代谢相关脂肪性肝病与颈动脉粥样硬化斑块及狭窄的关联分析
DOI: 10.12449/JCH240814
Association of metabolic associated fatty liver disease with carotid atherosclerotic plaque and stenosis
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摘要:
目的 分析代谢相关脂肪性肝病(MAFLD)与颈动脉粥样硬化斑块的相关性。 方法 随机纳入2014年7月—2022年12月在昆明医科大学第二附属医院住院期间同时完善腹部超声、头颈动脉CT血管成像的1 107例患者。收集基线资料、临床诊断,根据病史、临床检验及影像学指标分为MAFLD组(n=499)和非MAFLD组(n=608)。颈动脉斑块根据CT值分为钙化斑块、非钙化斑块及混合斑块。根据北美症状性颈动脉内膜剥脱试验(NASCET)标准,颈动脉狭窄分为:正常血管、轻微狭窄、轻度狭窄、中度狭窄、重度狭窄及闭塞。符合正态分布的计量资料两组间比较采用成组t检验;不符合正态分布的计量资料两组间比较采用Mann-Whitney U秩和检验;计数资料两组间比较采用χ2检验。采用单因素和多因素Logistic回归分析颈动脉粥样硬化的影响因素。 结果 MAFLD组患者钙化斑块、非钙化斑块、混合斑块的比例均高于非MAFLD组(74.3% vs 63.3%、27.1% vs 17.1%、27.3% vs 20.7%),差异均有统计学意义(P值均<0.05);MAFLD组患者颈动脉轻度狭窄、中度狭窄、重度狭窄及闭塞的比例均高于非MAFLD组(50.9% vs 44.9%、14.6% vs 8.4%、6.6% vs 3.5%),差异均有统计学意义(P值均<0.05)。单因素Logistic回归分析结果显示,MAFLD是颈动脉钙化斑块、非钙化斑块和混合斑块的危险因素,也是颈动脉轻度、中度、重度狭窄及闭塞的危险因素(P值均<0.05)。校正混杂因素后,多因素Logistic回归分析结果显示MAFLD仍是颈动脉钙化斑块、非钙化斑块、混合斑块以及颈动脉中度狭窄的独立危险因素(P值均<0.05)。 结论 MAFLD是颈动脉中度狭窄,颈动脉钙化斑块、非钙化斑块及混合斑块的独立危险因素。 Abstract:Objective To investigate the association between metabolic associated fatty liver disease (MAFLD) and carotid atherosclerotic plaque. Methods A total of 1 107 patients who were hospitalized in The Second Affiliated Hospital of Kunming Medical University from July, 2014 to December, 2022 were enrolled, and all patients underwent abdominal ultrasound and CT angiography of the head and neck arteries. Baseline data and clinical diagnosis were collected, and the patients were divided into MAFLD group with 499 patients and non-MAFLD group with 608 patients based on medical history, clinical tests, and imaging findings. According to the CT value, carotid plaques were classified into calcified plaques, non-calcified plaques, and mixed plaques. According to the NASCET criteria, carotid stenosis was categorized as normal vessel, slight stenosis, mild stenosis, moderate stenosis, and severe stenosis/occlusion. The independent-samples t test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U rank sum test was used for comparison of non-normally distributed continuous data between two groups; the chi-square test was used for comparison of categorical data between two groups. Univariate and multivariate Logistic regression analyses were used to investigate the influencing factors for carotid atherosclerosis. Results Compared with the non-MAFLD group, the MAFLD group had a significantly higher proportion of patients with calcified plaques (74.3% vs 63.3%, P<0.05), non-calcified plaques (27.1% vs 17.1%, P<0.05), or mixed plaques (27.3% vs 20.7%, P<0.05), as well as a significantly higher proportion of patients with