A comparative study on the characteristics of carotid plaques in overweight and non-overweight people
-
摘要: 目的 比较超重和非超重人群颈动脉粥样硬化斑块之间不同的病理特征,探索BMI水平和斑块特征的关系。方法 入选患者80例,根据体重指数(BMI)分为超重/肥胖组(40例)和正常/偏瘦组(40例)。收集入选者一般临床资料及血清学指标,对斑块进行组织病理学检查。结果 超重/肥胖组斑块平滑肌细胞、钙化中重度染色比例显著低于正常/偏瘦组(P < 0.05);2组患者斑块在巨噬细胞、胶原纤维、斑块内出血、脂核大小上差异无统计学意义(P>0.05)。超重/肥胖组斑块新生血管密度显著高于正常/偏瘦组(P < 0.05)。BMI水平与斑块内新生血管密度存在正相关(r=0.240,P < 0.05),BMI为斑块钙化的独立保护因素(P < 0.05)。超重/肥胖组斑块易损指数显著高于正常/偏瘦组(P < 0.05),BMI与斑块易损指数呈显著正相关(r=0.267,P < 0.05)。结论 超重人群颈动脉粥样硬化严重狭窄部位斑块钙化程度低,新生血管密度高,超重人群斑块比非超重人群斑块易损指数更高。Abstract: Objective To compare the different pathological features of carotid atherosclerotic plaques between overweight and non-overweight people, and to explore the relationship between BMI level and plaque characteristics.Methods A total of 80 patients were divided into the overweight/obesity group (n= 40) and normal/lean group (n= 40) according to body mass index (BMI). The general clinical data and serological indexes were collected, and the plaques were examined by histopathology.Results The proportion of moderate and severe staining of smooth muscle cells and calcification in the overweight/obesity group was significantly lower than that in the normal/lean group (P < 0.05). There was no significant difference in macrophage, collagen fiber, plaque hemorrhage, and fat core size between the two groups (P > 0.05). The neovascularization density in the overweight/obesity group was significantly higher than that in the normal/lean group (P < 0.05). There was a positive correlation between BMI level and neovascularization density in plaque (r= 0.240, P < 0.05), and BMI was an independent protective factor of plaque calcification. The plaque vulnerability index in overweight/obesity group was significantly higher than that in normal/lean group (P < 0.05), and there was a significant positive correlation between BMI and plaque vulnerability index (r= 0.267, P < 0.05).Conclusion Carotid atherosclerotic plaque calcification is lower and neovascularization density is higher in overweight people. The plaque vulnerability index in overweight people is higher than that in non-overweight people.
-
Key words:
- atherosclerosis /
- obesity /
- BMI /
- calcification /
- neovascularization /
- vulnerable plaque
-
表 1 2组一般资料比较
Table 1. Comparison of general data between the two groups
例(%), X±S, M(P25, P75) 项目 超重/肥胖(40例) 正常/偏瘦(40例) P 年龄/岁 64.73±7.07 66.33±7.58 0.332 男性 35(87.5) 35(87.5) 1.000 BMI/(kg·m-2) 27.37±1.66 22.17±1.50 0.000 有症状 23(57.5) 20(50.0) 0.501 高血压史 37(92.5) 21(52.5) 0.000 糖尿病史 10(25.0) 8(20.0) 0.592 血脂异常史 35(87.5) 30(75.0) 0.152 冠心病史 16(40.0) 11(27.5) 0.237 吸烟史 22(56.4) 24(60.0) 0.746 饮酒史 22(56.4) 18(45.0) 0.311 他汀类药物 28(70.0) 23(57.5) 0.245 阿司匹林/氯吡格雷 34(85.0) 27(67.5) 0.066 TC/(mmol·L-1) 3.64±0.82 3.54±0.71 0.571 TG/(mmol·L-1) 1.41(1.04,1.71) 1.03(0.90,1.38) 0.007 HDL-C/(mmol·L-1) 1.02±0.28 1.11±0.27 0.162 LDL-C/(mmol·L-1) 2.05±0.57 1.91±0.53 0.251 sdLDL-C/(mmol·L-1) 0.55(0.41,0.76) 0.37(0.32,0.63) 0.004 FPG/(mmol·L-1) 5.71±1.20 5.32±1.04 0.134 BUN/(mmol·L-1) 5.51±1.20 5.58±1.82 0.846 Cr/(μmol·L-1) 73.65±11.30 76.13±19.17 0.484 Hcy/(μmol·L-1) 12.75(10.35,16.23) 14.50(10.60,17.20) 0.757 UA/(μmol·L-1) 350.71±84.56 317.97±77.75 0.081 表 2 2组斑块特征比较
