Importance: Traditionally, elevated troponin concentrations were synonymous with myocardial infarction. But with improvements in troponin assays, elevated concentrations without overt myocardial ischemia are now more common; this is referred to as myocardial injury. Physicians may be falsely reassured by the absence of myocardial ischemia; however, recent evidence suggests that myocardial injury is associated with even more detrimental outcomes. Accordingly, this article reviews the definition, epidemiology, differential diagnosis, diagnostic evaluation, and management of myocardial injury. Observations: Current epidemiological evidence suggests that myocardial injury without overt ischemia represents about 60% of cases of abnormal troponin concentrations when obtained for clinical indications, and 1 in 8 patients presenting to the hospital will have evidence of myocardial injury. Myocardial injury is a concerning prognosis; the 5-year mortality rate is approximately 70%, with a major adverse cardiovascular event rate of 30% in the same period. The differential diagnosis is broad and can be divided into acute and chronic precipitants. The initial workup involves an assessment for myocardial ischemia. If infarction is ruled out, further evaluation includes a detailed history, physical examination, laboratory testing, a 12-lead electrocardiogram, and (if there is no known history of structural or valvular heart disease) an echocardiogram. Unfortunately, no consensus exists on routine management of patients with myocardial injury. Identifying and treating the underlying precipitant is the most practical approach. Conclusion and Relevance: Myocardial injury is the most common cause of abnormal troponin results, and its incidence will likely increase with an aging population, increasing prevalence of cardiovascular comorbidities, and greater sensitivity of troponin assays. Myocardial injury represents a challenge to clinicians; however, given its serious prognosis, it warrants a thorough evaluation of its underlying precipitant. Future strategies to prevent and/or manage myocardial injury are needed.
Bibliographical noteFunding Information:
reports having received honoraria from Abbott Diagnostics and AstraZeneca. Dr Apple has acted as a consultant for LumiraDx and Banyon Biomarkers; is on the board of directors at HyTest Ltd; has received advisory honoraria from Instrumentation Laboratory and Siemens Healthineers; has been a research principal investigator through the Hennepin Healthcare Research Institute (formerly Minneapolis Medical Research Foundation); has had nonsalaried grant relationships with Abbott Diagnostics, Abbott POC, Roche Diagnostics, Siemens Healthcare, Quidel/Alere, Ortho-Clinical Diagnostics, Qurvo, Becton Dickinson, Beckman Coulter, Amgen, and Singulex; and has received personal fees from Clinical Chemistry during the conduct of the study. Dr Mills has acted as a consultant for Abbott Diagnostics, Beckman-Coulter, Roche, and Singulex; has received grants from Abbott Diagnostics; has received grants and personal fees from Siemens Healthineers outside the submitted work; and is supported by a Butler Senior Clinical Research Fellowship (grant FS/16/14/32023) and Research Excellence Award (grant RE/18/5/34216) from the British Heart Foundation. Dr Januzzi has received grant support from Roche Diagnostics, Abbott Diagnostics, Singulex, Prevencio, and Cleveland Heart Labs; has received consulting income from Roche Diagnostics, MyoKardia, Abbott, and Critical Diagnostics; and has participated in clinical end point committees and/or data safety monitoring boards for Boehringer-Ingelheim, Amgen, AbbVie, Janssen, Abbott, and Siemens Diagnostics. Dr Sandoval reports present participation in an advisory board for Abbott Diagnostics and past, nonsalaried advisory board participation for Roche Diagnostics. No other disclosures were reported.
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