mild stenosis (50.9% vs 44.9%, P<0.05), moderate stenosis (14.6% vs 8.4%, P<0.05), or severe stenosis/occlusion (6.6% vs 3.5%, P<0.05). The univariate logistic regression analysis showed that MAFLD was a risk factor for calcified carotid plaques, non-calcified plaques, and mixed plaques, and it was also a risk factor for mild stenosis, moderate stenosis, and severe stenosis/occlusion of the carotid artery (all P<0.05). After adjustment for confounding factors, the multivariate Logistic regression analysis showed that MAFLD was an independent risk factor for calcified plaque, non-calcified plaque, mixed plaque, and moderate stenosis of the carotid arteries (all P<0.05). Conclusion MAFLD is an independent risk factor for moderate stenosis, calcified plaques, non-calcified plaques, and mixed plaques of the carotid arteries. -
表 1 非MAFLD组与MAFLD组基线特征比较
Table 1. Comparison of general data between non-MAFLD group and MAFLD group
组别 合计(n=1 107) 非MAFLD(n=608) MAFLD(n=499) 统计值 P值 年龄(岁) 61.31±12.95 60.68±14.20 62.09±11.20 t=1.855 0.064 性别[例(%)] χ2=4.044 0.044 男 664(60.0) 381(62.7) 283(56.7) 女 443(40.0) 227(37.3) 216(43.3) 2型糖尿病[例(%)] χ2=57.888 <0.001 有 333(30.1) 125(20.6) 208(41.8) 无 774(69.9) 483(79.4) 291(58.3) 吸烟[例(%)] χ2=9.834 0.002 有 363(32.8) 175(28.8) 188(37.7) 无 744(67.2) 433(71.2) 311(62.3) 服用降脂药[例(%)] χ2=11.550 0.001 有 867(78.3) 453(74.5) 414(83.0) 无 240(21.7) 155(25.5) 85(17.0) 胰岛素抵抗[例(%)] χ2=21.965 <0.001 有 94(8.5) 30(4.9) 64(12.8) 无 1013(91.5) 578(95.1) 435(87.2) 高血压[例(%)] χ2=30.450 <0.001 有 715(64.6) 349(57.4) 366(73.3) 无 392(35.4) 259(42.6) 133(26.7) 身高(m) 1.63±0.08 1.63±0.08 1.64±0.08 t=0.142 0.887 体质量(kg) 64.94±11.09 62.05±10.46 68.47±10.82 t=10.007 <0.001 BMI(kg/m2) 24.24±3.39 23.15±3.04 25.56±3.32 t=12.601 <0.001 SBP(mmHg) 135.72±22.30 132.41±22.29 139.77±21.65 t=5.536 <0.001 DBP(mmHg) 82.99±13.51 81.32±13.48 85.03±13.27 t=4.583 <0.001 TG(mmol/L) 1.47(1.07~2.05) 1.29(0.96~1.75) 1.71(1.31~2.36) Z=-9.844 <0.001 HDL(mmol/L) 1.07(0.92~1.25) 1.12(0.95~1.28) 1.03(0.89~1.20) Z=-5.445 <0.001 LDL(mmol/L) 2.69(2.16~3.22) 2.64(2.14~3.17) 2.78(2.23~3.30) Z=-2.717 0.007 FPG(mmol/L) 5.13(4.59~6.19) 4.91(4.45~5.70) 5.49(4.75~6.87) Z=-7.765 <0.001 ALT(U/L) 18(13~27) 17(12~25) 21(14~30) Z=-5.125 <0.001 AST(U/L) 21(17~26) 21(17~26) 21(17~27) Z=-1.268 0.205 表 2 非MAFLD组与MAFLD组颈动脉斑块比较
Table 2. Comparison of carotid plaque between non-MAFLD group and MAFLD group
颈动脉斑块类型 合计(n=1 107) 非MAFLD(n=608) MAFLD(n=499) χ2值 P值 钙化斑块[例(%)] 756(68.3) 385(63.3) 371(74.3) 15.388 <0.001 非钙化斑块[例(%)] 239(21.6) 104(17.1) 135(27.1) 16.024 <0.001 混合斑块[例(%)] 262(23.7) 126(20.7) 136(27.3) 6.470 0.011 表 3 单因素Logistic回归分析
