Non-ACS Troponin Elevation and Outcomes

Study Questions:

Are elevations in cardiac troponin (cTn) levels not attributed to acute coronary syndromes (ACS) associated with outcomes in acutely admitted patients?


The authors queried the SWEDEHEART (Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies) registry, which routinely collects information on patients hospitalized for suspected acute coronary syndromes (ACS) in all Swedish hospitals. They identified 48,872 patients in whom cTn was measured, and who were discharged without a specific diagnosis, and examined the association between cTn levels, clinical characteristics, and long-term outcomes in three nested subcohorts: patients without previous ACS, revascularization, stroke, or heart failure (subcohort 1, n = 38,281), of which another subcohort was selected excluding those with significant renal dysfunction (estimated glomerular filtration rate <60 ml/min/1.73 m2; subcohort 2, n = 31,822), and a third subcohort excluding those with a ejection fraction ≤50% or significant coronary artery disease ≥50% stenosis on angiography (n = 1,951).


The vast majority of patients included (95%) had been admitted for chest pain. The prevalence of cardiovascular risk factors and left ventricular dysfunction increased across cTn strata. Fifteen percent of patients (n = 7,529) experienced a major adverse event (MAE; mortality, ACS, heart failure, or stroke) during a median follow-up of 4.9 years. Overall, the incidence of MAE increased in stepwise fashion across strata of higher cTn levels, with survival curves diverging early (<6 months of follow-up). Results were mostly consistent between all three subcohorts and with multivariable analyses. Notably, high cTn levels in those with no evident risk factors for myocardial injury (subcohort 3) were associated with a 3.5-fold increase in the risk of MAE.


Elevated cTn is associated with increased risk of MAE, even in patients with no evidence of coronary artery disease, heart failure, or kidney dysfunction.


This study reiterates what has previously been shown in smaller cohorts: elevations in cTn, regardless of etiology, portend a worse prognosis, even in those without heart failure, obstructive coronary artery disease, or significant kidney dysfunction. The authors rightfully emphasize that troponin elevations should not be taken lightly, and every effort should be pursued to identify an etiology and optimize cardiovascular risk factors in these patients. It is important to note that the study does not distinguish between acute and chronic elevations in troponinn or excludes other causes of cTn elevation such as pulmonary emboli, arrhythmias, myopericarditis, or demand ischemia and is limited to patients presenting with chest pain. Thus, the occasional puzzling patients with truly no discernable cardiovascular disease and an unexplainable elevated cTn likely represents a very small proportion of this cohort.

Clinical Topics: Acute Coronary Syndromes, Dyslipidemia, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Prevention, Valvular Heart Disease, Atherosclerotic Disease (CAD/PAD), Lipid Metabolism, Acute Heart Failure, Interventions and ACS, Interventions and Coronary Artery Disease, Interventions and Imaging, Interventions and Structural Heart Disease, Angiography, Nuclear Imaging

Keywords: Acute Coronary Syndrome, Angiography, Chest Pain, Constriction, Pathologic, Coronary Artery Disease, Glomerular Filtration Rate, Heart Failure, Heart Valve Diseases, Risk Factors, Secondary Prevention, Stroke, Stroke Volume, Troponin, Troponin C, Ventricular Dysfunction, Left

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