Kwon Osung, Kang Soo-Jin, Kang Se Hun, Lee Pil Hyung, Yun Sung-Cheol, Ahn Jung-Min, Park Duk-Woo, Lee Seung-Whan, Kim Young-Hak, Lee Cheol Whan, Han Ki Hoon, Park Seong-Wook, Park Seung-Jung
From the Department of Cardiology (O.K., S.-J.K., S.H.K., P.H.L., J.-M.A., D.-W.P., S.-W.L., Y.-H.K., C.W.L., K.H.H., S.-W.P., S.-J.P.) and Department of Biostatistics (S.-C.Y.), University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
Circ Cardiovasc Imaging. 2017 Jul;10(7). doi: 10.1161/CIRCIMAGING.116.005934.
The mechanism of statin for atheroma stabilization remains unclear. We aimed to assess the relationship between on-treatment changes in serum inflammatory biomarker levels and plaque composition in differed nonculprit coronary lesions.
The changes in serum biochemical values, and intravascular ultrasound data were evaluated in 218 patients with virtual histology (VH)-intravascular ultrasound-defined fibroatheroma-containing segments after 12-month rosuvastatin treatment. When stratifying patients into quartiles according to the change in high-sensitivity C-reactive protein (hsCRP), there was a significant positive linear relationship for the changes in %necrotic core (coefficient, 1.31; standard error, 0.54) and %dense calcium volumes (coefficient, 0.80; standard error, 0.27), but a negative linear relationship for the changes in %fibrous (coefficient, -0.94; standard error, 0.45) and %fibrofatty volumes (coefficient, -1.17; standard error, 0.56; all <0.05). The decrease in hsCRP (-1.2±3.9 versus 0.5±3.4 mg/L; =0.02) was greater in those without VH-defined thin-cap fibroatheroma (TCFA, defined as >30° of necrotic core abutting the lumen in 3 consecutive slices) than those with VH-TCFA at follow-up. Diabetes mellitus, a larger normalized total atheroma volume, and the presence of VH-TCFA at baseline predicted the presence of VH-TCFA at follow-up (odds ratio, 4.01, 1.18, and 9.21, respectively; all <0.05), whereas the change in hsCRP showed a trend (odds ratio, 1.19; =0.07). The change in low-density lipoprotein-cholesterol had no relationship with the changes in hsCRP or plaque compositions.
With 12-month rosuvastatin therapy, a greater hsCRP reduction (not low-density lipoprotein-cholesterol) was associated with a greater decrease in %necrotic core volume and the absence of VH-TCFA, indicating a link between the anti-inflammatory action of statin and plaque stabilization by reducing NC and reinforcing fibrous cap.
URL: https://www.clinicaltrials.gov. Unique identifier: NCT00997880.
他汀类药物稳定动脉粥样硬化斑块的机制尚不清楚。我们旨在评估不同非罪犯冠状动脉病变中治疗期间血清炎症生物标志物水平变化与斑块成分之间的关系。
对218例经瑞舒伐他汀治疗12个月后采用虚拟组织学（VH）-血管内超声定义的含纤维粥样斑块节段的患者，评估血清生化值和血管内超声数据的变化。根据高敏C反应蛋白（hsCRP）变化将患者分为四分位数，坏死核心百分比（系数为1.31；标准误为0.54）和致密钙体积百分比（系数为0.80；标准误为0.27）的变化呈显著正线性关系，而纤维百分比（系数为-0.94；标准误为0.45）和纤维脂肪体积百分比（系数为-1.17；标准误为0.56；均P<0.05）的变化呈负线性关系。随访时，无VH定义的薄帽纤维粥样斑块（TCFA，定义为连续3个切片中坏死核心邻接管腔>30°）患者的hsCRP降低幅度（-1.2±3.9 对0.5±3.4 mg/L；P=0.02）大于有VH-TCFA的患者。糖尿病、更大的标准化总粥样斑块体积以及基线时存在VH-TCFA可预测随访时存在VH-TCFA（比值比分别为4.01、1.18和9.21；均P<0.05），而hsCRP变化呈趋势性（比值比为1.19；P=0.07）。低密度脂蛋白胆固醇变化与hsCRP或斑块成分变化无关。
瑞舒伐他汀治疗12个月时，hsCRP更大幅度降低（而非低密度脂蛋白胆固醇）与坏死核心体积百分比更大幅度降低及无VH-TCFA相关，表明他汀类药物的抗炎作用与通过减少坏死核心和加固纤维帽实现斑块稳定之间存在联系。
