Cardiac troponins: from myocardial infarction to chronic disease.
Cardiac troponins: from myocardial infarction to chronic disease.
复制标题
DOI：
10.1093/cvr/cvx183
复制
发表时间：
2017-12-01
影响因子：
10.8
通讯作者：
Marber MS
中科院分区：
文献类型：
--
作者：
Park KC;Gaze DC;Collinson PO;Marber MS
1973年肌钙蛋白生理学上不同亚基的阐明极大地促进了我们对心脏收缩的理解。虽然肌钙蛋白在骨骼肌和心肌中表达，但肌钙蛋白I/T的同种型在心脏中选择性表达。通过利用这些蛋白质中的心脏限制性表位，迄今为止最成功的诊断测试之一已经开发出来：心肌肌钙蛋白（cTn）测定。在过去的十年中，cTn一直被认为是急性心肌坏死的金标准标志物：急性心肌梗死（AMI）的病理标志。虽然cTn是排除疑似急性冠状动脉综合征（ACS）患者中AMI的基石，但在没有提示AMI的临床体征的患者中经常观察到cTn升高，通常反映了“来源不明”的心肌损伤。cTn通常在急性非ACS疾病以及慢性疾病中升高。目前尚不清楚为什么会出现这些升高;但不能忽视，因为慢性不适患者的cTn水平与预后直接相关。奇怪的是，检测灵敏度的提高意味着由于特异性降低，必须考虑更多的鉴别诊断，因为现在在这些非ACS疾病中更容易检测到cTn。重要的是要意识到cTn对心肌损伤具有高度特异性，这可能归因于无数的潜在原因，强调cTn是器官特异性而非疾病特异性生物标志物的概念。此外，在极端运动后使用高灵敏度测定检测cTn升高的能力令人不安。有人认为肌钙蛋白释放可以在没有心肌细胞坏死的情况下发生，这与传统的教条相矛盾，强调需要了解这种释放的机制。这篇综述讨论了肌钙蛋白的基本生物学，其在血清中检测背后的生理学，其在AMI诊断中的应用，以及为什么cTn可以在慢性疾病中升高的一些关键概念和实验证据。
Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to date has been developed: cardiac troponin (cTn) assays. For the past decade, cTn has been regarded as the gold-standard marker for acute myocardial necrosis: the pathological hallmark of acute myocardial infarction (AMI). Whilst cTn is the cornerstone for ruling-out AMI in patients presenting with a suspected acute coronary syndrome (ACS), elevated cTn is frequently observed in those without clinical signs indicative of AMI, often reflecting myocardial injury of ‘unknown origin’. cTn is commonly elevated in acute non-ACS conditions, as well as in chronic diseases. It is unclear why these elevations occur; yet they cannot be ignored as cTn levels in chronically unwell patients are directly correlated to prognosis. Paradoxically, improvements in assay sensitivity have meant more differential diagnoses have to be considered due to decreased specificity, since cTn is now more easily detected in these non-ACS conditions. It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasizing the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasizing a need to understand the mechanisms of such release. This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases.
登录
查看更多内容
影响因子：
37.8
作者：
Apple, FS;Murakami, MM;Herzog, CA
通讯作者：
Herzog, CA
DOI：
10.1016/j.jacbts.2017.03.008
发表时间：
2017-04
期刊：
JACC. Basic to translational science
影响因子：
--
作者：
Amgalan D;Pekson R;Kitsis RN
通讯作者：
Kitsis RN
影响因子：
20.1
作者：
ANDERSON, PAW;MALOUF, NN;ALLEN, PD
通讯作者：
ALLEN, PD
影响因子：
39.3
作者：
Alpert, JS;Antman, E;Wood, D
通讯作者：
Wood, D
影响因子：
9.3
作者：
Collinson, Paul O.;Heung, Yen Ming;Apple, Fred S.
通讯作者：
Apple, Fred S.