Key result
Angiogenesis in vulnerable plaques was significantly associated with vascular occlusion, inflammation, fibrosis, and lipid cores across 143 high-risk coronary lesions.
Cross-Sectional (n=121)
Angiogenesis in coronary atherosclerotic plaques is significantly associated with features of plaque vulnerability, suggesting it may play a role in anticipating plaque rupture.
Angiogenesis correlates with multiple vulnerability features in high-risk lesions; hypothesis-generating and requires prospective validation before any clinical application.
Background Angiogenesis or neovascularization involves the formation of new blood vessels in the adjacency of preexisting vessels . This vascular proliferation is prevalent in various clinical circumstances, such as atherosclerosis. Microvessels in coronary artery atherosclerotic plaques may contribute to plaque instability. Objectives To correlate the presence of angiogenesis in atherosclerotic plaques with the criteria of vulnerable plaque used by the American Heart Association (AHA). Ma terial and Methods A total of 121 hearts from non-diabetic and apparently healthy transplant donors older than 40 years were selected. The coronary arteries were examined and all areas of cross-sectional luminal narrowing underwent histological, immunohistochemical and morphometric studies. We used a semi-quantitative score (scale 0-3) for identification of angiogenesis. Univariate and multivariate logistic regression analysis was performed to identify angiogenesis-related risk factors. Results We found 143 high-risk lesions (AHA type IV, V and VI) in the left anterior descending coronary artery (46.3%), in the circumflex coronary artery (28.9%) and in the right coronary artery (43%). Angiogenesis had a statistically significant association with the severity of vascular occlusion, inflammatory cell infiltration, the presence of a lipid core, fibrosis and periarteritis. The history of HT was associated with angiogenesis only in lesions of the LAD artery. According to the AHA classification we detected angiogenesis in one lesion Type II; five in plaques Type III; 21 in lesions Type IV; 22 in Type V; and 7 in plaques Type VI. Conclusions Angiogenesis in vulnerable plaques was associated with the severity of vascular occlusion, inflammatory cell infiltration, fibrosis and the presence of a lipid core, HT in lesions of the LAD. There was no association between plaque hemorrhage or calcification, suggesting that angiogenesis may anticipate plaque rupture.
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Duronto et al. (2012) conducted a cross-sectional in Atherosclerosis (n=121). Angiogenesis vs. Absence or lower degree of angiogenesis was evaluated on Association of angiogenesis with AHA criteria for vulnerable plaques. Angiogenesis in vulnerable plaques was significantly associated with vascular occlusion, inflammation, fibrosis, and lipid cores across 143 high-risk coronary lesions.
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