Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death.
BACKGROUND
Coronary thrombosis has been reported to occur most frequently in lipid-rich plaques with rupture of a thin fibrous cap and contact of the thrombus with a pool of extracellular lipid. However, the frequency of coronary artery thrombosis with or without fibrous cap rupture in sudden coronary death is unknown. In this study, we compared the incidence and morphological characteristics of coronary thrombosis associated with plaque rupture versus thrombosis in eroded plaques without rupture.


RESULTS
Fifty consecutive cases of sudden death due to coronary artery thrombosis were studied by histology and immunohistochemistry. Plaque rupture of a fibrous cap with communication of the thrombus with a lipid pool was identified in 28 cases. Thrombi without rupture were present in 22 cases, all of which had superficial erosion of a proteoglycan-rich plaque. The mean age at death was 53 +/- 10 years in plaque rupture cases versus 44 +/- 7 years in eroded plaques without rupture (P < .02). In the plaque-rupture group, 5 of 28 (18%) were women versus 11 of 22 (50%) with eroded plaques (P = .03). The mean percent luminal area stenosis was 78 +/- 12% in plaque rupture and 70 +/- 11% in superficial erosion (P < .03). Plaque calcification was present in 69% of ruptures versus 23% of erosions (P < .002). In plaque ruptures, the fibrous cap was infiltrated by macrophages in 100% and T cells in 75% of cases compared with 50% (P < .0001) and 32% (P < .004), respectively, in superficial erosions. Clusters of smooth muscle cells adjacent to the thrombi were present in 95% of erosions versus 33% of ruptures (P < .0001). HLA-DR expression was more often seen in macrophages and T cells in ruptures (25 of 28 cases) compared with expression in macrophages in superficial erosion arteries (8 of 22 cases, P = .0002).


CONCLUSIONS
Erosion of proteoglycan-rich and smooth muscle cell-rich plaques lacking a superficial lipid core or plaque rupture is a frequent finding in sudden death due to coronary thrombosis, comprising 44% of cases in the present study. These lesions are more often seen in younger individuals and women, have less luminal narrowing and less calcification, and less often have foci of macrophages and T cells compared with plaque ruptures.
Farb
A
A
Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
Burke
A P
AP
Tang
A L
AL
Liang
T Y
TY
Mannan
P
P
Smialek
J
J
Virmani
R
R
D000328:Adult; D002114:Calcinosis / Q000473:pathology; D003324:Coronary Artery Disease / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D003328:Coronary Thrombosis / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D003331:Coronary Vessels / Q000737:chemistry / Q000473:pathology; D016757:Death, Sudden, Cardiac / Q000453:epidemiology / Q000209:etiology*; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D015994:Incidence; D008055:Lipids / Q000032:analysis*; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism; D012422:Rupture, Spontaneous; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D014657:Vasculitis / Q000276:immunology / Q000473:pathology
D006684:HLA-DR Antigens; D008055:Lipids; D011509:Proteoglycans