Plaque erosion and acute coronary syndromes: phenotype, molecular characteristics and future directions

Although acute coronary syndromes (ACS) remain one of the leading causes of death, the clinical presentation has changed over the past three decades with a decline in the incidence of ST-segment elevation myocardial infarction (STEMI) and an increase in non-STEMI. This epidemiological shift is at least partially explained by changes in plaque biology as a result of the widespread use of statins. Historically, atherosclerotic plaque rupture of the fibrous cap was thought to be the main culprit in ACS. However, plaque erosion with an intact fibrous cap is now responsible for about one third of ACS and up to two thirds of non-STEMI. Two major research approaches have enabled a better understanding of plaque erosion. First, advanced intravascular imaging has provided opportunities for an 'optical biopsy' and extensive phenotyping of coronary plaques in living patients. Second, basic science experiments have shed light on the unique molecular characteristics of plaque erosion. At present, patients with ACS are still uniformly treated with coronary stents irrespective of the underlying pathobiology. However, pilot studies indicate that patients with plaque erosion might be treated conservatively without coronary stenting. In this Review, we discuss the patient phenotype and the molecular characteristics in atherosclerotic plaque erosion and provide our vision for a potential major shift in the management of patients with plaque erosion.