联合N端脑钠肽前体、估算的肾小球滤过率及超敏C-反应蛋白对急性心肌梗死患者院内发生1型心肾综合征的危险分层评估
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摘要
目的观察N端脑钠肽前体(NT-proBNP)、估算的肾小球滤过率(eGFR)及超敏C-反应蛋白(hs-CRP)对急性心肌梗死患者在院内发生1型心肾综合征(CRS1)及危险分层中的作用。方法回顾性分析2012年12月至2017年2月北京友谊医院心血管中心数据库中急性心肌梗死患者2 094例。收集包括NT-proBNP、eGFR及hs-CRP在内的临床资料。按照每组人数大致相等的原则,分段考察NT-proBNP、eGFR及hs-CRP的值与CRS1发生率和院内死亡率之间的关系。采用SPSS 22.0统计软件进行统计学分析。Kaplan-Meier生存分析及COX比例风险回归评估异常指标的数目对院内死亡的影响。结果随着NT-proBNP的升高、eGFR的下降以及hs-CRP的升高,急性心肌梗死患者的院内CRS1发生率及院内死亡率均有升高趋势(P<0.05)。随着CRS1加重,eGFR有下降趋势,NT-proBNP及hs-CRP在CRS1达到重度之前具有升高趋势。Kaplan-Meier生存分析显示,患者的院内累积生存率随着异常指标数目的增加而降低(P<0.001)。≥2个指标异常是患者院内死亡的独立危险因素(RR=2.452,95%CI 1.105～5.440;P=0.027)。结论联合NT-proBNP、eGFR和hs-CRP将有助于对急性心肌梗死患者院内发生CRS1进行危险分层。
Objective To observe the effectiveness of N-terminal pro-brain natriuretic peptide(NT-proBNP), estimated glomerular filtration rate(eGFR) and high sensitivity C-reactive protein(hs-CRP) in risk stratification for the development of type 1 cardiorenal syndrome(CRS1) in patients with acute myocardial infarction(AMI). Methods A retrospective analysis was made of the available data of NT-proBNP, eGFR, and hs-CRP for 2 094 AMI patients in Cardiovascular Center of Beijing Friendship Hospital Database Bank(CBD BANK). The patients were divided into quartiles of an approximately equal number to assess the relationship of the three biomarkers with CRS1 incidence and in-hospital mortality. Statistical analyses were performed using SPSS 22.0. Kaplan-Meier survival analysis and COX proportional hazard regression were used to assess the effect of the number of abnormal biomarkers on in-hospital mortality. Results The incidence of CRS1 and in-hospital mortality increased in AMI patients as NT-proBNP and hs-CRP increased, and eGFR decreased(P<0.05). As CRS1 was aggravated, eGFR tended to decrease, and NT-proBNP and hs-CRP tended to increase before CRS1 became severe. Kaplan-Meier survival analysis showed that the in-hospital mortality in the AMI patients was correlated with the number of abnormal biomarkers(P<0.001). Abnormal biomarkers ≥2 was an independent risk factor for in-hospital death(RR=2.452, 95%CI 1.105-5.440; P=0.027). Conclusion The combination of NT-proBNP, eGFR, and hs-CRP at presentation may assist risk stratification for the development of CRS1 in AMI patients.
