Key result
Elevated hs-cTnT is linked to a ~190% higher mortality risk in stable COPD.
Why the study?
The prognostic value of circulating high-sensitive cardiac troponin T in stable COPD patients without overt cardiovascular disease was unknown.
Does elevated hs-cTnT predict all-cause mortality in patients with stable COPD without overt CVD?
Cohort (n=275)
Yes
Does elevated hs-cTnT predict all-cause mortality in patients with stable COPD without overt CVD?
Hazard Ratio: 2.9 (95% CI 1.2–7.2)
Absolute Event Rate: 11% vs 2.8%
p-value: p=<0.001
Elevated hs-cTnT is frequently present in stable COPD patients without overt CVD and is independently associated with increased all-cause mortality.
Elevated hs-cTnT may identify higher-risk stable COPD patients; hypothesis-generating for troponin monitoring outside exacerbations.
BACKGROUND: Cardiovascular disease (CVD) is a common comorbidity in chronic obstructive pulmonary disease (COPD). Cardiac troponin (cTn) elevation, indicating myocardial injury, is frequent during acute COPD exacerbations and associated with increased mortality. The prognostic value of circulating cTnT among COPD patients in the stable state of the disease is still unknown. The purpose of the present study was to assess the association between circulating cTnT measured by a high sensitive assay (hs-cTnT) and all-cause mortality among patients with stable COPD without overt CVD. METHODS: In a prospective cohort study we included 275 patients from the Akershus University Hospital's outpatient clinic and from Glittre, a pulmonary rehabilitation clinic. COPD-severity and cardiovascular risk factors were assessed, and time to all-cause death was recorded during a mean follow-up time of 2.8 years. RESULTS: One hundred-eighty patients (65%) had hs-cTnT concentrations ≥ the level of detection (5.0 ng/L) and 66 patients (24%) had hs-cTnT above the normal range (≥14.0 ng/L). In total, 47 patients (17%) died. hs-cTnT concentrations in the ranges <5.0, 5.0-13.9 and ≥14 ng/L were associated with crude mortality rates of 2.8, 4.4 and 11.0 per 100 patient-years, respectively. In adjusted analyses the hazard ratios (95% confidence intervals) for death were 1.7 (0.8-3.9) and 2.9 (1.2-7.2) among patients with hs-cTnT concentrations 5.0-13.9 and ≥14 ng/L, respectively, compared to patients with hs-cTnT <5.0 ng/L. CONCLUSIONS: hs-cTnT elevation is frequently present in patients with stable COPD without overt CVD, and associated with increased mortality, independently of COPD-severity and other cardiovascular risk factors.
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Neukamm et al. (2016) conducted a cohort in Stable chronic obstructive pulmonary disease (COPD) (n=275). High-sensitive cardiac troponin T (hs-cTnT) ≥14 ng/L vs. hs-cTnT <5.0 ng/L was evaluated on All-cause mortality (HR 2.9, 95% CI 1.2-7.2, p=<0.001). High-sensitive cardiac troponin T concentrations ≥14 ng/L were associated with increased all-cause mortality in patients with stable COPD compared to levels <5.0 ng/L (HR 2.9, 95% CI 1.2-7.2).
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