Table 3. Univariate Logistic regression analysis
指标 钙化斑块 非钙化斑块 混合斑块 OR(95%CI) P值 OR(95%CI) P值 OR(95%CI) P值 MAFLD 1.679(1.295~2.177) <0.001 1.797(1.346~2.400) <0.001 1.433(1.085~1.893) 0.011 性别 1.221(0.944~1.578) 0.129 2.233(1.624~3.072) <0.001 1.565(1.168~2.098) 0.003 年龄 1.099(1.084~1.114) <0.001 1.029(1.017~1.042) <0.001 1.056(1.042~1.070) <0.001 吸烟 1.123(0.856~1.474) 0.402 2.073(1.546~2.780) <0.001 1.658(1.245~2.207) 0.001 BMI 1.004(0.967~1.042) 0.833 1.024(0.982~1.068) 0.263 1.004(0.963~1.046) 0.859 TG 0.952(0.868~1.044) 0.295 0.951(0.846~1.070) 0.405 1.008(0.910~1.118) 0.872 HDL 0.538(0.346~0.837) 0.006 0.432(0.247~0.755) 0.003 0.317(0.182~0.555) <0.001 LDL 0.869(0.739~1.021) 0.088 1.035(0.862~1.242) 0.713 0.813(0.679~0.974) 0.250 2型糖尿病 2.677(1.957~3.663) <0.001 2.098(1.558~2.823) <0.001 1.655(1.237~2.214) 0.001 FPG 1.149(1.077~1.226) <0.001 1.103(1.050~1.159) <0.001 1.043(0.992~1.097) 0.104 高血压 3.284(2.520~4.280) <0.001 2.394(1.707~3.358) <0.001 2.292(1.660~3.165) <0.001 胰岛素抵抗 1.680(1.016~2.777) 0.043 2.233(1.427~3.495) <0.001 1.186(0.734~1.917) 0.485 ALT 0.990(0.984~0.997) 0.005 0.996(0.987~1.004) 0.319 1.000(0.994~1.007) 0.899 表 4 多因素Logistic回归分析
Table 4. Multifactorial Logistic regression analysis
项目 钙化斑块 非钙化斑块 混合斑块 OR(95%CI) P值 OR(95%CI) P值 OR(95%CI) P值 模型1:MAFLD 1.725(1.279~2.326) <0.001 1.840(1.360~2.489) <0.001 1.452(1.080~1.951) 0.013 模型2:MAFLD 1.674(1.211~2.314) 0.002 1.806(1.312~2.486) <0.001 1.414(1.035~1.932) 0.029 模型3:MAFLD 1.615(1.156~2.255) 0.005 1.840(1.324~2.556) <0.001 1.441(1.044~1.989) 0.026 模型4:MAFLD 1.554(1.107~2.181) 0.011 1.801(1.294~2.509) <0.001 1.445(1.045~1.999) 0.026 模型5:MAFLD 1.507(1.072~2.119) 0.018 1.748(1.253~2.439) 0.001 1.443(1.042~1.999) 0.027 模型6:MAFLD 1.483(1.052~2.091) 0.024 1.703(1.218~2.380) 0.002 1.424(1.027~1.975) 0.034 注:模型1,校正性别、吸烟、年龄后;模型2:校正性别、吸烟、年龄、BMI后;模型3,校正性别、吸烟、年龄、BMI、高血压后;模型4,校正性别、吸烟、年龄、BMI、高血压、HDL后;模型5,校正性别、吸烟、年龄、BMI、高血压、HDL、PFG后;模型6,校正性别、吸烟、年龄、BMI、高血压、HDL、PFG、2型糖尿病后。
表 5 非MAFLD组与MAFLD组颈动脉狭窄程度比较
Table 5. Comparison of carotid stenosis between non-MAFLD group and MAFLD group
颈动脉狭窄程度 合计(n=1 107) 非MAFLD(n=608) MAFLD(n=499) Z值 P值 正常血管[例(%)] 319(28.8) 215(35.4) 104(20.8) -5.305 <0.001 轻微狭窄[例(%)] 83(7.5) 48(7.9) 35(7.0) -0.553 0.580 轻度狭窄[例(%)] 527(47.6) 273(44.9) 254(50.9) -1.988 0.047 中度狭窄[例(%)] 124(11.2) 51(8.4) 73(14.6) -3.275 0.001 重度狭窄/闭塞[例(%)] 54(4.9) 21(3.5) 33(6.6) 2.427 0.015 表 6 单因素Logistic回归分析
Table 6. Univariate Logistic regression analysis
