Abstract
Plaque erosion is the second most common cause of acute coronary syndromes. It occurs in the absence of fibrous cap rupture, and typically shows luminal thrombi in direct contact with an intimal surface that lacks endothelial cells (ECs) but is enriched in smooth muscle cells and proteoglycan matrix. First described almost thirty years ago, plaque erosion accounts for an increasing fraction of acute coronary syndromes, but its frequency decreases with age in both men and women. Although a higher prevalence of erosion in women was suggested based on early observations, this has not been clearly borne out in more recent studies. The pathogenesis of plaque erosion is largely unknown; nevertheless, potential etiologic factors include disturbed flow and altered endothelial shear stress, elements of the innate and adaptive immune systems, hyaluronan and Toll-like receptor 2 signaling, activation of the NRF2 transcription factor, matrix metallopeptidase-mediated disruption of EC-extracellular matrix interactions, and distinct thrombotic mechanisms. While several of these factors are also linked to plaque rupture, existing evidence suggests that the biology of plaque erosion is substantially different from that of rupture; therefore, a deeper understanding of the molecular basis of coronary thrombosis associated with plaque erosion may guide the development of biomarkers and specific preventive or therapeutic strategies for acute coronary syndromes with intact fibrous cap. Such progress would pave the way for personalized care of these patients.