体重指数对冠心病行经皮冠状动脉介入治疗术后患者血小板高反应性及长期预后的影响
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摘要
目的:探讨体重指数(BMI)对冠心病行经皮冠状动脉介入治疗(PCI)后患者血小板高反应性(HTPR)及与长期预后的影响。方法:本研究纳入2013年1月至2013年12月于阜外医院行PCI且有术后12~72 h血栓弹力图(TEG)检测结果的冠心病患者4 567例。血栓弹力图二磷酸腺苷诱导的纤维蛋白凝块强度(MAADP)大于47 mm定义为HTPR。所有患者根据BMI分为三组:正常体重组(18.5~24 kg/m~2,n=1 107)、超重组(24~28 kg/m~2,n=2 328)和肥胖组(≥28 kg/m~2,n=1132)。主要终点为2年主要不良心脑血管事件(MACCE)包括死亡、心肌梗死、血运重建、支架内血栓、脑卒中。结果:在行PCI的4 567例冠心病患者中,1 317(28.8%)例患者存在HTPR;三组(正常体重组、超重组和肥胖组)患者HTPR的发生率无明显差异(28.5%vs 29.3%vs 28.4%, P=0.818)。Logistic多因素分析显示HTPR仅与糖尿病相关,与BMI及其他因素无明显相关性。2年随访期间,三组患者MACCE差异亦无统计学意义(11.7%vs 10.7%vs 13.1%,P=0.109)。Cox多因素分析显示,HTPR并非MACCE的预测因子。结论:对于行PCI的冠心病患者,BMI与TEG所发现的HTPR无相关性;2年随访期间三组患者的MACCE发生率差异无统计学意义,且HTPR与患者预后无相关性。
Objectives: To investigate the impact of body mass index(BMI) on high on-treatment platelet reactivity(HTPR) and the relationship with clinical prognosis in patients with coronary heart disease(CHD) who underwent percutaneous coronary intervention.Methods: A total of 4 567 patients with coronary heart disease, who underwent stent implantation at Fuwai Hospital in 2013 and had 12-72 h postoperative thrombus elasticity data, were included in this study. Thrombosis Elasticity Maximum clot strength(MAADP) greater than 47 mm is defined as HTPR. All patients were divided into three groups according to BMI: normal body weight group(18.5 kg/m~2 ≤ BMI < 24 kg/m~2, n=1 107), overweight group(24 kg/m~2 ≤ BMI < 28 kg/m~2, n=2 328) and the obese group(BMI ≥ 28 kg/m~2, n=1 132). The primary endpoint was the 2-year major adverse cardiovascular and cerebrovascular event(MACCE) including death, myocardial infarction, revascularization, stent thrombosis, and stroke.Results: HTPR was detected in 1 317(28.8%) patients. There was no significant difference in the incidence of HTPR between the three groups(28.5% vs 29.3% vs 28.4%, P=0.818). Logistic multivariate analysis showed that HTPR was onlyassociated with diabetes and had no significant association with BMI and other factors. There were no significant differences in MACCE events between the three groups during the 2-year follow-up period(11.7% vs 10.7% vs 13.1%, P=0.109). COX multivariate analysis showed that HTPR is not a predictor of MACCE. Conclusions: In patients with coronary artery disease undergoing interventional therapy, there is no significant correlation between BMI and HTPR. There is also no significant difference in the incidence of MACCE between the patients with various BMI during the 2-year follow-up period and there is no significant correlation between HTPR and outcome of patients in this cohort.
Objectives: To investigate the impact of body mass index(BMI) on high on-treatment platelet reactivity(HTPR) and the relationship with clinical prognosis in patients with coronary heart disease(CHD) who underwent percutaneous coronary intervention.Methods: A total of 4 567 patients with coronary heart disease, who underwent stent implantation at Fuwai Hospital in 2013 and had 12-72 h postoperative thrombus elasticity data, were included in this study. Thrombosis Elasticity Maximum clot strength(MAADP) greater than 47 mm is defined as HTPR. All patients were divided into three groups according to BMI: normal body weight group(18.5 kg/m~2 ≤ BMI < 24 kg/m~2, n=1 107), overweight group(24 kg/m~2 ≤ BMI < 28 kg/m~2, n=2 328) and the obese group(BMI ≥ 28 kg/m~2, n=1 132). The primary endpoint was the 2-year major adverse cardiovascular and cerebrovascular event(MACCE) including death, myocardial infarction, revascularization, stent thrombosis, and stroke.Results: HTPR was detected in 1 317(28.8%) patients. There was no significant difference in the incidence of HTPR between the three groups(28.5% vs 29.3% vs 28.4%, P=0.818). Logistic multivariate analysis showed that HTPR was onlyassociated with diabetes and had no significant association with BMI and other factors. There were no significant differences in MACCE events between the three groups during the 2-year follow-up period(11.7% vs 10.7% vs 13.1%, P=0.109). COX multivariate analysis showed that HTPR is not a predictor of MACCE. Conclusions: In patients with coronary artery disease undergoing interventional therapy, there is no significant correlation between BMI and HTPR. There is also no significant difference in the incidence of MACCE between the patients with various BMI during the 2-year follow-up period and there is no significant correlation between HTPR and outcome of patients in this cohort.
