Which pathologic findings are characteristic of plaque erosion in atherosclerosis?

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

Although plaque rupture is the most common cause of coronary thrombosis, acute coronary syndromes may occur in the absence of rupture. As mentioned earlier, thrombi may occur as a result of three different events: plaque rupture, plaque erosion, or, rarely, a calcified nodule (see Etiology). Plaque erosion is characterized by absence of the endothelium at the site of erosion, with exposed intima composed of smooth muscle cells and proteoglycans, as well as typically minimal inflammation.

In a series of 20 patients who died with acute myocardial infarction, van der Wal et al found plaque ruptures in 60% of lesions with thrombi, whereas the remaining 40% showed "superficial erosion." [26] The term "erosion" was chosen because the luminal surface beneath the thrombus lacked endothelial cells. In these lesions, the thrombus was confined to the most luminal portion of the plaque, and there was an absence of ruptures following serial sectioning of these lesions.

In addition, the authors' laboratory studied nearly 100 cases of sudden coronary death and found that 60% of all thrombi could be attributed to plaque rupture and 40% to erosions. Morphologically, major differences exist in the cellular composition of ruptured versus erosion lesions. Unlike the prominent fibrous cap inflammation described in ruptures, eroded surfaces contain few macrophages (rupture 100% vs erosion 50%, P< 0.0001) and T lymphocytes (rupture 75% vs erosion 32%, P< 0.004). Cell activation, indicated by human lymphocyte antigen (HLA)-DR staining, was identified in macrophages and T cells in 89% of plaque ruptures and in 36% of plaque erosions (P = 0.0002). [27] The smooth muscle cells near the erosion site appeared "activated," often displaying bizarre shapes with hyperchromatic nuclei and prominent nucleoli. The incidence of calcification was also less common in erosion than in ruptures.

The authors have also shown that more than 85% of thrombi in erosions exhibited 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 one half of thrombi showed healing. [28] 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. [29] Also, circulation blood myeloperoxidase levels are elevated in patients with acute coronary sinus with erosion compared with those with rupture, suggesting that elevations in selective inflammatory biomarkers may reflect specific acute coronary events.

Probe electrospray ionization mass spectrometry appears to have the potential to detect new biomarkers of atherosclerosis (eg, cholesterol sulfate, phospholipid PE18:0/24:0), although current findings are from animal models (rabbits). [30]


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