Intraplaque neovascularization attenuated statin benefit on atherosclerotic plaque in CAD patients: A follow-up study with combined imaging modalities
Intraplaque neovascularization attenuated statin benefit on atherosclerotic plaque in CAD patients: A follow-up study with combined imaging modalities
复制标题
斑块内新生血管形成减弱了他汀类药物对 CAD 患者动脉粥样硬化斑块的益处:联合成像模式的后续研究
DOI:
10.1016/j.atherosclerosis.2019.06.912
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发表时间:
2019-08-01
期刊:
影响因子:
5.3
通讯作者:
Yu, Bo
中科院分区:
文献类型:
--
作者:
Liu, Xinxin;Sun, Changbin;Yu, Bo
Background and aims: Plaque progression increases the risk of a cardiovascular event. This study aims to determine whether intraplaque neovascularization (NV) associates with a greater risk of plaque progression.Methods: Baseline and 12-month follow-up IVUS was used in combination with baseline OCT to assess 164 non-culprit plaques in 118 CAD patients. A generalized estimating equation approach with exchangeable correlation structure was used to correct for the dependency of repeated measurements.Results: Patients were divided into two groups according to NV (52 patients with 62 NV plaques, 66 patients with 102 non-NV plaques). Non-culprit plaques in the NV group exhibited a more frequent occurrence of TCFA (p= 0.004), macrophage (p= 0.005), cholesterol crystal (p= 0.012), calcification (p= 0.030), thinner fibrous cap thickness (FCT) [(86.8 +/- 55.1) vs. (127.4 +/- 70.1) mu m, p= 0.015], larger lipid arc [(219.5 +/- 66.9) vs. (179.8 +/- 61.4), p= 0.002] compared to the non-NV group. A large change in percent atheroma volume (PAV), plaque plus media cross-sectional area (P&M CSA), plaque volume, and plaque burden was observed from baseline to follow-up in the NV group. Changes in P&M CSA, plaque volume, and plaque burden showed significant differences in fibroatheroma with NV. Intraplaque NV could predict a high risk of plaque progression despite statin therapy [OR 6.521 (95% CI 2.457-17.308), p < 0.001].Conclusions: NV might attenuate the benefits of statin therapy in plaque progression. This study may provide a new basis for anti-angiogenic strategies to prevent atherosclerotic plaque progression.