指标 轻度狭窄 中度狭窄 重度狭窄/闭塞 OR(95%CI) P值 OR(95%CI) P值 OR(95%CI) P值 MAFLD 1.272(1.003~1.613) 0.047 1.872(1.281~2.735) 0.001 1.979(1.130~3.476) 0.017 性别 1.144(0.899~1.456) 0.275 0.685(0.461~1.020) 0.062 0.562(0.306~1.032) 0.063 年龄 1.049(1.038~1.060) <0.001 1.043(1.026~1.061) <0.001 1.023(1.000~1.047) 0.049 吸烟 1.054(0.820~1.355) 0.683 1.339(0.911~1.969) 0.137 1.556(0.894~2.709) 0.118 BMI 0.994(0.959~1.029) 0.714 1.066(1.010~1.125) 0.020 0.989(0.912~1.073) 0.787 TG 1.004(0.919~1.097) 0.933 1.026(0.898~1.171) 0.710 0.886(0.680~1.156) 0.373 HDL 0.996(0.657~1.512) 0.986 0.433(0.209~0.897) 0.024 0.305(0.100~0.926) 0.036 LDL 0.943(0.811~1.097) 0.446 1.033(0.791~1.273) 0.979 0.817(0.572~1.168) 0.268 2型糖尿病 1.427(1.103~1.847) 0.007 2.259(1.546~3.301) <0.001 3.347(1.920~5.835) <0.001 FPG 1.022(0.976~1.069) 0.359 1.145(1.083~1.211) <0.001 1.128(1.047~1.216) 0.002 高血压 2.089(1.622~2.692) <0.001 2.648(1.653~4.240) <0.001 2.512(1.250~5.049) 0.010 胰岛素抵抗 1.277(0.836~1.950) 0.258 2.027(1.167~3.519) 0.012 1.371(0.571~3.293) 0.481 ALT 0.995(0.988~1.001) 0.102 0.996(0.985~1.007) 0.472 0.999(0.985~1.014) 0.924 表 7 多因素Logistic回归分析
Table 7. Multifactorial Logistic regression analysis
项目 轻度狭窄 中度狭窄 重度狭窄/闭塞 OR(95%CI) P值 OR(95%CI) P值 OR(95%CI) P值 模型1:MAFLD 1.296(1.019~1.649) 0.035 1.920(1.306~2.825) 0.001 2.033(1.150~3.594) 0.015 模型2:MAFLD 1.265(0.985~1.626) 0.066 1.947(1.316~2.882) 0.001 2.020(1.141~3.576) 0.016 模型3:MAFLD 1.265(0.967~1.655) 0.086 1.698(1.124~2.563) 0.012 2.200(1.206~4.012) 0.010 模型4:MAFLD 1.224(0.935~1.604) 0.142 1.668(1.103~2.523) 0.015 2.124(1.163~3.879) 0.014 模型5:MAFLD 1.270(0.962~1.676) 0.091 1.658(1.088~2.527) 0.019 1.976(1.074~3.637) 0.029 模型6:MAFLD 1.289(0.975~1.703) 0.075 1.568(1.024~2.402) 0.039 1.893(1.023~3.501) 0.042 模型7:MAFLD 1.285(0.971~1.701) 0.080 1.553(1.012~2.383) 0.044 1.759(0.945~3.271) 0.075 注:模型1,校正性别、吸烟后;模型2,校正性别、吸烟、年龄后;模型3:校正性别、吸烟、年龄、BMI后;模型4,校正性别、吸烟、年龄、BMI、高血压后;模型5,校正性别、吸烟、年龄、BMI、高血压、HDL后;模型6,校正性别、吸烟、年龄、BMI、高血压、HDL、PFG;模型7,性别、吸烟、年龄、BMI、高血压、HDL、PFG、2型糖尿病后。
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[1] FILIPOVIC B, MARJANOVIC-HALJILJI M, MIJAC D, et al. Molecular aspects of MAFLD-new insights on pathogenesis and treatment[J]. Curr Issues Mol Biol, 2023, 45( 11): 9132- 9148. DOI: 10.3390/cimb45110573. [2] XUE R, FAN JG. Brief introduction of an international expert consensus statement: A new definition of metabolic associated fatty liver disease[J]. J Clin Hepatol, 2020, 36( 6): 1224- 1227. DOI: 10.3969/j.issn.1001-5256.2020.06.007.薛芮, 范建高. 代谢相关脂肪性肝病新定义的国际专家共识简介[J]. 