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A parallel physiological pathway for elastic changes is hypothesized for declines in arterial elasticity and lung function. Endothelial dysfunction and inflammation could potentially decrease elasticity of both vasculature and lung tissue. We examined biomarkers, large arterial elasticity and small arterial elasticity (SAE), and forced vital capacity (FVC) in a period cross-sectional design in the multiethnic study of atherosclerosis, which recruited 1823 women and 1803 men, age range 45 to 84 years, black, white, Hispanic, and Chinese, free of clinically recognized cardiovascular disease. Radial artery tonometric pulse waveform registration was performed and large arterial elasticity and SAE were derived from diastole. Spirometric data and markers of endothelial dysfunction and inflammation (soluble intracellular adhesion molecule-1, fibrinogen, hs-C-reactive protein, and interleukin-6) were obtained. Mean large arterial elasticity was 13.7 ± 5.5 mL/mm Hg × 10 and SAE was 4.6 ± 2.6 mL/mm Hg × 100. Mean FVC was 3192 ± 956.0 mL and forced expiratory volume in 1 second was 2386 ± 734.5 mL. FVC was about 40 ± 5 mL higher per SD of SAE, stronger in men than women. The association was slightly weaker with large arterial elasticity, with no sex interaction. After regression adjustment for demographic, anthropometric, and cardiovascular risk factors, the biomarkers tended to be related to reduced SAE and FVC, particularly in men. These biomarker associations suggest important cardiovascular disease risk alterations that occur concurrently with lower arterial elasticity and lung function. The observed positive association of SAE with FVC and with forced expiratory volume in 1 second in middle-aged to older free-living people is consistent with the hypothesis of parallel physiological pathways for elastic changes in the vasculature and in lung parenchymal tissue.

Associations Among Lung Function, Arterial Elasticity, and Circulating Endothelial and Inflammation Markers