Episodes of Acute Heart Failure Syndrome Are Associated With Increased Levels of Troponin and Extracellular Matrix Markers
Episodes of Acute Heart Failure Syndrome Are Associated With Increased Levels of Troponin and Extracellular Matrix Markers
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DOI：
10.1161/circheartfailure.108.844324
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发表时间：
2010-01-01
影响因子：
9.7
通讯作者：
Colucci, Wilson S.
中科院分区：
文献类型：
--
作者：
Biolo, Andreia;Fisch, Mark;Colucci, Wilson S.
背景：心肌细胞丢失和细胞外基质（ECM）周转增加是导致慢性心力衰竭（HF）病理性心肌重塑的核心机制。我们测试了以下假设：急性心力衰竭综合征 (AHFS) 发作与心肌细胞损伤标记物和 ECM 更新的短暂增加相关，超出了慢性稳定型心力衰竭中观察到的水平。方法和结果 - 对 80 名患者进行了评估，前瞻性地将其分为 3 组：AHFS（n=39）；AHFS（n=39）；慢性稳定收缩性心力衰竭 (n=21)；和无 HF 的对照受试者 (n=20)。通过测量血浆肌钙蛋白 I 来评估心肌细胞损伤。通过测量血浆基质金属蛋白酶、基质金属蛋白酶的组织抑制剂以及 I 型原胶原 N 端和 III 型原胶原 N 端肽来评估 ECM 周转。在 AHFS 组中，（1）在因心力衰竭失代偿而入院时，（2）出院时，以及（3）恢复到慢性稳定代偿状态的患者出院几周后，获得了生物标志物。在稳定心力衰竭患者中（与非心力衰竭对照组相比），肌钙蛋白 I 略有增加，并且 ECM 转换的任何标志物几乎没有差异或没有差异。在 AHFS 患者中，肌钙蛋白 I 和 3 种 ECM 更新标志物（基质金属蛋白酶 - 2、基质金属蛋白酶组织抑制剂 - 1 和 III 型前胶原 N 端肽）升高（与慢性稳定型心力衰竭相比），并且在恢复代偿状态的患者中，所有肌钙蛋白 I 和 3 个 ECM 更新标志物均下降至慢性心力衰竭水平。 结论：AHFS 发作与肌细胞损伤和 ECM 更新标志物的短暂增加有关，这可能反映了加速AHFS 期间病理性心肌重构的影响。 （循环心力衰竭。2010；3：44-50。）
Background-Increased myocyte loss and extracellular matrix (ECM) turnover are central mechanisms that contribute to pathological myocardial remodeling in chronic heart failure (HF). We tested the hypothesis that episodes of acute HF syndrome (AHFS) are associated with transient increases in markers of myocyte injury and ECM turnover beyond those observed in chronic stable HF.Methods and Results-Markers of myocyte injury and ECM turnover were assessed in 80 patients prospectively divided into 3 groups: AHFS (n=39); chronic stable systolic HF (n=21); and control subjects without HF (n=20). Myocyte injury was assessed by measuring plasma troponin I. ECM turnover was assessed by measuring plasma matrix metalloproteinases, tissue inhibitors of matrix metalloproteinases, and procollagen N-terminal type I and procollagen type III N-terminal peptides. In the AHFS group, biomarkers were obtained (1) at the time of hospital admission for an episode of HF decompensation, (2) at the time of hospital discharge, and (3) several weeks after discharge in patients who had returned to a chronic stable compensated state. In patients with stable HF (versus non-HF controls), there was a small increase in troponin I and little or no difference in any marker of ECM turnover. In patients with AHFS, troponin I and 3 markers of ECM turnover (matrix metalloproteinases-2, tissue inhibitors of matrix metalloproteinases-1, and procollagen type III N-terminal peptides) were elevated (versus chronic stable HF), and all fell toward chronic HF levels in patients who returned to a compensated state.Conclusion-Episodes of AHFS are associated with transient increases in markers of myocyte injury and ECM turnover that may reflect an acceleration of pathological myocardial remodeling during AHFS. (Circ Heart Fail. 2010; 3: 44-50.)