Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain
Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain
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DOI：
10.1067/mhj.2001.111767
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发表时间：
2001-02-01
影响因子：
4.8
通讯作者：
Solal, AC
中科院分区：
文献类型：
--
作者：
Logeart, D;Beyne, P;Solal, AC
背景心肌细胞死亡在心力衰竭（HF）中起一定作用，与是否存在冠状动脉疾病无关。该研究的目的是评估这一假设通过使用的心肌肌钙蛋白I（cTnI）assay.Methods和结果71例非缺血性HF，纽约心脏协会（NYHA）II-IV级，与正常冠状动脉造影和排除心肌病后，在研究中进行了评价。对照组包括9名健康受试者和15名因严重非心源性呼吸困难住院的患者。在入院时用研究试剂（cTnlus）测定心脏Tnl浓度，其特征在于检测限为0.026 ng/ml，分析灵敏度高，为0.002 ng/ml。在19名HF患者中，cTnlus水平大于0.026 ng/mL，范围在0.027和0.463 ng/ml之间，而在对照组中未检测到cTnlus水平。使用参考测定，仅2例HF患者cTnI值异常。根据NYHA IV级或肺水肿的存在，在这19例患者中的17例中观察到重度HF。cTnlus水平升高的患者具有更严格的二尖瓣多普勒模式（P <0.001）和更明显的左心室（LV）向心性重构（P <0.0001），而两个HF组的IV选举分数相似。cTnl水平的增加也与LV壁应变生物标志物相关，即脑钠肽血浆水平的增加（P <0.001）。结论：cTnl测定是一种有前途的检测HF心肌溶解的生化方法，与冠状动脉疾病的存在无关。这种轻微的肌溶解可能部分与左心室壁应变严重增加有关。
Background Myocyte death could play a role in heart failure (HF) irrespective of the presence of coronary artery disease. The study aimed to assess this hypothesis by use of the cardiac troponin I (cTnl) assay.Methods and Results Seventy-one patients with nonischemic HF, New York Heart Association (NYHA) class II-IV, with a normal coronary angiogram and after exclusion of myocardiopathies were evaluated in the study. The control group included 9 healthy subjects and 15 patients hospitalized for severe noncardiac dyspnea. Cardiac Tnl concentrations were determined at admission with a research reagent (cTnlus) characterized by a detection limit of 0.026 ng/ml and a high analytic sensitivity of 0.002 ng/ml. cTnlus levels were more than 0.026 ng/mL in 19 HF patients, ranging between 0.027 and 0.463 ng/ml, whereas no cTnlus level was detectable in the control group. With use of a reference assay, only 2 HF patients had abnormal cTnl values. Severe HF was observed in 17 of these 19 patients, assessed by NYHA class IV or by the presence of pulmonary edema. Patients with an increased cTnlus level had a more restrictive mitral Doppler pattern (P < .001) and a more distinctive left ventricular (LV) concentric remodeling (P < .0001), whereas IV election fraction was similar in both HF groups. The increased cTnlus level was also associated with a LV wall strain biologic marker tie, an increased brain natriuretic peptide plasma level) (P < .001).Conclusions: cTnl assay is a promising biochemical method for detecting cardiac myolysis in HF, independent of the presence of coronary artery disease. This subtle myolysis could be in part related to the severely increased LV wall strain.