Editorial Comment: Serotonin: another player in the complex pathogenesis of no-reflow phenomenon

Myocardial no-reflow after primary percutaneous coronary intervention (PCI) or thrombolysis may negate advantages of reperfusion therapy. Indeed, compromised microcirculation does not allow providing normal blood flow to the myocardium despite an epicardial vessel reopening. No-reflow has a prognostic role for both mortality and adverse left ventricular remodelling which is the cause of left ventricular failure (1). In humans, no-reflow is caused by the variable combination of four pathogenetic components: 1) distal atherothrombotic embolization; 2) ischemic injury; 3) reperfusion injury; and 4) susceptibility of coronary microcirculation to injury. For each of them, it is possible to detect different predictors thus allowing specific therapies to be used in order to prevent no-reflow phenomenon (2). Importantly, both distal embolization and ischemiareperfusion injury are associated with release of potent vasoconstrictors, which further impair the microcirculation.