What is the pathophysiology of vulnerable plaque erosion?

Updated: Dec 30, 2019
  • Author: Elena R Ladich, MD; Chief Editor: Allen Patrick Burke, MD  more...
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Answer

Plaque erosion is defined as an acute thrombus in direct contact with the intima in an area of denuded endothelium. [9]  Thus, plaque events ensue as a result of an intimal fibroatheroma in the coronary artery wall becoming vulnerable to erosion or rupture. [2] Histologically, luminal thrombus is present with an underlying base rich in proteoglycans and smooth muscle cells with minimal inflammation. Most erosions lack a necrotic core but when present, a thick fibrous cap sequesters the necrotic core, preventing communication with the lumen. In addition, eroded lesions tend to be eccentric and are rarely calcified. These plaques account for 25-40% of all coronary thrombi in sudden coronary death (see the following image).

Vulnerable plaque pathology. Case study: Plaque er Vulnerable plaque pathology. Case study: Plaque erosion in a 33-year-old female. The patient complained of chest pain for 2 weeks and was discharged form the emergency department with a diagnosis of anxiety. A: The left anterior descending coronary artery contains a luminal thrombus (Th) with a more than 80% cross-sectional luminal narrowing by atherosclerotic plaque. The underlying lesion shows a necrotic core (NC) consistent with a fibroatheroma (Movat actin positive smooth; pentachrome, ×20). B: The eroded surface contains muscle cells (smooth muscle cells [SMCs]) (×200). C: Macrophages. D: T cells. E and F: Platelet (PLT) (anti-CD61) and fibrin (anti-fibrin II) staining show partial organization of the thrombus (×100).

Plaque erosion occurs primarily in patients younger than age 50 years and represents the majority of acute coronary thrombi in premenopausal women, especially women with a history of tobacco use. Approximately, 20-25% of acute myocardial infarctions occurring in hospitalized patients are due to plaque erosion, and the relative proportion of erosions (compared with plaque rupture) is higher in women than men.

Autopsy studies in sudden coronary death victims have shown that greater than 85% of thrombi in erosions exhibit late stages of healing characterized by acute inflammatory cell lysis, invasion by smooth muscle cells and/or endothelial cells, or organized layers of smooth muscle cells and proteoglycans with varying degrees of platelet/fibrin layering, whereas in ruptures only half of thrombi show healing. [10] Postmortem coronary thrombi superimposed on eroded plaques have been shown to contain a higher density of myeloperoxidase-positive cells than those superimposed on ruptured plaques. [11] In addition, circulation blood myeloperoxidase levels are elevated in patients with ACS with erosion as compared with those with rupture, suggesting that elevations in selective inflammatory biomarkers may reflect specific acute coronary events. [11]


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