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Relation between cardiac troponin I and mortality in acute decompensated heart failure
John J You1, Peter C Austin, David A Alter
1Institute for Clinical Evaluative Sciences, University of Toronto, Ontario, Canada.
Insights
Elevated cardiac troponin I levels in acute decompensated heart failure (ADHF) independently predict mortality. This troponin testing offers valuable prognostic information beyond traditional markers, aiding clinical decisions.
Area of Science:
- Cardiology
- Biomarkers
- Heart Failure Research
Background:
- Elevated troponin levels are common in acute decompensated heart failure (ADHF).
- The prognostic significance of troponin elevations beyond established predictors in heart failure remains unclear.
Purpose of the Study:
- To investigate the association between cardiac troponin I levels and all-cause mortality in patients hospitalized for ADHF.
- To determine if cardiac troponin I provides prognostic value independent of traditional risk factors.
Main Methods:
- The EFFECT study analyzed data from 2025 patients hospitalized for heart failure in Ontario, Canada.
- Cardiac troponin I levels were measured, and their association with all-cause mortality was assessed.
- Statistical models were used to adjust for potential confounding factors.
Main Results:
- Cardiac troponin I levels >0.5 microg/L were observed in 34.5% of patients.
- Elevated cardiac troponin I was an independent predictor of mortality (aHR 1.49).
- A significant dose-response relationship existed between troponin I levels and mortality (aHR 1.10 per 1 microg/L increase).
Conclusions:
- Cardiac troponin I is an independent predictor of all-cause mortality in hospitalized ADHF patients.
- Troponin testing offers valuable prognostic information beyond traditional predictors.
- Cardiac troponin measurements can assist in medical decision-making for ADHF patients.
Background:
Troponin level elevations are common in patients with acute decompensated heart failure (ADHF), yet their prognostic value above and beyond traditional predictors of outcomes in heart failure is uncertain.
Methods:
In the EFFECT study, we determined the association between cardiac troponin I and all-cause mortality in 2025 patients hospitalized for heart failure in Ontario, Canada, between April 1, 1999, and March 31, 2001.
Results:
Cardiac troponin I levels >0.5 microg/L (median 1.7 microg/L, interquartile range 0.9-4.8 microg/L) occurred in 699 (34.5%) patients and was an independent predictor of mortality (adjusted hazard ratio 1.49, 95% CI 1.25-1.77, P < .001). Furthermore, we observed a dose-response relationship between cardiac troponin I and mortality that persisted after adjustment for potential confounding factors (adjusted hazard ratio 1.10 per 1 microg/L increase, 95% CI 1.05-1.15, P < .001). The association between cardiac troponin I and mortality was similar for patients with and without other features of acute ischemia on presentation (P > .05 for interaction).
Conclusions:
In patients hospitalized for ADHF who had cardiac troponin levels measured during the course of clinical practice, cardiac troponin I was an independent predictor of all-cause mortality. Cardiac troponin testing is easily accessible, has predictive value above and beyond traditional clinical predictors of mortality, and may help guide medical decision making in patients with ADHF.
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