Abstract 170: Luminal Neovascular Sprouting with Inflammation Contributes to Symptomatic Intraplaque Hemorrhage in Carotid Stenosis
Background and Purpose: Neovascularization of carotid plaques is associated with plaque vulnerability. However, the role of neovascularization in the development of intraplaque hemorrhage (IPH) and the clinical contribution of neovascularization to IPH and symptomatic presentation remain undetermined.
Methods: Consecutive patients with moderate to severe carotid atherosclerosis who underwent carotid endarterectomy were prospectively analyzed from 2010 to 2014. The neovessel appearance was categorized into three groups based on dynamic intraoperative indocyanine green videoangiography: neovessels derived from the endothelium (NVe), neovessels derived from the vasa vasorum (NVv), and no neovessels. Each neovessel pattern was evaluated with respect to clinical, radiological, and pathological findings.
Results: Of 57 patients, 13 exhibited NVe, 33 exhibited NVv, and 11 exhibited no neovessels. There were no significant differences in baseline characteristics among the three groups with the exception of a higher percentage of symptomatic presentations among patients with NVe. Moreover, patients with NVe exhibited larger infarctions than did those with NVv (P=0.04). Pathologically, patients with NVe had more severe IPH (P=0.002), hemosiderin spots (P=0.04), neovessels (P=0.11) and inflammation (P=0.26), all of which were correlated with hyperintensity on time-of-flight magnetic resonance imaging. Interestingly, inflammation was significantly correlated with neovessel formation (R=0.43, P=0.008), hemosiderin spots (R=0.62, P<0.0001), and IPH (R=0.349, P=0.0097), suggesting that inflammation may be a key factor in plaque vulnerability.
Conclusions: Luminal neovascular sprouting with inflammation and lumen communication could clinically contribute to IPH and symptomatic presentation in patients with carotid stenosis. This condition may thus be a key therapeutic target against neovessel formation and inflammation.
Author Disclosures: N. Horie: None. Y. Morofuji: None. M. Morikawa: None. S. Yamaguchi: None. Y. Tateishi: None. T. Izumo: None. K. Hayashi: None. A. Tsujino: None. I. Nagata: None.
- © 2015 by American Heart Association, Inc.