Purpose: This study was undertaken to determine the association between cardiac function and therapy with beta2-adrenoceptor agonists (β2-agonists), β-blockers, or β-blocker-β-agonist combination therapy in elderly male patients with chronic obstructive pulmonary disease (COPD).
Patients and methods: This was a retrospective cohort study of 220 elderly male COPD patients (mean age 84.1 ± 6.9 years). The patients were divided into four groups on the basis of the use of β-blockers and β2-agonists. N-terminal fragment pro-B-type natriuretic peptide (NT pro-BNP), left ventricular ejection fraction (LVEF), and other relevant parameters were measured and recorded. At follow-up, the primary end point was all-cause mortality.
Results: Multiple linear regression analysis revealed no significant associations between NT pro-BNP and the use of β2-agonists (β = 35.502, P = 0.905), β-blockers (β = 3.533, P = 0.989), or combination therapy (β = 298.635, P = 0.325). LVEF was not significantly associated with the use of β2-agonists (β = -0.360, P = 0.475), β-blockers (β = -0.411, P = 0.284), or combination therapy (β = -0.397, P = 0.435). Over the follow-up period, 52 patients died, but there was no significant difference in mortality among the four groups (P = 0.357). Kaplan-Meier analysis showed no significant difference among the study groups (log-rank test, P = 0.362). After further multivariate adjustment, use of β2-agonists (hazard ratio [HR] 0.711, 95% confidence interval [CI] 0.287-1.759; P = 0.460), β-blockers (HR 0.962, 95% CI 0.405-2.285; P = 0.930), or combination therapy (HR 0.638, 95% CI 0.241-1.689; P < 0.366) were likewise not correlated with mortality.
Conclusion: There was no association between the use of β2-agonists, β-blockers, or β-blocker-β2-agonist combination therapy with cardiac function and all-cause mortality in elderly male COPD patients, which indicated that they may be used safely in this population.
Keywords: cardiac function; elderly COPD patients; mortality; β-blocker; β-blockers; β2-agonist combination; β2-agonists.