The Role of Troponin for Acute Heart Failure

To review the mechanisms, clinical interpretation, prognostic role, and future research regarding cardiac troponin (cTn) in the assessment of acute heart failure (AHF) patients presenting to the emergency department (ED).

cTn has become a necessary component of the evaluation of AHF patients in the ED, largely because of its independently predictive value as a prognosticator of poor outcome. High-sensitivity assays (hs-cTn) may add risk stratification value beyond conventional assays, specifically with regard to identifying low-risk AHF patients. Moreover, as the complex mechanisms of cTn release in AHF continue to be elucidated, recent studies suggest that many of the key hemodynamic derangements that define specific AHF syndromes may also be direct culprits in cTn release. cTn is released in AHF in response to both non-ischemic (e.g., increased afterload, increased preload, inflammatory signaling, altered calcium handling) and ischemic mechanisms. cTn detectable on conventional sensitivity assays predicts poor prognosis when measured in the ED or when noted in historical data such as past ED visits or at the time of discharge from the most recent AHF hospitalization. hs-cTn assays provide detectable values in nearly all AHF patients. Evidence is evolving on using hs-cTn levels below the upper limit of normal to potentially identify low-risk ED patients, and further research is needed. Among the classically cited risk factors for AHF mortality, cTn and natriuretic peptides stand as independent and synergistic prognostic factors even after adjustment for confounders. Many other risk factors, such as ejection fraction, often failed to retain ED prognostic value beyond these two biomarkers.