Cardiology Division, Massachusetts General Hospital, Yawkey 5984, 32 Fruit Street, Boston, MA 02114, USA.
Eur Heart J. 2012 Sep;33(18):2265-71. doi: 10.1093/eurheartj/ehs191. Epub 2012 Jun 28.
Cardiac troponin testing is commonly performed in patients with heart failure (HF). Despite being strongly linked to spontaneous (Type I) acute myocardial infarction (MI)--a common cause of acute HF syndromes--it is well recognized that concentrations of circulating troponins above the 99 th percentile of a normal population in the context of both acute and chronic HF are highly prevalent, and frequently unrelated to Type I MI. Other mechanism(s) leading to troponin elevation in HF syndromes remain elusive in many cases but prominently includes supply-demand inequity (Type II MI), which may be associated with coronary artery obstruction and endothelial dysfunction, or may occur in the absence of coronary obstruction due to increased oxygen demand related to increased wall tension, anaemia, or other factors provoking subendocardial injury. Non-coronary triggers, such as cellular necrosis, apoptosis, or autophagy in the context of wall stress may explain the troponin release in HF, as can toxic effects of circulating neurohormones, toxins, inflammation, and infiltrative processes, among others. Nonetheless, across a wide spectrum of HF syndromes, when troponin elevation occurs, independent of mechanism, it is strongly predictive of an adverse outcome. Clinicians should be aware of the high frequency of troponin elevation when measuring the marker in patients with HF, should keep in mind the possible causes of this phenomenon, and, independent of a diagnosis of 'acute MI', should recognize the considerable ramifications of troponin elevation in this setting.
在心力衰竭（HF）患者中，通常会进行心肌肌钙蛋白检测。尽管心肌肌钙蛋白与自发性（I 型）急性心肌梗死（MI）密切相关——这是急性 HF 综合征的常见原因——但人们已经认识到，在急性和慢性 HF 情况下，循环肌钙蛋白浓度高于正常人群第 99 百分位数的情况非常普遍，并且常常与 I 型 MI 无关。在许多情况下，导致 HF 综合征中肌钙蛋白升高的其他机制仍然难以捉摸，但主要包括供应-需求不平衡（II 型 MI），这可能与冠状动脉阻塞和内皮功能障碍有关，或者可能发生在没有冠状动脉阻塞的情况下，因为与增加壁张力、贫血或其他引起心内膜下损伤的因素相关的增加的氧气需求。在壁应力的情况下，非冠状动脉触发因素，如细胞坏死、细胞凋亡或自噬，可能解释了 HF 中的肌钙蛋白释放，循环神经激素、毒素、炎症和浸润性过程等的毒性作用也可能解释了肌钙蛋白释放。尽管如此，在广泛的 HF 综合征范围内，当肌钙蛋白升高发生时，无论机制如何，它都强烈预示着不良预后。临床医生在测量 HF 患者的标志物时应注意肌钙蛋白升高的高频率，应牢记这种现象的可能原因，并且，即使没有“急性 MI”的诊断，也应认识到在这种情况下肌钙蛋白升高的重大影响。