Objective To observe the effectiveness of N-terminal pro-brain natriuretic peptide(NT-proBNP), estimated glomerular filtration rate(eGFR) and high sensitivity C-reactive protein(hs-CRP) in risk stratification for the development of type 1 cardiorenal syndrome(CRS1) in patients with acute myocardial infarction(AMI). Methods A retrospective analysis was made of the available data of NT-proBNP, eGFR, and hs-CRP for 2 094 AMI patients in Cardiovascular Center of Beijing Friendship Hospital Database Bank(CBD BANK). The patients were divided into quartiles of an approximately equal number to assess the relationship of the three biomarkers with CRS1 incidence and in-hospital mortality. Statistical analyses were performed using SPSS 22.0. Kaplan-Meier survival analysis and COX proportional hazard regression were used to assess the effect of the number of abnormal biomarkers on in-hospital mortality. Results The incidence of CRS1 and in-hospital mortality increased in AMI patients as NT-proBNP and hs-CRP increased, and eGFR decreased(P<0.05). As CRS1 was aggravated, eGFR tended to decrease, and NT-proBNP and hs-CRP tended to increase before CRS1 became severe. Kaplan-Meier survival analysis showed that the in-hospital mortality in the AMI patients was correlated with the number of abnormal biomarkers(P<0.001). Abnormal biomarkers ≥2 was an independent risk factor for in-hospital death(RR=2.452, 95%CI 1.105-5.440; P=0.027). Conclusion The combination of NT-proBNP, eGFR, and hs-CRP at presentation may assist risk stratification for the development of CRS1 in AMI patients.
引文
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[5] 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: 10.1093/eurheartj/ehr236.
[6] Steg PG, James SK, Atar D, et al. ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation[J]. Eur Heart J, 2012, 33(20): 2569-2619. DOI: 10.1093/eurheartj/ehs215.
[7] Mccullough PA, Kellum JA, Haase M, et al. Pathophysiology of the cardiorenal syndromes: executive summary from the eleventh consensus conference of the Acute Dialysis Quality Initiative (ADQI)[J]. Contrib Nephrol, 2013, 182: 82-98. DOI: 10.1159/000349966.
[8] Chen KP, Cavender S, Lee J, et al. Peripheral edema, central venous pressure, and risk of AKI in critical illness[J]. Clin J Am Soc Nephrol, 2016, 11(4): 602-608. DOI: 10.2215/cjn.08080715.
[9] F Gnanaraj J, von Haehling S, Anker SD, et al. The relevance of congestion in the cardio-renal syndrome[J]. Kidney Int, 2013, 83(3): 384-391. DOI: 10.1038/ki.2012.406.
[10] Virzi GM, Torregrossa R, Cruz DN, et al. Cardiorenal syndrome type 1 may be immunologically mediated: a pilot evaluation of monocyte apoptosis[J]. Cardiorenal Med, 2012, 2(1): 33-42. DOI: 000335499.
[11] Lassus JP, Harjola VP, Peuhkurinen K, et al. Cystatin C, NT-proBNP, and inflammatory markers in acute heart failure: insights into the cardiorenal syndrome[J]. Biomarkers, 2011, 16(4): 302-310. DOI: 10.3109/1354750x.2011.555822.
[12] Hou FF, Yang X. Advances in the management of acute cardiorenal syndrome in China: biomarkers for predicting development and outcomes[J]. Kidney Dis (Basel), 2017, 2(4): 145-150. DOI: 10.1159/000449026.
[13] Yamashita T, Seino Y, Ogawa A, et al. N-terminal pro-BNP is a novel biomarker for integrated cardio-renal burden and early risk stratification in patients admitted for cardiac emergency[J]. J Cardiol, 2010, 55(3): 377-383. DOI: 10.1016/j.jjcc.2010.01.008.
[14] Aimo A, Januzzi JL Jr, Vergaro G, et al. High-sensitivity troponin T, NT-proBNP and glomerular filtration rate: a multimarker strategy for risk stratification in chronic heart failure[J]. Int J Cardiol, 2019, 277: 166-172. DOI: 10.1016/j.ijcard.2018.10.079.
[15] Ma QQ, Yang XJ, Yang NQ, et al. Study on the levels of uric acid and high-sensitivity C-reactive protein in ACS patients and their relationships with the extent of the coronary artery lesion[J]. Eur Rev Med Pharmacol Sci, 2016, 20(20): 4294-4298.
