Swedish researchers report a strong, graded association between all detectable levels of cardiac troponin measured by a high-sensitivity assay (hs-cTnT) and increased risk of myocardial infarction (MI), heart failure, and cardiovascular- and noncardiovascular-related deaths (J Am Coll Cardiol 2017;70:2226-36). The findings, which build on prior studies with similar outcomes, suggest a need for better evaluation and management strategies to reduce risk in patients with elevated hs-cTnT, according to the researchers.
The study involved 22,589 patients older than age 25 who presented with chest pain at the Karolinska University Hospital emergency department in Stockholm. After excluding patients who had an MI associated with their initial visit or who had acute illnesses that might have affected hs-cTnT, the researchers followed 19,460 patients for a mean 3.3±1.2 years. During this time, 6.9% of patients died, and 62%, 21%, 8.6%, 5.7%, 1.5%, and 0.7% had baseline hs-cTnT levels <5 ng/L, 5-9 ng/L, 10-14 ng/L, 15-29 ng/L, 30-49 ng/L, and ≥50 ng/L, respectively.
The adjusted hazard ratios for all-cause death in comparison to individuals with undetectable hs-cTnT (<5 ng/L) were 2.00, 2.92, 4.07, 6.77, and 9.68 for those with hs-cTnT 5-9 ng/L, 10-14 ng/L, 15-29 ng/L, 30-49 ng/L, and ≥50 ng/L, respectively. The researchers observed similar increased adjusted hazard ratios associated with rising hs-cTnT levels for cardiovascular-related mortality, noncardiovascular-related mortality, MI, and heart failure. However, this graded risk relationship was particularly pronounced in the case of heart failure, with adjusted hazard ratios of 3.66, 6.04, 10.7, 13.1, and 13.3 for those with hs-cTnT 5-9 ng/L, 10-14 ng/L, 15-29 ng/L, 30-49 ng/L, and ≥50 ng/L, respectively, in comparison to the reference population with undetectable levels of hs-cTnT.
The latter finding and other studies suggesting continuous but small release of cTnT from the myocardium during heart failure may indicate that “chronic troponin release may be mediated by functional and structural heart diseases rather than by ischemic heart disease,” wrote the researchers.