临床肝胆病杂志, 2020, 36( 6): 1224- 1227. DOI: 10.3969/j.issn.1001-5256.2020.06.007. [3] ESLAM M, NEWSOME PN, SARIN SK, et al. A new definition for metabolic dysfunction-associated fatty liver disease: An international expert consensus statement[J]. J Hepatol, 2020, 73( 1): 202- 209. DOI: 10.1016/j.jhep.2020.03.039. [4] LEI F, WANG XM, WANG CQ, et al. Metabolic dysfunction-associated fatty liver disease increased the risk of subclinical carotid atherosclerosis in China[J]. Front Endocrinol, 2023, 14: 1109673. DOI: 10.3389/fendo.2023.1109673. [5] GBD 2019 Stroke Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990-2019: A systematic analysis for the Global Burden of Disease Study 2019[J]. Lancet Neurol, 2021, 20( 10): 795- 820. DOI: 10.1016/S1474-4422(21)00252-0. [6] ZHOU XD, CAI JJ, TARGHER G, et al. Metabolic dysfunction-associated fatty liver disease and implications for cardiovascular risk and disease prevention[J]. Cardiovasc Diabetol, 2022, 21( 1): 270. DOI: 10.1186/s12933-022-01697-0. [7] National Workshop on Fatty Liver and Alcoholic Liver Disease, Chinese Society of Hepatology, Chinese Medical Association; Fatty Liver Expert Committee, Chinese Medical Doctor Association. Guidelines of prevention and treatment for nonalcoholic fatty liver disease: a 2018 update[J]. J Clin Hepatol, 2018, 34( 5): 947- 957. DOI: 10.3969/j.issn.1001-5256.2018.05.007.中华医学会肝病学分会脂肪肝和酒精性肝病学组, 中国医师协会脂肪性肝病专家委员会. 非酒精性脂肪性肝病防治指南(2018年更新版)[J]. 临床肝胆病杂志, 2018, 34( 5): 947- 957. DOI: 10.3969/j.issn.1001-5256.2018.05.007. [8] CUI L, PENG XM, TANG QJ. Analysis of CTA in head and neck in evaluating carotid stenosis and plaque properties in patients with cerebral infarction[J]. Mod Med Imageology, 2021, 30( 4): 715- 717.崔凌, 彭细美, 唐庆健. 头颈部CTA在评估脑梗死患者颈动脉狭窄及斑块性质的价值分析[J]. 现代医用影像学, 2021, 30( 4): 715- 717. [9] CHALASANI N, YOUNOSSI Z, LAVINE JE, et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases[J]. Hepatology, 2018, 67( 1): 328- 357. DOI: 10.1002/hep.29367. [10] LEI F, QIN JJ, SONG XH, et al. The prevalence of MAFLD and its association with atrial fibrillation in a nationwide health check-up population in China[J]. Front Endocrinol(Lausanne), 2022, 13: 1007171. DOI: 10.3389/fendo.2022.1007171. [11] DELLA TS. Beyond the X factor: Relevance of sex hormones in NAFLD pathophysiology[J]. Cells, 2021, 10( 9): 2502. DOI: 10.3390/cells10092502. [12] LEE CB, KIM J, HAN J, et al. Formyl peptide receptor 2 determines sex-specific differences in the progression of nonalcoholic fatty liver disease and steatohepatitis[J]. Nat Commun, 2022, 13( 1): 578. DOI: 10.1038/s41467-022-28138-6. [13] GEORGE ES, FORSYTH A, ITSIOPOULOS C, et al. Practical dietary recommendations for the prevention and management of nonalcoholic fatty liver disease in adults[J]. Adv Nutr, 2018, 9( 1): 30- 40. DOI: 10.1093/advances/nmx007. [14] QIN S. LDL and HDL oxidative modification and atherosclerosis[M/OL]//JIANG XC. Lipid transfer in lipoprotein metabolism and cardiovascular