急性冠状动脉综合征和稳定型心绞痛罪犯病变和非罪犯病变组织学特征比较Comparison of tissue characteristics between acute coronary syndrome and stable angina pectoris culprit and non-culprit lesions
许康世,单守杰,刘志忠,张俊杰,金国珍
摘要(Abstract):
目的应用彩色编码血管内超声(iMAP-IVUS)比较急性冠状动脉综合征(ACS)患者和稳定型心绞痛(SAP)患者罪犯病变与非罪犯病变斑块组织学特征。方法连续纳入2014年5月至2016年10月于南京市第一医院行经皮冠状动脉介入治疗(PCI)的冠心病患者152例。术前行IVUS检查,根据入院时临床症状特征分为ACS组(62例)和SAP组(90例),共检出213处罪犯病变(ACS组76处,SAP组137处)和164处非罪犯病变(ACS组68处,SAP组96处)。使用i MAP-IVUS系统计算具有最小管腔横截面积的节段纤维面积百分比(纤维面积/斑块面积)和脂质面积百分比(脂质面积/斑块面积)。结果 ACS组患者罪犯病变处重构指数[(1.05±0.21)比(0.97±0.13),P=0.008]和偏心指数[(0.64±0.09)比(0.59±0.07),P=0.007]显著高于非罪犯病变。i MAP-IVUS分析显示:和SAP组患者相比,ACS组患者罪犯病变和非罪犯病变纤维面积百分比显著增加[(37±19)%比(30±16)%,P=0.003]和[(37±20)%比(31±17)%,P=0.027],而脂质面积百分比显著减少[(60±14)%比(63±13)%,P=0.032]和[(57±17)%比(63±15)%,P=0.031]。logistic多因素回归分析显示,ACS患者罪犯病变(OR 4.98,95%CI 1.54~17.90,P=0.006),非罪犯病变(OR 7.36,95CI 1.95~28.70,P=0.004)是预测富含脂质斑块独立预测因子。结论 ACS患者冠状动脉非罪犯病变与富含脂质斑块显著相关,提示此类患者广泛存在斑块易损性。
关键词(KeyWords): 急性冠状动脉综合征;斑块;彩色编码血管内超声
基金项目(Foundation):
作者(Author): 许康世,单守杰,刘志忠,张俊杰,金国珍
参考文献(References):
- [1] Narula J, Nakano M, Virmani R, et al. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J Am Coll Cardiol, 2013, 61(10):1041-1051.
- [2] Ambrose JA, Srikanth S. Vulnerable plaques and patients:improving prediction of future coronary events. Am J Med, 2010, 123(1):10-16.
- [3] Uchida Y, Hiruta N. Histological characteristics of glistening yellow coronary plaques seen on angioscopy. With special reference to vulnerable plaques. Circ J, 2011, 75(8):1913-1919.
- [4] Uchida Y, Uchida Y, Kawai S, et al. Detection of vulnerable coronary plaques by color fluorescent angioscopy. JACC Cardiovasc Imaging, 2010, 3(4):398-408.
- [5] Koga S, Ikeda S, Miura M, et al. iMap-Intravascular ultrasound radiofrequency signal analysis reflects plaque components of optical coherence tomography-derived thin-cap fibroatheroma. Circ J,2015, 79(10):2231-2237.
- [6] Takahashi K, Kakuta T, Yonetsu T, et al. In vivo detection of lipid-rich plaque by using a 40-MHz intravascular ultrasound:a comparison with optical coherence tomography findings. Cardiovasc Interv Ther, 2013, 28(4):333-343.
- [7] Zhao Z, Witzenbichler B, Mintz GS, et al. Dynamic nature of nonculprit coronary artery lesion morphology in STEMI:a serial IVUS analysis from the HORIZONS-AMI trial. JACC Cardiovasc Imaging, 2013, 6(1):86-95.
- [8] Liu J, Wang Z, Wang WM, et al. Feasibility of diagnosing unstable plaque in patients with acute coronary syndrome using iMap-IVUS. J Zhejiang Univ Sci B, 2015, 16(11):924-930.
- [9] Kashiyama K, Sonoda S, Muraoka Y, et al. Coronary plaque progression of non-culprit lesions after culprit percutaneous coronary intervention in patients with moderate to advanced chronic kidney disease:intravascular ultrasound and integrated backscatter intravascular ultrasound study. Int J Cardiovasc Imaging, 2015, 31(5):935-945.
- [10] Asakura M, Ueda Y, Yamaguchi O, et al. Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction:an angioscopic study. J Am Coll Cardiol,2001, 37(5):1284-1288.
- [11] Cutlip DE, Chhabra AG, Baim DS, et al. Beyond restenosis:fiveyear clinical outcomes from second-generation coronary stent trials.Circulation, 2004, 110(10):1226-1230.
- [12] Glaser R, Selzer F, Faxon DP, et al. Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention. Circulation, 2005, 111(2):143-149.
- [13] Stone GW, Maehara A, Lansky AJ, et al. A prospective naturalhistory study of coronary atherosclerosis. N Engl J Med, 2011, 364(3):226-235.
- [14] Ando H, Amano T, Matsubara T, et al. Comparison of tissue characteristics between acute coronary syndrome and stable angina pectoris. An integrated backscatter intravascular ultrasound analysis of culprit and non-culprit lesions. Circ J, 2011, 75(2):383-390.
- [15] Liu HL, Zhang J, Ma DX, et al. Coronary plaque characterization of nonculprit or nontarget lesions assessed by analysis of in vivo intracoronary ultrasound radio-frequency data. Chin Med J(Engl),2009, 122(6):622-626.
- [16] Sano K, Kawasaki M, Ishihara Y, et al. Assessment of vulnerable plaques causing acute coronary syndrome using integrated backscatter intravascular ultrasound. J Am Coll Cardiol, 2006, 47(4):734-741.
- [17] Nakamura M, Nishikawa H, Mukai S, et al. Impact of coronary artery remodeling on clinical presentation of coronary artery disease:an intravascular ultrasound study. J Am Coll Cardiol, 2001, 37(1):63-69.
- [18]郑婕舒,张元春,刘祖恒,等.急性冠状动脉综合征患者血清超敏C反应蛋白及抵抗素浓度与罪犯病变虚拟组织学-血管内超声特点的相关性.中国介入心脏病学杂志,2014, 22(1):30-34.
- [19] Nair A, Kuban BD, Tuzcu EM, et al. Coronary plaque classification with intravascular ultrasound radiofrequency data analysis.Circulation, 2002, 106(17):2200-2206.
- [20]谢剑昶,黄进宇.基于血管内超声斑块组织学检测方法的历史及现状.中国介入心脏病学杂志,2018, 26(11):645-648.
- [21] Rioufol G, Finet G, Ginon I, et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome:a three-vessel intravascular ultrasound study. Circulation, 2002, 106(7):804-808.
- [22] Soysal D, Karakus V, Yavas HH, et al. C-reactive protein in unstable angina pectoris and its relation to coronary angiographic severity and diffusion scores of coronary lesions. Anadolu Kardiyol Derg, 2010, 10(5):421-428.
- [23] Tsimikas S, Willerson JT, Ridker PM. C-reactive protein and other emerging blood biomarkers to optimize risk stratification of vulnerable patients. J Am Coll Cardiol,2006, 47(8 Suppl):C19-C31.