Microvascular obstruction is caused by atherothrombosis in patients with acute coronary syndrome undergoing percutaneous coronary intervention.

The diagnosis of acute coronary syndrome (ACS) is primarily based on the mode of clinical presentation and is a term used for any conditions suggesting the acute induction of myocardial ischemia. The precise molecular and cellular triggers that lead to ACS remain poorly understood; however, histopathologic studies have illustrated several mechanisms that may explain the sudden onset of symptoms in ACS patients. The most common substrate underlying ACS is thought to be rupture of a vulnerable plaque that contains a necrotic core covered by a fibrous cap. The term, thin-cap fibroatheroma (TCFA) is used to describe vulnerable plaque because histomorphometric analysis of ruptured plaques revealed fibrous cap thickness to be 65 m in 95% of the lesions.1 Once the disruption of the fibrous cap occurs, the lesion is no longer classified as a TCFA. In morphological measurement, plaque ruptures have the largest necrotic core, 3.8 5.5 mm, followed by TCFAs, 1.7 1.1 mm, with 75% of the lesions involving 120 degree of circumferential arc; whereas thick cap fibroatheromas have the smallest necrotic core (1.2 2.2 mm).2,3 The highest positive remodeling index is seen in plaque ruptures, followed by plaque hemorrhage, TCFA, healed plaque rupture, and fibroatheroma.4 Also, plaque rupture and TCFA are located predominantly in the proximal portions of the coronary tree.5 Following the rupture of plaque, the exposure of necrotic core material to blood flow leads to thrombotic luminal obstruction with or without distal embolization of platelet-rich thrombus, or less commonly, atherosclerotic debris.