Table 2. Comparison of plaque characteristics between the two groups
例(%), X±S, M(P25, P75) 项目 超重/肥胖(40例) 正常/偏瘦(40例) P 巨噬细胞 0.653 无/轻度 17(42.5) 19(47.5) 中/重度 23(57.5) 21(52.5) 平滑肌细胞 0.044 无/轻度 23(57.5) 14(35.0) 中/重度 17(42.5) 26(65.0) 胶原纤维 0.592 无/轻度 10(25.0) 8(20.0) 中/重度 30(75.0) 32(80.0) 钙化 0.041 无/轻度 28(70.0) 19(47.5) 中/重度 12(30.0) 21(52.5) 斑块内出血 0.633 无 26(65.0) 28(70.0) 有 14(35.0) 12(30.0) 脂核大小 0.361 ≤10% 14(35.0) 18(45.0) > 10% 26(65.0) 22(55.0) 巨噬细胞含量/% 0.62(0.27,0.99) 0.45(0.17,0.97) 0.398 平滑肌细胞含量/% 4.81±2.79 5.40±2.38 0.328 胶原纤维含量/% 37.79±16.80 38.53±16.62 0.845 新生血管密度/(个·热点-1) 7.32±3.93 5.52±3.00 0.024 表 3 斑块钙化的单因素logistic回归模型
Table 3. Univariate logistic regression analysis of calcification
因素 标准回归系数 OR值 95% CI P 年龄 0.049 1.050 0.985~1.120 0.134 BMI -0.176 0.839 0.716~0.983 0.029 吸烟史 -0.168 0.845 0.340~2.098 0.717 饮酒史 -0.269 0.764 0.312~1.873 0.556 他汀类药物 -0.216 0.806 0.317~2.047 0.650 TC -0.239 0.787 0.431~1.438 0.437 TG 0.160 1.173 0.575~2.396 0.661 HDL-C 0.123 1.130 0.222~5.744 0.882 LDL-C -0.648 0.523 0.221~1.237 0.140 sdLDL-C -0.348 0.706 0.131~3.808 0.686 FPG -0.140 0.869 0.573~1.318 0.509 BUN 0.275 1.317 0.960~1.807 0.088 Cr 0.047 1.048 1.011~1.086 0.011 Hcy 0.014 1.014 0.955~1.076 0.654 UA 0.003 1.003 0.997~1.008 0.364 表 4 钙化的多因素logistic回归模型
Table 4. Multivariate logistic regression analysis of calcification
因素 标准回归系数 OR值 95% CI P值 BMI -0.188 0.828 0.701~0.979 0.027 Cr 0.049 1.051 1.012~1.091 0.010 -
[1] Libby P. The changing landscape of atherosclerosis[J]. Nature, 2021, 592(7855): 524-533. doi: 10.1038/s41586-021-03392-8
[2] Goncalves I, Sun J, Tengryd C, et al. Plaque Vulnerability Index Predicts Cardiovascular Events: A Histological Study of an Endarterectomy Cohort[J]. J Am Heart Assoc, 2021, 10(15): e021038. doi: 10.1161/JAHA.120.021038
[3] Bonati LH, Jansen O, de Borst GJ, et al. Management of atherosclerotic extracranial carotid artery stenosis[J]. Lancet Neurol, 2022, 21(3): 273-283. doi: 10.1016/S1474-4422(21)00359-8
[4] Heck D, Jost A. Carotid stenosis, stroke, and carotid artery revascularization[J]. Prog Cardiovasc Dis, 2021, 65: 49-54. doi: 10.1016/j.pcad.2021.03.005
[5] Bostrom JA, Mottel B, Heffron SP. Medical and Surgical Obesity Treatments and Atherosclerosis: Mechanisms beyond Typical Risk Factors[J]. Curr Atheroscler Rep, 2021, 23(10): 60. doi: 10.1007/s11883-021-00961-0
[6] Nagarajan SR, Cross E, Sanna F, et al. Dysregulation of hepatic metabolism with obesity: factors influencing glucose and lipid metabolism[J]. Proc Nutr Soc, 2021: 1-11.
[7] Voisin M, Shrestha E, Rollet C, et al. Inhibiting LXRα phosphorylation in hematopoietic cells reduces inflammation and attenuates atherosclerosis and obesity in mice[J]. Commun Biol, 2021, 4(1): 420. doi: 10.1038/s42003-021-01925-5
[8] Geeraerts X, Bolli E, Fendt SM, et al. Macrophage Metabolism As Therapeutic Target for Cancer, Atherosclerosis, and Obesity[J]. Front Immunol, 2017, 8: 289.
