From Lungs to Vascular Health: Airflow Obstruction, Not Lung Function Decline, Predicts Atherosclerosis Progression Independent of Smoking Status

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Objectives To prospectively evaluate the relationship between 4-year changes in lung function and the progression of subclinical atherosclerosis among 1623 middle-aged adults with at least one cardiovascular risk factor participating in ILERVAS, and to determine whether individuals who develop airflow obstruction (AO) are especially susceptible to accelerated atherosclerosis progression. Methods This prospective cohort study included 1623 middle-aged adults from the ILERVAS cohort, recruited in primary care centers in the province of Lleida (Catalonia, Spain), with baseline assessments conducted between 2015 and 2018 and follow-up visits between 2019 and 2021 (mean follow-up, 3.99 [SD, 0.22] years). Pulmonary function was assessed by spirometry at baseline and at 4-year follow-up. Subclinical atherosclerosis was evaluated using vascular ultrasound of 12 carotid and femoral territories at baseline and at follow-up, with total plaque area quantified. Associations were analyzed using multivariable linear regression models, adjusting for clinical variables and baseline plaque burden. Analyses were stratified by smoking status. Results Median annual declines were −95 mL (−2.04%) for FVC and −78 mL (−2.00%) for FEV 1 . Categorization of annual pulmonary function decline by tertiles showed no significant association with plaque progression. In contrast, incident AO was associated with greater annual FEV 1 decline (−146.73 vs −74.90 mL; P < .001) and with greater plaque burden, reflected by an increase in affected vascular territories (0.26 [IQR, 0.00–0.75]; P < .001). Multivariable models confirmed larger annual increases in total (4.40 mm 2 ; P < .001), carotid (2.33 mm 2 ; P < .001), and femoral (1.99 mm 2 ; P = .031) plaque areas among participants with incident AO, with consistent results across smoking strata. Sensitivity analyses using a lower limit of normal-based definition of AO showed similar findings, with effect estimates consistent with the primary fixed-ratio analyses. Conclusions In this two-time-point analysis, lung function decline was not independently associated with subclinical atherosclerosis progression. In contrast, incident AO was consistently associated with greater plaque progression across smoking strata. These findings support incident AO as a spirometric marker associated with vascular risk.

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