Key result
Higher hsTnI linked to ~4.3-fold higher cardiovascular mortality alongside faster CAD progression.
Why the study?
Does elevated high-sensitivity troponin I (hsTnI) predict worse angiographic coronary artery disease severity, disease progression, and incident adverse cardiovascular outcomes?
Cohort (n=3,087)
Yes
Does elevated high-sensitivity troponin I (hsTnI) predict worse angiographic coronary artery disease severity, disease progression, and incident adverse cardiovascular outcomes?
Hazard Ratio: 4.3 (95% CI 2.68–6.9)
p-value: p=<0.0001
Elevated baseline hsTnI levels independently predict angiographic coronary disease severity, accelerated plaque progression, and long-term adverse cardiovascular outcomes in patients undergoing cardiac catheterization.
hsTnI may aid risk stratification in catheterization patients; extends observational links to CAD severity and progression but leaves causal inference open.
Background The associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity. Methods and Results In 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all‐cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD , 20% had 1‐vessel CAD, 20% had 2‐vessel CAD, and 26% had 3‐vessel CAD . After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18–0.44; P <0.001) and with CAD progression (log 2 ß=0.36; 95% confidence interval, 0.14–0.58; P =0.001). hsTnI level was also a significant predictor of incident death, cardiovascular death, myocardial infarction, revascularization, and cardiac hospitalizations, independent of the aforementioned covariates and CAD severity. Conclusions Higher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD , and higher risk of all‐cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation.
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Tahhan et al. (2018) conducted a cohort in Coronary artery disease (CAD) (n=3,087). High-sensitivity troponin I (hsTnI) levels vs. Lower hsTnI levels (lowest quartile or continuous reference) was evaluated on Incident cardiovascular death (Quartile 4 vs Quartile 1 of hsTnI) (HR 4.30, 95% CI 2.68-6.9, p=<0.0001). Higher hsTnI levels were independently associated with greater coronary artery disease severity, more rapid progression, and an increased risk of cardiovascular death (adjusted HR 4.30 for highest vs lowest quartile).
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