disease: Vol. 1276. Singapore: Springer Singapore, 2020: 157- 169[2023-11-08]. https://link.springer.com/10.1007/978-981-15-6082-8_10. DOI: 10.1007/978-981-15-6082-8_10 [15] SAKURAI Y, KUBOTA N, YAMAUCHI T, et al. Role of insulin resistance in MAFLD[J]. Int J Mol Sci, 2021, 22( 8): 4156. DOI: 10.3390/ijms22084156. [16] DUAN YM, PAN XF, LUO JY, et al. Association of inflammatory cytokines with non-alcoholic fatty liver disease[J]. Front Immunol, 2022, 13: 880298. DOI: 10.3389/fimmu.2022.880298. [17] SATISH M, SAXENA SK, AGRAWAL DK. Adipokine dysregulation and insulin resistance with atherosclerotic vascular disease: Metabolic syndrome or independent sequelae?[J]. J Cardiovasc Transl Res, 2019, 12( 5): 415- 424. DOI: 10.1007/s12265-019-09879-0. [18] MU W, CHENG XF, LIU Y, et al. Potential nexus of non-alcoholic fatty liver disease and type 2 diabetes mellitus: Insulin resistance between hepatic and peripheral tissues[J]. Front Pharmacol, 2019, 9: 1566. DOI: 10.3389/fphar.2018.01566. [19] KHAN RS, BRIL F, CUSI K, et al. Modulation of insulin resistance in nonalcoholic fatty liver disease[J]. Hepatology, 2019, 70( 2): 711- 724. DOI: 10.1002/hep.30429. [20] BIAN F, YANG XY, XU G, et al. CRP-induced NLRP3 inflammasome activation increases LDL transcytosis across endothelial cells[J]. Front Pharmacol, 2019, 10: 40. DOI: 10.3389/fphar.2019.00040. [21] POZNYAK AV, BHARADWAJ D, PRASAD G, et al. Anti-inflammatory therapy for atherosclerosis: Focusing on cytokines[J]. Int J Mol Sci, 2021, 22( 13): 7061. DOI: 10.3390/ijms22137061. [22] SHAH PK. Inflammation, infection and atherosclerosis[J]. Trends Cardiovasc Med, 2019, 29( 8): 468- 472. DOI: 10.1016/j.tcm.2019.01.004. [23] DURKOVICOVA Z, FAKTOROVA X, JAKABOVICOVA M, et al. Molecular mechanisms in the pathogenesis of metabolically associated fatty liver disease[J]. Bratisl Lek Listy, 2023, 124( 6): 427- 436. DOI: 10.4149/BLL_2023_065. [24] KAPIL S, DUSEJA A, SHARMA BK, et al. Small intestinal bacterial overgrowth and toll-like receptor signaling in patients with non-alcoholic fatty liver disease[J]. J Gastroenterol Hepatol, 2016, 31( 1): 213- 221. DOI: 10.1111/jgh.13058. [25] YANG LD, DAI YZ, HE H, et al. Integrative analysis of gut microbiota and fecal metabolites in metabolic associated fatty liver disease patients[J]. Front Microbiol, 2022, 13: 969757. DOI: 10.3389/fmicb.2022.969757. [26] XU YY, ZHU YD, HU SW, et al. Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease[J]. Mol Metab, 2021, 51: 101244. DOI: 10.1016/j.molmet.2021.101244. [27] BADI I, MANCINELLI L, POLIZZOTTO A, et al. MiR-34a promotes vascular smooth muscle cell calcification by downregulating SIRT1(sirtuin 1) and axl(AXL receptor tyrosine kinase)[J]. Arterioscler Thromb Vasc Biol, 2018, 38( 9): 2079- 2090. DOI: 10.1161/ATVBAHA.118.311298. [28] GUO YC, ZHOU Y, GAO X, et al. Association between nonalcoholic fatty liver disease and carotid artery disease in a community-based Chinese population: A cross-sectional study[J]. Chin Med J(Engl), 2018, 131( 19): 2269- 2276. DOI: 10.4103/0366-6999.241797. [29] TANG CH, GUO L, LI Q, et al. Interpretation on the report of global stroke data 2022[J]. J Diagn Concepts Pract, 2023, 22( 3): 238- 246. DOI: 10.16150/j.1671-2870.2023.03.06.唐春花, 郭露, 李琼, 等. 2022年全球卒中数据报告解读[J]. 诊断学理论与实践, 2023, 22( 3): 238- 246. DOI: 10.16150/j.1671-2870.2023.03.06. [30] HAO WC, LIU YR, ZHANG JH, et al. Detected condition of carotid artery plaque and its risk factors during physical examination[J]. Clin Misdiagn Misther, 2022, 35( 1): 90- 93. DOI: 10.3969/j.issn.1002-3429.2022.01.021.郝文超, 刘艳如, 张婧环, 等. 健康体检颈动脉斑块检出情况及危险因素分析[J]. 临床误诊误治, 2022, 35( 1): 90- 93. DOI: 10.3969/j.issn.1002-3429.2022.01.021. [31] SCHINDLER A, SCHINNER R, ALTAF N, et al. Prediction of stroke risk by detection of hemorrhage in carotid plaques: Meta-analysis of individual patient data[J]. JACC Cardiovasc Imaging, 2020, 13( 2 Pt 1): 395- 406. DOI: 10.1016/j.jcmg.2019.03.028. [32] JIANG ZM, CHEN YH, ZHANG ZJ, et al. Influence of metabolic associated fatty liver disease on the degree of carotid stenosis[J]. J Clin Hepatol, 2023, 39( 8): 1874- 1879. DOI: 10.3969/j.issn.1001-5256.2023.08.016.姜梓萌, 陈宇航, 张志娇, 等. 代谢相关脂肪性肝病对颈动脉狭窄程度的影响[J]. 临床肝胆病杂志, 2023, 39( 8): 1874- 1879. DOI: 10.3969/j.issn.1001-5256.2023.08.016. [33] JOSEPHSON SA, BRYANT SO, MAK HK, et al. Evaluation of carotid stenosis using CT angiography in the initial evaluation of stroke and TIA[J]. Neurology, 2004, 63( 3): 457- 460. DOI: 10.1212/01.wnl.0000135154.53953.2c. [34] NETUKA D, BELŠÁN T, BROULÍKOVÁ K, et al. Detection of carotid artery stenosis using histological specimens: A comparison of CT angiography, magnetic resonance angiography, digital subtraction angiography and Doppler ultrasonography[J]. Acta Neurochir(Wien), 2016, 158( 8): 1505- 1514. DOI: 10.1007/s00701-016-2842-0. [35] JIAO YG, QIN YH, ZHANG ZG, et al. Early identification of carotid vulnerable plaque in asymptomatic patients[J]. BMC Cardiovasc Disord, 2020, 20( 1): 429. DOI: 10.1186/s12872-020-01709-5. [36] WEN W, LI H, WANG C, et al. Metabolic dysfunction-associated fatty liver disease and cardiovascular disease: A meta-analysis[J]. Front Endocrinol(Lausanne), 2022, 13: 934225. DOI: 10.3389/fendo.2022.934225.
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