[9] Yuan T, Yang T, Chen H, et al. New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis[J]. Redox Biol, 2019, 20: 247-260. doi: 10.1016/j.redox.2018.09.025
[10] 中华医学会外科学分会血管外科学组. 颈动脉狭窄诊治指南[J]. 中国血管外科杂志(电子版), 2017, 9(3): 169-175. doi: 10.3969/j.issn.1674-7429.2017.03.003
[11] Fassaert L, Timmerman N, van Koeverden ID, et al. Preoperative hypertension is associated with atherosclerotic intraplaque hemorrhage in patients undergoing carotid endarterectomy[J]. Atherosclerosis, 2019, 290: 214-221. doi: 10.1016/j.atherosclerosis.2019.09.008
[12] Georgakis MK, van der Laan SW, Asare Y, et al. Monocyte-Chemoattractant Protein-1 Levels in Human Atherosclerotic Lesions Associate With Plaque Vulnerability[J]. Arterioscler Thromb Vasc Biol, 2021, 41(6): 2038-2048. doi: 10.1161/ATVBAHA.121.316091
[13] Libby P, Buring JE, Badimon L, et al. Atherosclerosis[J]. Nat Rev Dis Primers, 2019, 5(1): 56. doi: 10.1038/s41572-019-0106-z
[14] Goncalves I, Sun J, Tengryd C, et al. Plaque Vulnerability Index Predicts Cardiovascular Events: A Histological Study of an Endarterectomy Cohort[J]. J Am Heart Assoc, 2021, 10(15): e021038. doi: 10.1161/JAHA.120.021038
[15] Emdin CA, Khera AV, Natarajan P, et al. Genetic Association of Waist-to-Hip Ratio With Cardiometabolic Traits, Type 2 Diabetes, and Coronary Heart Disease[J]. JAMA, 2017, 317(6): 626-634. doi: 10.1001/jama.2016.21042
[16] Bi H, Zhang Y, Qin P, et al. Association of Chinese Visceral Adiposity Index and Its Dynamic Change With Risk of Carotid Plaque in a Large Cohort in China[J]. J Am Heart Assoc, 2022, 11(1): e022633. doi: 10.1161/JAHA.121.022633
[17] Liu L, Shi Z, Ji X, et al. Adipokines, adiposity, and atherosclerosis[J]. Cell Mol Life Sci, 2022, 79(5): 272. doi: 10.1007/s00018-022-04286-2
[18] Ratushnyy A, Lobanova M, Buravkova LB. Expansion of adipose tissue-derived stromal cells at "physiologic" hypoxia attenuates replicative senescence[J]. Cell Biochem Funct, 2017, 35(4): 232-243. doi: 10.1002/cbf.3267
[19] Schüler R, Seebeck N, Osterhoff MA, et al. VEGF and GLUT1 are highly heritable, inversely correlated and affected by dietary fat intake: Consequences for cognitive function in humans[J]. Mol Metab, 2018, 11: 129-136. doi: 10.1016/j.molmet.2018.02.004
[20] Mantella LE, Colledanchise KN, Hétu MF, et al. Carotid intraplaque neovascularization predicts coronary artery disease and cardiovascular events[J]. Eur Heart J Cardiovasc Imaging, 2019, 20(11): 1239-1247. doi: 10.1093/ehjci/jez070
[21] Zeng ZL, Yuan Q, Zu X, et al. Insights Into the Role of Mitochondria in Vascular Calcification[J]. Front Cardiovasc Med, 2022, 9: 879752. doi: 10.3389/fcvm.2022.879752
[22] Kwiecinski J, Tzolos E, Adamson PD, et al. Coronary 18F-Sodium Fluoride Uptake Predicts Outcomes in Patients With Coronary Artery Disease[J]. J Am Coll Cardiol, 2020, 75(24): 3061-3074. doi: 10.1016/j.jacc.2020.04.046
[23] Shi X, Gao J, Lv Q, et al. Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?[J]. Front Physiol, 2020, 11: 56. doi: 10.3389/fphys.2020.00056
[24] Xiao X, Liu YZ, Cheng ZB, et al. Adipokines in vascular calcification[J]. Clin Chim Acta, 2021, 516: 15-26. doi: 10.1016/j.cca.2021.01.009
[25] Raman P, Khanal S. Leptin in Atherosclerosis: Focus on Macrophages, Endothelial and Smooth Muscle Cells[J]. Int J Mol Sci, 2021, 22(11).
[26] Kronmal RA, McClelland RL, Detrano R, et al. Risk factors for the progression of coronary artery calcification in asymptomatic subjects: results from the Multi-Ethnic Study of Atherosclerosis(MESA)[J]. Circulation, 2007, 115(21): 2722-2730. doi: 10.1161/CIRCULATIONAHA.106.674143
[27] Fujiyoshi A, Sekikawa A, Shin C, et al. A cross-sectional association of obesity with coronary calcium among Japanese, Koreans, Japanese Americans, and U.S. whites[J]. Eur Heart J Cardiovasc Imaging, 2013, 14(9): 921-927. doi: 10.1093/ehjci/jet080