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Serial Measurement of Cardiac Troponin T Using a Highly Sensitive Assay in Patients With Chronic Heart Failure: Data From Two Large Randomized Clinical Trials
Study Questions:
Are changes in high-sensitivity cardiac troponin T (hs-cTnT) levels prognostic in patients with chronic stable heart failure?
Methods:
This was a secondary analysis of data collected from the Val-HeFT (n = 4,053) and GISSI (n = 1,231) heart failure trials. Hs-cTnT using two different assays was measured at baseline and again at 3 months (GISSI-HF) or 4 months (Val-HeFT) following trial enrollment. Events were compared in patients with positive (hs-cTnT ≥13.5 ng/L) and negative (hs-cTnT <13.5 ng/L) hs-cTnT levels.
Results:
Patients with positive cTnT tended to be older, and were more likely to have diabetes, renal dysfunction, worse New York Heart Association class, and higher N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations. Compared with a negative hs-cTnT at baseline, an elevated hs-cTnT level was associated with a higher adjusted mortality (hazard ratio [95% confidence interval], 1.6 [1.4-1.8] and 1.9 [1.5-2.3] for Val-HeFT and GISSI-HF, respectively) and cardiovascular rehospitalization (1.4 [1.3-1.5] and 1.5 [1.2-1.9], respectively) at the end of the studies. There was a graded increase in mortality based on changes in hs-cTnT levels at follow-up (log rank p < 0.001).
Conclusions:
The authors concluded that baseline and serial changes in cTnT are prognostic in heart failure.
Perspective:
Using two very large clinical trials in heart failure, the authors show that even small releases of cTns from the myocardium are associated with worse outcome. The etiology for troponin release in heart failure remains a subject of debate and speculation. Regardless of cause, serum troponin positivity (above the 99th percentile for ‘normals’) identifies an unstable myocardium. Similar findings have been shown with BNP levels. In this analysis, hs-cTnT was correlated with NT-BNP and, in fact, the authors state that the hs-cTnT added little risk discrimination to a model that included baseline NT-BNP. The biggest question is: ‘What is the appropriate clinical response’ to a high hs-cTnT level? Can an intervention in response to a change in hs-cTnT change the course of events?
Keywords: Fluorobenzenes, Chronic Disease, Troponin T, Pyrimidines, Tetrazoles, Myocardium, Heart Diseases, Natriuretic Peptides, Prognosis, Biomarkers, Cardiology, Heart Failure, Sulfonamides
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