引文
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[15] Calle EE, Thun MJ, Petrelli JM, et al. Body mass index and mortality in a prospective cohort of U. S. adults[J]. N Engl J Med, 1999, 341(15):1097-1105. DOI:10. 1056/NEJM199910073411501.
[16] Braekkan SK, van der Graaf Y, Visseren FL, et al. Obesity and risk of bleeding:the SMART study[J]. J Thromb Haemost, 2016, 14(1):65-72.DOI:10. 1111/jth. 13184.
[17] Romero CA, Montori VM, Somers VK, et al. Association of body weightwith total mortality and with cardiovascular events in coronary artery disease:a systematic review of cohort studies[J]. Lancent, 2006,368:666-678. DOI:DOI:10. 1016/S0140-6736(06)69251-9.
[18] Akin I, Schneider H, Nienaber CA. Lack of"obesity paradox"in patients presenting with ST-segment elevation myocardial infarctionincluding cardiogenic shock:a multicenter German network registry analysis[J]. BMC Cardiovasc Disord, 2015, 15(1):67-75. DOI10. 1186/s 12872-015-0065-6.
[19] Bonello N, Armero S, Paganelli F, et al. Relation of body mass indextohighon-treatmentplateletreactivityand of failed clopidogrel dose adjustment according to platelet reactivity monitoring in patients undergoing percutaneous coronary intervention[J]. Am J Cardiol, 2009,104(11):1511-1515.DOI:10. 1016/j. amjcard. 2009. 07.015.
[20]成万钧,周玉杰,赵迎新,等.体重对冠状动脉介入术患者氯吡格雷负荷剂量后血小板聚集率的影响[J].中国循环杂志,2010, 25(1):18-21. DOI:10. 3969/j. issn. 1000-3614. 2010. 01. 007.
[21] Montalescot G,Range G,Silvain J,et al. High on-treatment platelet reactivity as a risk factor for secondary preventnion after coronary stent revascularization:A landmark analysis of the ARCTIC study[J]. Circulation, 2014, 129(21):2136-2143. DOI:10. 1161/CIRCULATIONAHA. 113. 007524.
[22] Mangiacapra F,Colaiori I,Ricottini E,et al. Impact of platelet reactivity on 5-year clinical outcomes following percutaneous coronary intervention:a landmark analysis[J]. J Thromb Thrombolysis, 2018, 45(4):1-8. DOI:10. 1007/s11239-018-1630-5.
[23] Gurbel PA, Bliden KP, Navickas IA, et al. Adenosine diphosphateinduced platelet-fibrin clot strength:a new thromblastographic indicator of long-term post-stenting ischemic events[J]. Am Heart J, 2010,160(2):346-354. DOI:10.1016/j.ahj.2010.05.034.
[2] Wisman PP, Roest M, Asselbergs FW, et al. Platelet-reactivity tests identify patients at risk of secondary cardiovascular events:a systematic review and meta-analysis[J]. J Thromb Haemost, 2014, 12(5):736-747. DOI:10. 1111/jth. 12538.
[3] Hamm CW, Bassand JP, Agewall S, et al. ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation:the task force for the management of acute coronary syndromes(ACS)in patients presenting without persistent ST-segment elevation of the European Society of Cardiology(ESC)[J]. Eur Heart J, 2011, 32(23):2999-3054. DOI:10.4414/smw. 2012. 13514.
[4] Lavie CJ, De Schutte A, Parto P, et al. Obesity and prevalence of cardiovascular diseses and prognosis-the ovesity paradox updated.Prog Cardiovasc Dis, 2016, 58(5):537-547. DOI:10. 1016/j. pcad.2016.01.008.
[5] Kaneko H, Yajima J, Oikawa Y, et al. Obesity paradox in Japanese patients after percutaneous coronary intervention:an observation cohort study[J]. J Cardiol, 2013, 62(1):18-24. DOI:10. 1016/j. jjcc. 2013. 02.009.
[6] Gupta T, Kolte D, Mohananey D, et al. Relation of obesity to survival after in-hospital cardiac arrest[J]. Am J Cardiol, 2016, 118:662-667.
[7] Wang ZJ, Zhou YJ, Liu YY, et al. Obesity and cardiovascular thrombotic events in patients undergoing percutaneous coronary intervention with drug-eluting stent[J]. Heart, 2009, 95(19):m1587-1592. DOI:10. 1136/hrt. 2009. 172395.
