Plaque erosion: a new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes

Abstract

Pathology and in vivo imaging studies have identified superficial plaque erosion as a frequent and important mechanism underlying acute coronary syndromes (ACS). In contrast with plaque rupture, the pathophysiological mechanisms leading to plaque erosion remain poorly understood. The advent of intravascular imaging techniques, particularly optical coherence tomography, has aided understanding of this mode of ACS in vivo by complementing previous insights from pathology studies. Appreciation of the distinct biological and clinical mechanisms of plaque erosion points to the possibility of tailored management strategies for patients presenting with ACS.

Figure 1

Left: a thin cap fibroatheroma with ruptured fibrous cap and luminal thrombi is shown. A large necrotic core communicates with the lumen. Middle: erosion occurs over lesions rich in proteoglycans and smooth muscle cells. Thrombus is attached in an area that lacks endothelium. These lesions have few inflammatory cells, in particular of mononuclear leukocytes. Right: a calcified nodule is protruding into the lumen through a disrupted thin fibrous cap (adapted from Virmani et al.¹⁰). NC, necrotic core; Th, thrombi.

Figure 2

A schema of a potential pathophysiological pathway to superficial erosion (adapted from Quillard et al.²¹). PAMPs, pathogen-associated molecular patterns; DAMPs, danger-associated molecular patterns; TLR2, Toll-like receptor-2; MMP, matrix metalloproteinase; HOCl, hypochlorous acid; MPO, myeloperoxidase; NETs, neutrophil extracellular traps.

Figure 3

An intact fibrous cap separates erosion from rupture or calcified nodule. In lesions without an intact fibrous cap, other characteristics of the underlying plaque further categorize the atheroma disruption as due to rupture or to penetration by a calcified nodule (adapted from Jia et al.³⁴). OCT, optical coherence tomography.

Figure 4

Optical coherence tomography imaging of a ruptured plaque shows circumferential superficial lipid and ruptured fibrous cap at 6 o’clock communicating with an empty cavity. A plaque complicated by erosion shows preserved vascular structure with larger lumen and the appearance of a platelet-rich thrombus. A calcific nodule resides at 1–3 o’clock. Such deposits are often seen in the area of substantive calcification.