AECOPD不伴AMI住院患者高敏心肌肌钙蛋白T动态增高的病因分析
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摘要
目的探讨慢性阻塞性肺疾病急性加重(AECOPD)不伴急性心肌梗死(AMI)住院患者高敏心肌肌钙蛋白T(hs-cTnT)动态增高的病因,为临床准确诊治提供帮助。方法选取2016年1月至2018年1月四川大学华西医院呼吸内科AECOPD不伴AMI住院患者为研究对象,患者因胸痛在12 h内测定两次hs-cTnT和其他实验室指标,两次hs-cTnT水平增高≥50%为病例组,水平增高<50%为对照组,收集患者实验室检查结果和临床资料,探讨AECOPD不伴AMI患者hs-cTnT动态增高的原因。结果病例组hs-cTnT水平在12 h内从78.4(33.9～129.0)ng/L大幅上升至185.9(126. 0～468. 2)ng/L(P <0. 05),而对照组hs-cTnT水平无变化(P> 0. 05);病例组在12 h内肾功能指标(Urea、Crea)和感染指标(WBC、PCT)水平大幅升高(P <0. 05),呼吸功能指标(PCO_2、PO_2)表现为PCO_2水平升高,而PO_2水平降低(P <0.05),对照组肾功能指标、感染指标及呼吸功能指标变化差异无统计学意义(P>0. 05);病例组在12 h内hs-cTnT变化率为132. 98%(87.27%～338. 98%),显著高于对照组的12.71%(6. 09%～30.54%)(P <0.05),病例组在12h内Urea、Crea、WBC、PCT、PCO_2、PO_2的变化率均高于对照组,差异有统计学意义(P<0.05)。结论加重的感染、呼吸功能减弱以及肾功能减退是AECOPD不伴AMI患者hs-cTnT动态升高的主要原因,临床诊治中应注意鉴别诊断。
Objective To investigate the etiology of high-sensitivity cardiac troponin T(hs-cTnT)in AECOPD patients without acute myocardial infarction(AMI),and to provide information for accurate clinical diagnosis and treatment. Methods AECOPD patients without AMI in the Department of Respiratory Medicine, West China Hospital of Sichuan University, from January 2016 to January 2018 were enrolled for the study. The levels of hs-cTnT and other laboratory indicators were determined twice within 12 hours after chest pain. The case group was defined as the increase rate as hs-cTnT≥50% from the first time to the second time,while the control group was defined as the increase rate <50%. The laboratory test results and clinical data from both groups were collected to address the reason of the dynamic increase of hs-cTnT in AECOPD patients without AMI.Results The hs-cTnT level in the case group increased significantly from 78.4(33. 9,129. 0) ng/L to185.9(126.0,468. 2)ng/L within 12 hours(P <0.05),while the hs-cTnT level in the control group did not change(P > 0. 05). The renal function index(Urea, Crea) and infection index(WBC,PCT)in the case group showed a significant increase within 12 hours(P <0.05),and the respiratory function index(PCO_2,PO_2) showed an increase in PCO_2 and a decrease in PO_2(P < 0.05). There were no significant differences in renal function index, infection index and respiratory function index between the case group and the control group(P >0.05). The change rate of hs-cTnT in the case group was 132.98%(87. 27%,338.98%) within12 hours,which was significantly higher than that of the control group with 12. 71 %(6. 09%,30. 54%)(P <0.05). The change rates of Urea,Crea,WBC,PCT,PC02 and P02 in the case group were higher than those in the control group within 12 hours, and the differences were significant(P <0. 05). Conclusion Aggravated infection, decreased respiratory function, and renal dysfunction are the main reasons for the significant increase of hs-cTnT in AECOPD patients without AMI. We should pay attention to differential diagnosis and treatment.
Objective To investigate the etiology of high-sensitivity cardiac troponin T(hs-cTnT)in AECOPD patients without acute myocardial infarction(AMI),and to provide information for accurate clinical diagnosis and treatment. Methods AECOPD patients without AMI in the Department of Respiratory Medicine, West China Hospital of Sichuan University, from January 2016 to January 2018 were enrolled for the study. The levels of hs-cTnT and other laboratory indicators were determined twice within 12 hours after chest pain. The case group was defined as the increase rate as hs-cTnT≥50% from the first time to the second time,while the control group was defined as the increase rate <50%. The laboratory test results and clinical data from both groups were collected to address the reason of the dynamic increase of hs-cTnT in AECOPD patients without AMI.Results The hs-cTnT level in the case group increased significantly from 78.4(33. 9,129. 0) ng/L to185.9(126.0,468. 2)ng/L within 12 hours(P <0.05),while the hs-cTnT level in the control group did not change(P > 0. 05). The renal function index(Urea, Crea) and infection index(WBC,PCT)in the case group showed a significant increase within 12 hours(P <0.05),and the respiratory function index(PCO_2,PO_2) showed an increase in PCO_2 and a decrease in PO_2(P < 0.05). There were no significant differences in renal function index, infection index and respiratory function index between the case group and the control group(P >0.05). The change rate of hs-cTnT in the case group was 132.98%(87. 27%,338.98%) within12 hours,which was significantly higher than that of the control group with 12. 71 %(6. 09%,30. 54%)(P <0.05). The change rates of Urea,Crea,WBC,PCT,PC02 and P02 in the case group were higher than those in the control group within 12 hours, and the differences were significant(P <0. 05). Conclusion Aggravated infection, decreased respiratory function, and renal dysfunction are the main reasons for the significant increase of hs-cTnT in AECOPD patients without AMI. We should pay attention to differential diagnosis and treatment.
