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22.05.2018 | Original Article | Ausgabe 11/2018 Open Access

Heart and Vessels 11/2018

Stabilization of symptomatic carotid atherosclerotic plaques by statins: a clinico-pathological analysis

Zeitschrift:
Heart and Vessels > Ausgabe 11/2018
Autoren:
Takao Konishi, Naohiro Funayama, Tadashi Yamamoto, Daisuke Hotta, Ryota Nomura, Yusuke Nakagaki, Takeo Murahashi, Kenji Kamiyama, Tetsuyuki Yoshimoto, Takeshi Aoki, Shinya Tanaka
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Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s00380-018-1193-6) contains supplementary material, which is available to authorized users.

Abstract

Human and animal studies have revealed a stabilization of atherosclerotic plaques by statins. However, the stabilization of human carotid plaques has not been thoroughly described pathologically. This analysis explored the relationship between statin therapy and plaque stability in carotid endarterectomy (CEA) specimens. We analyzed specimens harvested between May 2015 and February 2017, from 79 consecutive patients presenting with > 70% carotid artery stenoses, of whom 66 were untreated (group 1) and 13 treated (group 2) with a statin. Immunohistochemistry was performed, using an endothelial specific antibody to CD31, CD34 and platelet derived growth factor receptor-β. The prevalence of plaque ruptures (P = 0.009), lumen thrombi (P = 0.009), inflammatory cells (P = 0.008), intraplaque hemorrhages (P = 0.030) and intraplaque microvessels (P < 0.001) was significantly lower in group 2 than in group 1. Among 66 patients presenting with strokes and infarct sizes > 1.0 cm3 on magnetic resonance imaging, the mean infarct volume was significantly smaller (P = 0.031) in group 2 (4.2 ± 2.5 cm3) than in group 1 (8.2 ± 7.1 cm3). The difference in mean concentration of low-density lipoprotein cholesterol between group 1 (121 ± 32 mg/dl) and group 2 (105 ± 37 mg/dl) was non-significant (P = 0.118). This analysis of plaques harvested from patients undergoing CEA suggests that statin therapy mitigates the plaque instability, which, in patients presenting with strokes, might decrease infarct volume.

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