Abstract
Background: Pathologic angiogenesis has been implicated in the development of high-risk plaques where nascent immature leaky vessels become the primary source of intraplaque hemorrhage contributing to necrotic core expansion. The stage of lesion progression, however, favoring an angiogenic response has not been identified. Methods and Results: Multiple coronary lesions collected from 73 sudden coronary death victims at autopsy were examined. Plaque morphologies included pathologic intimal thickening (PIT), fibroatheromas whose cores were in an early stage (eFA) or late stage (lFA) of necrosis, thin-cap fibroatheromas (TCFA) and ruptures (pR). Lesions were characterized by immunostaining using specific markers directed against endothelial cells (CD31/CD34), smooth muscle cells (α-actin), macrophages (CD68), and T-lymphocytes (CD45RO, CD4). Mean intraplaque vessel densities per mm 2 between lesions with PIT and eFA increased significantly (PIT= 15.84±16.73 vs. eFA= 42.07±40.70, p=0.0054) where maximal numbers of vessels were found in pR (66.57±33.42). Overall, intraplaque vessels associated with actin 3 SMCs, were generally <10%, suggesting a more immature phenotype. Increased vessel densities coincided with greater numbers of inflammatory macrophages and T-cells. Notably, T-cell numbers in areas with high intraplaque vessel densities increased approximate 3-fold between lesions with PIT and eFA (PIT= 62.62±76.50 vs. eFA= 182.33±171.54, p=0.0043) with maximal numbers displayed in TCFAs and pRs, in particular at the intimal/medial border. Populations infiltrating T cells were predominantly CD4 3 and most of these appeared to be activated (human leukocyte antigen DR positive). Conclusion: Atherosclerotic coronary arteries express a latent proangiogenic phenotype coinciding with a localized increased in activated CD4 3 T-cells and early plaque necrosis.
Published Version
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