引文
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[10]段玉香,范晔,杨海峰,等.慢性阻塞性肺疾病急性加重期患者肺部真菌感染对血清炎症因子的影响[J].中华医院感染学杂志,2017,27(4):754-757.
[11] TAYLANM, DEMIR M, KAYA H, et al. Alterations of the neutrophil-lymphocyte ratio during the period of stable and acute exacerbation of chronic obstructive pulmonary disease patients[J].Clin Respir J,2017,11(3):311-317.
[12] COLAK A, YILMAZ C,TOPRAK B,et al. Procalcitonin and CRP as Biomarkers in iscrimination of Community-acquired Pneumonia and Exacerbation of COPD[J]. J Med Biochem,2017,36(2):122-126.
[13] WALLEY K R. Deeper understanding of mechanisms contributing to sepsis-induced myocardial dysfunction[J]. Crit Care,2014,18(3):137.
[14]苗强,李立新,唐江涛.脓毒血症患者高敏肌钙蛋白T水平及预后判断的价值研究[J].中国实验诊断学,2017,21(3):438-441.
[15] HUANG H,ZHU S,WANG W,et al. Diagnosis of acute myocardial infarction in patients with renal insufficiency using high-sensitivity troponin T[J]. Clin Chem Lab Med,2015,53(5):723-730.
[2] PICKERING J W,GREENSLADE J H,CULLEN L,et al. Validation of presentation and 3 h high-sensitivity troponin to rule-in and ruleout acute myocardial infarction[J]. Heart, 2016, 102(16):1270-1278.
[3] UREARNEY P G, PATEL J, NEWSON R, et al. Global and regional trends in COPD mortality, 1990-2010[J]. Eur Respir J, 2015,45(5):1239-1247.
[4] LOPEZ-CAMPOS J L,TAN W, SORIANO J B. Global burden of COPD[J]. Respirology,2016,21(1):14-23.
[5] ROTHNIE K J, YAN R, SMEETH L, et al. Risk of myocardial infarction(MI):and death following MI in people with chronic obstructive pulmonary disease(COPD):a systematic review and meta-analysis[J]. BMJ Open,2015,5(9):e007824.
[6]中华医学会呼吸病学分会慢性阻塞性肺疾病学组.慢性阻塞性肺疾病诊治指南(2007年修订版)[J].中华内科杂志,2007,46(3):254-261.
[7] WANG W Q,HUANG H L,ZHU S,et al. High-sensitivity cardiac troponin T in patients with acute myocardial infarction in acute exacerbation of chronic obstructive pulmonary disease[J]. Clin Lab,2015,61(8):1083-1093.
[8] S(?)YSETH V,BHATNAGAR R, HOLMEDAHL N H, et al. Acute exacerbation of COPD is associated with fourfold elevation of cardiac troponin T[J]. Heart,2013,99(2):122-126.
[9] KARADENIZ G, POLAT G, SENOL G, et al. C-reactive protein measurements as a marker of the severity of chronic obstructive pulmonary disease exacerbations[J]. Inflammation, 2013,36(4):948-953.
[10]段玉香,范晔,杨海峰,等.慢性阻塞性肺疾病急性加重期患者肺部真菌感染对血清炎症因子的影响[J].中华医院感染学杂志,2017,27(4):754-757.
[11] TAYLANM, DEMIR M, KAYA H, et al. Alterations of the neutrophil-lymphocyte ratio during the period of stable and acute exacerbation of chronic obstructive pulmonary disease patients[J].Clin Respir J,2017,11(3):311-317.
[12] COLAK A, YILMAZ C,TOPRAK B,et al. Procalcitonin and CRP as Biomarkers in iscrimination of Community-acquired Pneumonia and Exacerbation of COPD[J]. J Med Biochem,2017,36(2):122-126.
[13] WALLEY K R. Deeper understanding of mechanisms contributing to sepsis-induced myocardial dysfunction[J]. Crit Care,2014,18(3):137.
[14]苗强,李立新,唐江涛.脓毒血症患者高敏肌钙蛋白T水平及预后判断的价值研究[J].中国实验诊断学,2017,21(3):438-441.
[15] HUANG H,ZHU S,WANG W,et al. Diagnosis of acute myocardial infarction in patients with renal insufficiency using high-sensitivity troponin T[J]. Clin Chem Lab Med,2015,53(5):723-730.