Asthma and cardiovascular outcomes: a population-based matched cohort study

Asthma is a prevalent chronic inflammatory airway disease characterized by airway hyperresponsiveness and structural remodelling, and a major contributor to global disability.1,2 Asthma and cardiovascular disease (CVD) are leading public health challenges, each contributing substantially to morbidity and mortality.3 Emerging evidence suggests that asthma may increase cardiovascular (CV) risk through systemic inflammation and immune dysregulation, but prior studies have been limited by modest sample sizes, short follow-up, incomplete outcome assessment, and focus on a restricted set of atherosclerotic outcomes.4 Moreover, asthma is not recognized as a CV risk factor in current prevention guidelines, and its role in broader CV risk stratification remains unclear. To address these gaps, we leveraged the UK Biobank to map the association between asthma and 12 prespecified cardiovascular outcomes. The UK Biobank is a population-based cohort of over 500 000 adults aged 40–69 years recruited across the UK between 2006 and 2010. From this cohort, we identified participants with asthma, ascertained from linked health records using ICD-10 codes J45–J46, who were free of CVD at baseline. Up to five controls per asthma case were matched on age (±5 years), sex, ethnicity, and socioeconomic status (Townsend deprivation index quintile), and were free of asthma. Controls were assigned the same index date as their matched asthma case. Covariates included established cardiovascular risk factors. The primary outcome was the first occurrence of any CVD, defined as a composite of 12 conditions: ischaemic heart disease, stroke or transient ischaemic attack, peripheral arterial disease, atrial fibrillation/flutter, conduction disorders, supraventricular arrhythmias, valvular heart disease (excluding congenital and rheumatic), heart failure, venous thromboembolism or pulmonary embolism, myocarditis/pericarditis, aortic aneurysm/dissection, and infective endocarditis. Secondary outcomes were individual CVD conditions. Follow-up extended to 31 October 2022. Age-adjusted incidence rates were estimated using Poisson regression (events per 10 000 person-years), and multivariable Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), accounting for clustering within matched sets using robust sandwich variance estimators. Cumulative incidence was plotted using the Kaplan–Meier method, and 5-year absolute risks were derived from Cox models. Pre-specified subgroup and sensitivity analyses assessed the robustness of findings.