Troponin elevation in patients with heart failure: on behalf of the third Universal Definition of Myocardial Infarction Global Task Force: Heart Failure Section

被引:235
作者
Januzzi, James L., Jr. [1 ]
Filippatos, Gerasimos [2 ]
Nieminen, Markku [3 ]
Gheorghiade, Mihai [4 ]
机构
[1] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA
[2] Univ Athens, Hosp Attikon, Dept Cardiol, Heart Failure Unit, Athens, Greece
[3] Univ Helsinki, Cent Hosp, Div Cardiol, Helsinki, Finland
[4] Northwestern Univ, Feinberg Sch Med, Ctr Cardiovasc Innovat, Chicago, IL 60611 USA
关键词
Troponin; Heart failure; Prognosis; ACUTE CORONARY SYNDROME; BRAIN NATRIURETIC PEPTIDE; CARDIAC TROPONIN; AMBULATORY PATIENTS; PROGNOSTIC VALUE; SENSITIVE ASSAY; SERIAL CHANGES; I ELEVATION; CIRCULATING CONCENTRATIONS; RISK STRATIFICATION;
D O I
10.1093/eurheartj/ehs191
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 syndromesit is well recognized that concentrations of circulating troponins above the 99th 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 supplydemand 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 oacute MI', should recognize the considerable ramifications of troponin elevation in this setting.
引用
收藏
页码:2265 / +
页数:8
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