Department of Cardiology, Beijing Anzhen Hospital, Affiliated to Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Department of Emergency, Beijing Friendship Hospital, Capital Medical University, Beijing, China; and.
J Cardiovasc Pharmacol. 2021 Oct 1;78(4):544-550. doi: 10.1097/FJC.0000000000001088.
Our study aimed to investigate the effect of atorvastatin on plaque calcification by matching the results obtained by 18F-sodium fluoride (18F-NaF) positron emission tomography (PET)/computed tomography (CT) with data from histologic sections.
The rabbits were divided into 2 groups as follows: an atherosclerosis group (n = 10) and an atorvastatin group (n = 10). All rabbits underwent an abdominal aortic operation and were fed a high-fat diet to induce atherosclerosis. Plasma samples were used to analyze serum inflammation markers and blood lipid levels. 18F-NaF PET/CT scans were performed twice. The plaque area, macrophage number and calcification were measured, and the data from the pathological sections were matched with the 18F-NaF PET/CT scan results. The mean standardized uptake value (0.725 ± 0.126 vs. 0.603 ± 0.071, P < 0.001) and maximum standardized uptake value (1.024 ± 0.116 vs. 0.854 ± 0.091, P < 0.001) significantly increased in the atherosclerosis group, but only slightly increased in the atorvastatin group (0.616 ± 0.103 vs. 0.613 ± 0.094, P = 0.384; 0.853 ± 0.099 vs.0.837 ± 0.089, P < 0.001, respectively). The total calcium density was significantly increased in rabbits treated with atorvastatin compared with rabbits not treated with atorvastatin (1.64 ± 0.90 vs. 0.49 ± 0.35, P < 0.001), but the microcalcification level was significantly lower. There were more microcalcification deposits in the areas with increased radioactive uptake of 18F-NaF.
Our study suggests that the anti-inflammatory activity of atorvastatin may promote macrocalcification but not microcalcification within atherosclerotic plaques. 18F-NaF PET/CT can detect plaque microcalcifications.
本研究旨在通过将 18F-氟化钠(18F-NaF)正电子发射断层扫描(PET)/计算机断层扫描(CT)的结果与组织学切片数据相匹配,来探讨阿托伐他汀对斑块钙化的影响。
将兔子分为 2 组:动脉粥样硬化组(n = 10)和阿托伐他汀组(n = 10)。所有兔子均接受腹主动脉手术,并给予高脂饮食以诱导动脉粥样硬化。检测血浆样本以分析血清炎症标志物和血脂水平。进行了 2 次 18F-NaF PET/CT 扫描。测量斑块面积、巨噬细胞数量和钙化程度,并将病理切片数据与 18F-NaF PET/CT 扫描结果相匹配。动脉粥样硬化组的平均标准化摄取值(0.725 ± 0.126 比 0.603 ± 0.071,P < 0.001)和最大标准化摄取值(1.024 ± 0.116 比 0.854 ± 0.091,P < 0.001)显著增加,但阿托伐他汀组仅略有增加(0.616 ± 0.103 比 0.613 ± 0.094,P = 0.384;0.853 ± 0.099 比 0.837 ± 0.089,P < 0.001)。与未接受阿托伐他汀治疗的兔子相比,接受阿托伐他汀治疗的兔子的总钙密度显著增加(1.64 ± 0.90 比 0.49 ± 0.35,P < 0.001),但微钙化水平显著降低。在 18F-NaF 放射性摄取增加的区域有更多的微钙化沉积。
本研究表明,阿托伐他汀的抗炎活性可能促进动脉粥样硬化斑块内的大钙化,但不促进微钙化。18F-NaF PET/CT 可检测斑块微钙化。