Primary PCI: time to change focus from epicardial reperfusion towards protection of the microvasculature.

Myocardial tissue perfusion remains compromised in 30-40% of patients with ST-segment elevation myocardial infarction (STEMI) despite restored epicardial patency after primary percutaneous coronary intervention (pPCI). This phenomenon is attributed to microvascular dysfunction secondary to numerous pathophysiological mechanisms, including distal embolisation of plaque and thrombus material. Its association with larger post-infarction myocardial necrosis, impaired left ventricular recovery, and worse clinical outcome illustrates the pertinence of a comprehensive armamentarium for the diagnosis, protection and treatment of microvascular dysfunction in STEMI patients. Current strategies to protect the microvasculature during pPCI are based on the assumption that distal embolisation of thrombotic and atheromatous debris is the main mechanism precipitating impaired myocardial tissue perfusion. However, recent findings suggest that this assumption is only true for the border zone of the ischaemic myocardium, whereas the infarct core consists of intramyocardial haemorrhage secondary to microvascular destruction, rather than obstruction. This observation has pertinent implications for contemporary and future adjuvant treatment strategies in STEMI patients. In this review, we provide an overview of the currently available armamentarium to assess the microvasculature, review contemporary strategies in pPCI to protect the myocardium, and discuss novel insights into microvascular pathophysiology that may help guide our focus from the coronary arteries to the microvasculature.