Angiogenesis in Vulnerable Atherosclerotic Plaques in Apparently Healthy Human Hearts
pp 210-216
DOI:
https://doi.org/10.7775/rac.v80i3.2139Keywords:
Angiogenesis, Pathologic, Aorta, Plaque, Atherosclerotic, HearthAbstract
Background
Angiogenesis or neovascularization involves the formation of new blood vessels adjacent to preexisting vessels. This vascular proliferation is prevalent in various clinical conditions, such as atherosclerosis. Microvessels in coronary artery atherosclerotic plaques may contribute to plaque instability.
Objectives
The aim of this study was to correlate the presence of angiogenesis in atherosclerotic plaques with the criteria of plaque vulnerability used by the American Heart Association (AHA).
Methods
One hundred and twenty one 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. A semi-quantitative score (scale 0-3) was used to identify of angiogenesis. Univariate and multivariate logistic regression analysis was performed to identify angiogenesis-
related risk factors.
Results
On hundred and forty three high-risk lesions (AHA type IV, V and VI) in the left anterior descending coronary artery (46.3%), the circumflex coronary artery (28.9%) and the right coronary artery (43%) were identified. Angiogenesis had a statistically significant association with the severity of vascular occlusion, inflammatory cell infiltration, presence of a lipid core, fibrosis and periarteritis. A history of hypertension (HT) was associated with angiogenesis only in lesions of the left anterior descending coronary artery (LAD). According to the AHA classification angiogenesis was detected in 1 Type II, 5 Type III, 21 Type IV, 22 Type V, and 7 Type VI plaques.
Conclusions
Angiogenesis in vulnerable plaques was associated with the severity of vascular occlusion, inflammatory cell infiltration, fibrosis and presence of a lipid core, and with a history of HT in LAD lesions. There was no association between angiogenesis and plaque hemorrhage or calcification, suggesting that angiogenesis may anticipate plaque rupture.
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