Int J Chron Obstruct Pulmon Dis. 2026 Oct 12;21:640995. doi: 10.2147/COPD.S640995. eCollection 2026.
ABSTRACT
PURPOSE: COPD and vascular aging frequently coexist in later life. Whether widened pulse pressure identifies older adults with COPD at particularly high cardiovascular risk is uncertain.
PATIENTS AND METHODS: We analyzed CHARLS participants aged 60 years or older without baseline heart disease or stroke. Questionnaire-defined COPD and widened pulse pressure (≥60 mmHg) formed four phenotypes. The primary outcome was incident physician-reported heart disease or stroke; all-cause mortality was secondary, and heart disease and stroke were component outcomes. Weighted cause-specific Cox models used respondent weights and household-cluster robust standard errors. Because the joint phenotype was selected after an exploratory screen of candidate vascular indicators, this study should be interpreted as hypothesis-generating rather than confirmatory.
RESULTS: Among 4183 participants, 943 developed incident cardiovascular disease and 685 died. Relative to neither exposure, COPD alone (adjusted hazard ratio (HR) 1.15, 95% confidence interval (CI) 0.84-1.57) and widened pulse pressure alone (HR 0.93, 95% CI 0.70-1.25) were not associated with cardiovascular disease, whereas both exposures were (HR 1.86, 95% CI 1.26-2.76). The cardiovascular association was present for heart disease (HR 2.80, 95% CI 1.94-4.05) but not stroke (HR 0.84, 95% CI 0.43-1.65). The composite cardiovascular signal should therefore not be read as a uniform effect across cardiovascular systems. For all-cause mortality, the both-exposure group had 63 deaths among 209 participants and a fully adjusted HR of 2.05 (95% CI 1.54-2.73) versus neither exposure, but mortality was not clearly higher than in the COPD-only group (HR 1.37, 95% CI 0.96-1.95).
CONCLUSION: Coexisting questionnaire-defined COPD and widened pulse pressure was associated with a higher risk of incident cardiovascular disease, primarily reported heart disease, and with higher all-cause mortality than neither exposure, although mortality was not clearly higher than among participants with COPD alone. These findings are hypothesis-generating and warrant external validation using objective pulmonary and vascular measures.
PMID:42891288 | PMC:PMC13674289 | DOI:10.2147/COPD.S640995