Abstract Rationale Subclinical airflow obstruction (SAO)—defined as reduced FEV1/FVC ratio without dyspnea—affects 10-15% of adults globally but lacks longitudinal outcome data. Whether SAO predicts cardiovascular disease (CVD) mortality independent of clinical COPD diagnosis remains unclear. We leveraged publicly available NHANES and linked mortality data to examine this relationship. Methods We analyzed data from NHANES 2007-2012 cycles (n = 8,847 adults ≥40 years with complete spirometry and mortality follow-up through 2020). SAO was defined as FEV1/FVC 0.70 with FEV1 ≥80% predicted and no respiratory symptoms. Clinical COPD was defined as FEV1/FVC 0.70 with symptoms. Participants were stratified into: (1) normal spirometry (reference); (2) SAO only; (3) clinical COPD; (4) reduced FEV1 with normal ratio (restrictive pattern). Primary outcome CVD mortality through 2020. Cox proportional hazards models adjusted for age, sex, BMI, smoking status, hypertension, diabetes, and physical activity (publicly available NHANES variables). Results Mean follow-up: 11.8±2.1 years (97,521 person-years). Overall CVD mortality: 287 deaths (3.2%). SAO group (n = 1,204): 48 CVD deaths (3.9% crude rate); adjusted hazard ratio (aHR)=1.43 (95% CI: 1.02-2.01; p = 0.04) compared to normal spirometry. Clinical COPD group (n = 312): 31 CVD deaths (9.9% crude rate); aHR=2.87 (95% CI: 1.89-4.36; p 0.001). Restrictive pattern (n = 891): 34 CVD deaths (3.8%); aHR=1.41 (95% CI: 0.92-2.17; p = 0.12). In stratified analyses, SAO-associated CVD mortality was significant in smokers (aHR=1.89; 95% CI: 1.21-2.96) and nonsmokers (aHR=1.31; 95% CI: 0.78-2.20). Dose-response relationship observed: each 1-unit decrease in FEV1/FVC ratio associated with 18% increased CVD mortality risk (aHR per unit change=1.18; 95% CI: 1.06-1.31). Conclusions Subclinical airflow obstruction is independently associated with elevated long-term CVD mortality risk, with stronger associations in smokers. These findings support spirometric screening for CVD risk stratification and suggest novel cardiopulmonary mechanisms warrant investigation. Public NHANES data enables reproducible validation and cost-free international collaboration. This abstract is funded by: NA
Qamar et al. (2026) studied this question.