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

• Published in: European heart journal Vol. 33; no. 18; pp. 2265 - 2271
• Main Authors: JANUZZI, James L, FILIPPATOS, Gerasimos, NIEMINEN, Markku, GHEORGHIADE, Mihai
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.09.2012
• Subjects: Acute Disease; Biological and medical sciences; Biomarkers - metabolism; Cardiology. Vascular system; Chronic Disease; Coronary heart disease; Heart; Heart Failure - diagnosis; Heart Failure - etiology; Heart Failure - mortality; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Humans; Medical sciences; Myocardial Infarction - diagnosis; Myocardial Infarction - etiology; Myocardial Infarction - mortality; Myocarditis. Cardiomyopathies; Risk Assessment; Risk Factors; Sensitivity and Specificity; Troponin - metabolism; Human; Myocardial infarction; Heart failure; Prognosis; Force; Definition; Cardiovascular disease; Patient; Coronary heart disease; Myocardial disease; Section; Troponin; Circulatory system; Cardiology
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/eurheartj/ehs191

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.