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Cardiac Troponin I and Cardiovascular Risk in Patients With Chronic Obstructive Pulmonary Disease
Philip D Adamson1, Julie A Anderson2, Robert D Brook3
1British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom.
Insights
High-sensitivity cardiac troponin I levels in patients with chronic obstructive pulmonary disease (COPD) indicate a significant risk for cardiovascular events and death. Inhaled therapies did not alter these cardiac troponin I concentrations.
Area of Science:
- Cardiology
- Pulmonology
- Biomarkers
Background:
- Patients with chronic obstructive pulmonary disease (COPD) face an elevated risk of cardiovascular events.
- This study investigates cardiac troponin I as a predictor in this high-risk population.
Purpose of the Study:
- To evaluate the association between high-sensitivity cardiac troponin I (hs-cTnI) concentration and cardiovascular events in patients with COPD and heightened cardiovascular risk.
- To determine if inhaled therapies affect hs-cTnI levels in this population.
Main Methods:
- A double-blind randomized controlled trial involving 16,485 patients with COPD and cardiovascular risk factors.
- Plasma hs-cTnI concentrations were measured in 1,599 patients.
- Outcomes included on-treatment cardiovascular events, COPD exacerbations, and cardiovascular death.
Main Results:
- Elevated baseline hs-cTnI concentrations (≥7.7 ng/l) were associated with a significantly greater risk of cardiovascular events (HR 3.7) and cardiovascular death (HR 20.1) compared to the lowest quintile (<2.3 ng/l).
- Inhaled therapies did not impact hs-cTnI concentrations at 3 months (p > 0.05).
- No significant differences in COPD exacerbations were observed between hs-cTnI quintiles.
Conclusions:
- Plasma hs-cTnI is a specific and major indicator of future cardiovascular events and death in COPD patients with heightened cardiovascular risk.
- Inhaled therapies demonstrated a neutral effect on cardiovascular outcomes and mortality, consistent with their lack of impact on hs-cTnI levels.
Background:
Patients with chronic obstructive pulmonary disease (COPD) have increased risk of cardiovascular events.
Objectives:
This study evaluated the association between high-sensitivity cardiac troponin I concentration and cardiovascular events in patients with COPD and heightened cardiovascular risk.
Methods:
In a double-blind randomized controlled trial, 16,485 patients with COPD and cardiovascular disease or risk factors were randomized to once daily inhaled placebo, fluticasone furoate (100 microg), vilanterol (25 microg), or their combination. Plasma high-sensitivity cardiac troponin I concentrations were measured in a subgroup of 1,599 patients. Outcomes were on-treatment cardiovascular events and COPD exacerbations over a median of 18 months, and cardiovascular death over a median of 27 months.
Results:
Baseline plasma cardiac troponin I concentrations were above the limit of detection (1.2 ng/l) in 1,542 (96%) patients. Concentrations were unaffected by inhaled therapies at 3 months (p > 0.05). Compared with the lowest quintile (cardiac troponin <2.3 ng/l), patients in the highest quintile (≥7.7 ng/l) were at greater risk of cardiovascular events (hazard ratio [HR] 3.7; 95% confidence interval [CI]: 1.3 to 10.1; p = 0.012) and cardiovascular death (HR: 20.1; 95% CI: 2.4 to 165.2; p = 0.005) after adjustment for risk factors. By contrast, there were no differences in exacerbations between quintiles (HR: 1.1; 95% CI: 0.8 to 1.5; p = 0.548).
Conclusions:
In patients with COPD and heightened cardiovascular risk, plasma cardiac troponin I concentrations are a specific and major indicator of future cardiovascular events and cardiovascular death. Inhaled therapies did not affect cardiac troponin I concentrations consistent with their neutral effect on mortality and cardiovascular outcomes. (Study to Evaluate the Effect of Fluticasone Furoate/Vilanterol on Survival in Subjects With Chronic Obstructive Pulmonary Disease [SUMMIT]; NCT01313676).
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