Cardiac Troponin I and Cardiovascular Risk in Patients With Chronic Obstructive Pulmonary Disease

Abstract

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 μg), vilanterol (25 μg), 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).

Keywords: cardiac troponin; cardiovascular risk; chronic obstructive pulmonary disease.

Figure 1

Baseline High-Sensitivity Cardiac Troponin and Risk of CV Composite Events, CV Death, and COPD Exacerbations Patients were grouped into quintiles based on their baseline cardiac troponin I concentrations. Compared with the lowest quintile (<2.3 ng/l), those in the highest quintile (≥7.7 ng/l) were at greater risk of experiencing a CV composite event (A) and CV death (B). By contrast, there was no difference between the highest and lowest quintiles in the risk of moderate or severe COPD exacerbations (C). CI = confidence interval; COPD = chronic obstructive pulmonary disease; CV = cardiovascular.

Central Illustration

High-Sensitivity Cardiac Troponin I Concentration Is a Strong, Independent, and Specific Predictor of CV Death in Patients With COPD The association between baseline high-sensitivity cardiac troponin I and CV death (orange) and COPD exacerbations (blue) was examined using cardiac troponin as a continuous variable. Hazard ratios are compared with the median troponin concentration in the first quintile (1.7 ng/l) and are adjusted for age, sex, previous myocardial infarction, hypertension, and exacerbation history. Shaded areas represent 95% confidence intervals. COPD = chronic obstructive pulmonary disease; CV = cardiovascular.

Figure 2

High-Sensitivity Cardiac Troponin at Baseline or 3 Months and Risk of CV Composite Events, CV Death, and COPD Exacerbations Patients were grouped into those who had high-sensitivity cardiac troponin I concentrations <5 ng/l at both baseline and 3 months, and those with a concentration ≥5 ng/l at either baseline or 3 months. Patients with cardiac troponin concentrations ≥5 ng/l at either time point had increased rates of the composite CV endpoint (A) and CV death (B). By contrast, there was no difference in COPD exacerbations (C). Abbreviations as in Figure 1.