Troponins in Heart Failure - a Perpetual Challenge

Abstract

Increased troponin levels in HF are a frequent and significant finding, as it strongly correlates with the underlying pathogenic mechanisms, diagnosis and prognosis. The advent of hs-cTn testing, as opposed to conventional troponin testing, led to additional difficulties in result interpretation. Most frequently, though not exclusively, increased cTn levels in acute or chronic failure is correlated, with myocardial necrosis (AMI); the diagnosis of AMI is confirmed if other criteria are fulfilled, as described in the fourth Universal Definition of Myocardial Infarction. Increased cTn levels below the cut-off for AMI suggest acute or chronic injury, depending on the ascending and/or descending trend curve or stable levels of cTn on serial testing. In acute or chronic HF with reduced or preserved EF, increased cTn levels carry prognostic value for adverse outcomes. Acute and chronic HF, as well as other ischemic or non-ischemic conditions, may lead to a transient increase in cTn levels: hypertensive crises, tachyarrhythmias, valvular regurgitation, myocarditis, stroke, mandating differential diagnosis with ACS. There are multiple mechanisms that explain increased levels of cTn: myocardial necrosis or coronary thrombosis (type I MI), supply-demand mismatch with subendocardial ischemia/injury, cardiomyocyte apoptosis, inflammatory cytokines, neurohomonal changes. Screening for cTn levels in the population at high cardiovascular risk yields prognostic information on development of de novo HF or other cardiovascular adverse events.