Which pathologic findings are characteristic of plaque rupture in atherosclerosis?

Updated: Dec 30, 2019
  • Author: Elena R Ladich, MD; Chief Editor: Allen Patrick Burke, MD  more...
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Plaque rupture is defined as an area of fibrous cap disruption in which the overlying thrombus is in contact with the underlying necrotic core. The fibrous cap is composed of type I collagen with varying degrees of macrophages and lymphocytes and very few, if any, alpha-actin positive smooth muscle cells. The luminal thrombus is platelet rich at the rupture site. Plaque ruptures are most prevalent in the proximal coronary artery near branch points and are frequently found in the proximal left anterior descending coronary artery, followed by the right and left circumflex coronary arteries.

The causes of plaque rupture are poorly understood, but responsible factors include expression of factors that weaken the fibrous cap, such as MMPs, enzymes (eg, myeloperoxidases) produced by inflammatory cells, high shear regions, stress points, macrophage calcification, and iron deposition. Data are also beginning to emerge that demonstrate critical differences in gene expression between stable and unstable atherosclerotic plaques. [20] In one of these studies, differential expression of 18 genes associated with lesion instability included the metalloproteinase ADAMDEC1, retinoic acid receptor responser-1, cysteine protease legumain (a potential activator of MMPs) and cathepsins. [20]

More recently, in an autopsy study, investigators reported an association between B lymphocytes and macrophages in the perivascular adipose tissue (PvAT) with coronary atherosclerosis. [21]  They concluded that the "density of CD20+ B lymphocytes and CD68+ macrophages in periplaque PvAT was increased with plaque size, and the CD68+ macrophages were greater near unstable atherosclerotic plaques than near stable lesions." Moreover, there was more intense inflammation in the periplaque PvAT than in the PvAT distal to the atherosclerotic plaques. [21]

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