Key result
Elevated high-sensitivity troponin I was independently associated with an increased risk of major adverse cardiovascular events (HR 1.2) after adjusting for confounders including coronary artery disease severity, whereas troponin T was not.
Why the study?
The association between hsTnT and hsTnI and outcome when adjusted for confounders including angiographical CAD severity remains largely unknown.
Do high-sensitivity troponin T and I blood concentrations predict all-cause mortality and major adverse cardiovascular events in stable patients undergoing coronary angiography?
Cohort (n=1,829)
No
Do high-sensitivity troponin T and I blood concentrations predict all-cause mortality and major adverse cardiovascular events in stable patients undergoing coronary angiography?
In stable patients undergoing coronary angiography, both hsTnT and hsTnI independently predict all-cause mortality, but only hsTnI independently predicts MACE after adjusting for CAD severity and other confounders.
Answers are grounded in this paper and cite their sources.
hsTnI may refine MACE risk stratification in stable CAD; leaves open differential troponin isoform utility for prospective validation.
Background The association between high‐sensitivity troponin T (hsTnT) and high‐sensitivity troponin I (hsTnI) and outcome when adjusted for confounders including the angiographical severity of coronary artery disease (CAD) remains largely unknown. We therefore aimed to explore whether hsTnT and hsTnI blood levels increase with CAD severity and add independent predictive information for future major adverse cardiovascular events and all‐cause mortality in stable patients. Methods and Results Patients from the INTERCATH cohort with available coronary angiography and hsTnT and hsTnI concentrations were included. Troponin concentrations were quantified via hsTnT (Roche Elecsys) and hsTnI (Abbott ARCHITECT STAT). To investigate the association of hsTnT and hsTnI with outcome, a multivariable analysis adjusting for classical cardiovascular risk factors, low‐density lipoprotein cholesterol, estimated glomerular filtration rate, hs‐CRP (high‐sensitivity C‐reactive protein), NT‐proBNP (N‐terminal pro–brain natriuretic peptide), and Gensini score was carried out. Of 1829 patients, 27.9% were women, and the mean age was 68.6±10.9 years. Troponin blood concentrations were higher in patients with diagnosed CAD compared with those without. Using a linear regression model current smoking, arterial hypertension, estimated glomerular filtration rate, hs‐CRP, NT‐proBNP, and CAD severity as graded by the Gensini and SYNTAX scores were associated with high‐sensitivity troponin levels. Patients were followed for 4.4 years (25th and 75th percentiles: 4.3, 4.4). After multivariable adjustment, all‐cause mortality was predicted by hsTnT (hazard ratio [HR], 1.7 [95% CI, 1.5–2.2], P <0.001) as well as hsTnI (HR, 1.5 [95% CI, 1.2–1.8], P <0.001). However, only hsTnI (HR, 1.2 [95% CI, 1.0–1.4], P =0.032) remained as an independent predictor of major adverse cardiovascular events after adjusting for most possible confounders, including CAD severity (hsTnT: HR, 1.0 [95% CI, 0.9–1.2], P =0.95). Conclusions After adjusting for classical cardiovascular risk factors, low‐density lipoprotein cholesterol, estimated glomerular filtration rate, hs‐CRP, NT‐proBNP, and CAD severity, hsTnT and hsTnI were independently associated with all‐cause mortality, but only hsTnI was associated with major adverse cardiovascular events in stable patients undergoing coronary angiography. Registration URL: https://clinicaltrials.gov/ ; Unique identifier: NCT04936438.
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Bay et al. (2022) conducted a cohort in Stable patients undergoing coronary angiography (n=1,829). High-sensitivity troponin I (hsTnI) and T (hsTnT) vs. Lowest quartile of troponin concentration was evaluated on Major adverse cardiovascular events (MACE) (HR 1.2, 95% CI 1.0-1.4, p=0.032). Elevated high-sensitivity troponin I was independently associated with an increased risk of major adverse cardiovascular events (HR 1.2) after adjusting for confounders including coronary artery disease severity, whereas troponin T was not.
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