[8] Pankert M, Quilici J, Loundou AD, et al. Impact of obesity and the metabolic syndrome on response to clopidogrel or prasugrel and bleeding risk in patients treated after coronary stenting[J]. Am J Cardio,2014, 113(1):54-59. DOI:10. 1016/j. amjcard. 2013. 09. 011.
[9] Sibbing D, vonBeckerath O, Schomig A, et al. Impact of body mass index on platelet aggregation after administration of a high loading dose of 600 mg of clopidogrel before percutaneous coronary intervention[J].Am J Cardiol, 2007, 100(2):203-205. DOI:10. 1016/j. amjcard. 2007.02. 081.
[10] Michael A. Gaglia, Torguson R, et al. Relation of body mass index to on-treatment(clopidogrel+aspirin)platelet reactivity[J]. Am J Cardiol, 2011, 108(6):766-771. DOI:10. 1016/j. amjcard. 2011. 04.029.
[11] Tantry US, Bonello L, Aradi D, et al. Consensus and update on the definition of on-treatment platelet reactivity to adenosine diphosphate associated with ischemia and bleeding[J]. J Am Coll Cardiol, 2013,62(24):2261-2273. DOI:10. 1016/j.jacc. 2013. 07. 101.
[12] Thygesen K,Alpert JS, Jaffe AS,et al. Third universal definition of myocardial infarction[J]. Eur Heart J, 2012, 33(20):2551-2567. DOI:10. 1038/nrcardio. 2012. 122.
[13] Cutlip DE, Windecker S, Mehran R, et al. Clinical end points in coronary stent trials:a case for standardized definitions[J]. Circulation,2007, 115(17):2344-2351. DOI:10. 1161/CIRCULATIONAHA. 106.685313.
[14] Coorperative Meta-Analysis Group Of China Obesity Task Force.Predictive values of body mass index and waist circumference to risk factors of related diseases in Chinese adult population[J]. Chin J Epidemiol,2002, 23(1):5-10.
[15] Calle EE, Thun MJ, Petrelli JM, et al. Body mass index and mortality in a prospective cohort of U. S. adults[J]. N Engl J Med, 1999, 341(15):1097-1105. DOI:10. 1056/NEJM199910073411501.
[16] Braekkan SK, van der Graaf Y, Visseren FL, et al. Obesity and risk of bleeding:the SMART study[J]. J Thromb Haemost, 2016, 14(1):65-72.DOI:10. 1111/jth. 13184.
[17] Romero CA, Montori VM, Somers VK, et al. Association of body weightwith total mortality and with cardiovascular events in coronary artery disease:a systematic review of cohort studies[J]. Lancent, 2006,368:666-678. DOI:DOI:10. 1016/S0140-6736(06)69251-9.
[18] Akin I, Schneider H, Nienaber CA. Lack of"obesity paradox"in patients presenting with ST-segment elevation myocardial infarctionincluding cardiogenic shock:a multicenter German network registry analysis[J]. BMC Cardiovasc Disord, 2015, 15(1):67-75. DOI10. 1186/s 12872-015-0065-6.
[19] Bonello N, Armero S, Paganelli F, et al. Relation of body mass indextohighon-treatmentplateletreactivityand of failed clopidogrel dose adjustment according to platelet reactivity monitoring in patients undergoing percutaneous coronary intervention[J]. Am J Cardiol, 2009,104(11):1511-1515.DOI:10. 1016/j. amjcard. 2009. 07.015.
[20]成万钧,周玉杰,赵迎新,等.体重对冠状动脉介入术患者氯吡格雷负荷剂量后血小板聚集率的影响[J].中国循环杂志,2010, 25(1):18-21. DOI:10. 3969/j. issn. 1000-3614. 2010. 01. 007.
[21] Montalescot G,Range G,Silvain J,et al. High on-treatment platelet reactivity as a risk factor for secondary preventnion after coronary stent revascularization:A landmark analysis of the ARCTIC study[J]. Circulation, 2014, 129(21):2136-2143. DOI:10. 1161/CIRCULATIONAHA. 113. 007524.
[22] Mangiacapra F,Colaiori I,Ricottini E,et al. Impact of platelet reactivity on 5-year clinical outcomes following percutaneous coronary intervention:a landmark analysis[J]. J Thromb Thrombolysis, 2018, 45(4):1-8. DOI:10. 1007/s11239-018-1630-5.
[23] Gurbel PA, Bliden KP, Navickas IA, et al. Adenosine diphosphateinduced platelet-fibrin clot strength:a new thromblastographic indicator of long-term post-stenting ischemic events[J]. Am Heart J, 2010,160(2):346-354. DOI:10.1016/j.ahj.2010.05.034.