[2] Gonzalez RP, Comba PC, Esteban MR, et al. Incidence, mortality and positive predictive value of type 1 cardiorenal syndrome in acute coronary syndrome[J]. PLoS One, 2016, 11(12): e0167166. DOI: 10.1371/journal.pone.0167166.
[3] 杜辉, 刘桂峰, 杨洁. 老年心肾综合征患者的临床特征和预后分析[J]. 中华老年多器官疾病杂志, 2016, 15(5): 377-381. DOI: 10.11915/j.issn.1671-5403.2016.05.089. Du H, Liu GF, Yang J. Clinical characteristics and prognosis of cardiorenal syndrome in the elderly[J]. Chin J Mult Organ Dis Elderly, 2016, 15(5): 377-381. DOI: 10.11915/j.issn.1671-5403.2016.05.089.
[4] Zhang DQ, Li HW, Chen HP, et al. Combination of amino-terminal pro-BNP, estimated GFR, and high-sensitivity CRP for predicting cardiorenal syndrome type 1 in acute myocardial infarction patients[J]. J Am Heart Assoc, 2018, 7(19): e009162. DOI: 10.1161/jaha.118.009162.
[5] 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: 10.1093/eurheartj/ehr236.
[6] Steg PG, James SK, Atar D, et al. ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation[J]. Eur Heart J, 2012, 33(20): 2569-2619. DOI: 10.1093/eurheartj/ehs215.
[7] Mccullough PA, Kellum JA, Haase M, et al. Pathophysiology of the cardiorenal syndromes: executive summary from the eleventh consensus conference of the Acute Dialysis Quality Initiative (ADQI)[J]. Contrib Nephrol, 2013, 182: 82-98. DOI: 10.1159/000349966.
[8] Chen KP, Cavender S, Lee J, et al. Peripheral edema, central venous pressure, and risk of AKI in critical illness[J]. Clin J Am Soc Nephrol, 2016, 11(4): 602-608. DOI: 10.2215/cjn.08080715.
[9] F Gnanaraj J, von Haehling S, Anker SD, et al. The relevance of congestion in the cardio-renal syndrome[J]. Kidney Int, 2013, 83(3): 384-391. DOI: 10.1038/ki.2012.406.
[10] Virzi GM, Torregrossa R, Cruz DN, et al. Cardiorenal syndrome type 1 may be immunologically mediated: a pilot evaluation of monocyte apoptosis[J]. Cardiorenal Med, 2012, 2(1): 33-42. DOI: 000335499.
[11] Lassus JP, Harjola VP, Peuhkurinen K, et al. Cystatin C, NT-proBNP, and inflammatory markers in acute heart failure: insights into the cardiorenal syndrome[J]. Biomarkers, 2011, 16(4): 302-310. DOI: 10.3109/1354750x.2011.555822.
[12] Hou FF, Yang X. Advances in the management of acute cardiorenal syndrome in China: biomarkers for predicting development and outcomes[J]. Kidney Dis (Basel), 2017, 2(4): 145-150. DOI: 10.1159/000449026.
[13] Yamashita T, Seino Y, Ogawa A, et al. N-terminal pro-BNP is a novel biomarker for integrated cardio-renal burden and early risk stratification in patients admitted for cardiac emergency[J]. J Cardiol, 2010, 55(3): 377-383. DOI: 10.1016/j.jjcc.2010.01.008.
[14] Aimo A, Januzzi JL Jr, Vergaro G, et al. High-sensitivity troponin T, NT-proBNP and glomerular filtration rate: a multimarker strategy for risk stratification in chronic heart failure[J]. Int J Cardiol, 2019, 277: 166-172. DOI: 10.1016/j.ijcard.2018.10.079.
[15] Ma QQ, Yang XJ, Yang NQ, et al. Study on the levels of uric acid and high-sensitivity C-reactive protein in ACS patients and their relationships with the extent of the coronary artery lesion[J]. Eur Rev Med Pharmacol Sci, 2016, 20(20): 4294-4298.