery in the early phase of an acute myocardial infarction does not mandatorily translate into an effective myocardial reperfusion. This is the case of the socalled “no-reflow phenomenon”, which refers to the failure to restore perfusion to themicrovasculature supplying themyocardium, generally due to thrombotic occlusion of the pre-capillary and capillary bed. In STelevationmyocardial infarction (STEMI), the incidence of no-reflow has been reported to be comprised between 11 and 41%, with a variability depending on patient, vessel, and lesion factors [1] Its appearance is associated with a worse prognosis, especially in term of short and long mortality [2,3]. Angiographic diagnosis requires documentation of an impaired (≤2) Myocardial Blush Grade (MGB), whereas a preserved TIMI flow (grade 3) alone, although associated with a lower risk of noreflow, is not sufficient. Since there is no definitive treatment of noreflow once it has occurred, prevention plays a pivotal role to avoiding this harmful complication. Although the mechanisms determining noreflow are not still completely understood, it is now clear that its pathogenesis is multifactorial. In fact, injury related to ischemia, reperfusion, endothelial dysfunction, distal thromboembolism and microvascular spasm are considered the principal underlying determinants [4]. A number of clinical, serologic, angiographic and procedural parameters have been identified in several studies as predictors of no-reflow. Due to heterogeneity of the populations studied, there is a disagreement on the relative importance of some of these parameters. Not surprisingly, a high thrombus burden increases the risk of no-reflow [5,6], due to dislodgement of atherothrombotic debris causing distal embolization [7]. However, thrombus burden is only one predictor of no reflow with other mechanisms that have to be searched in the concomitant presence of multiple, especially clinical, pro-thrombotic and/or pro-inflammatory patient characteristics. In fact, Mazhar et al. [6] showed in a cohort of 781 patients underwent primary percutaneous coronary intervention (pPCI) that no-reflow occurred more frequently in the older (N60 years), in the presence of high thrombus burden and in case of delayed presentation from symptom onset (N4 h). Interestingly, no lesion and pharmacological associations were documented.