Preserved ratio impaired spirometry (PRISm) is a recently recognized spirometric pattern defined by forced expiratory volume in 1 second (FEV1) / Forced vital capacity ratio ≥0.70 and FEV1 <80% of reference. For unclear reasons, PRISm is associated with increased cardiovascular (CV) morbidity and mortality. Arterial stiffness is a major mechanism of CV disease, which can be measured by carotid-femoral pulse wave velocity (cfPWV). We explored the hypothesis that cfPWV would be increased in individuals with PRISm and airflow limitation (AL). We measured forced spirometry, lung volumes by body plethysmography, and cfPWV in 9,466 subjects recruited from the general population in the Austrian cross-sectional LEAD study, and tested the association of arterial stiffness with PRISm and AL by multivariable linear regression analysis. Individuals aged 18 years and under as well as those with missing cfPWV or co-variates were excluded from further analysis. Individuals with PRISm (n = 431, 4.6%) were of similar age to those with normal spirometry (n = 8136, 85.9%) and significantly younger than those with AL (n = 899, 9.5%). Arterial hypertension, diabetes mellitus, coronary artery disease, heart failure and peripheral arterial occlusive disease were significantly more common in individuals with PRISm compared to normal lung function and similar to those with AL. There was a significant association between PRISm and arterial stiffness on bivariate linear regression analysis (crude model; ß = 0.038; 95% CI, 0.016 - 0.058), which persisted after robust adjustment for clinical confounders upon multivariable analysis (final model; ß = 0.017; 95% CI, 0.001 - 0.032). CfPWV was significantly higher in individuals with PRISm irrespective of the presence of established CV disease or pulmonary restriction. AL also showed a significant association with arterial stiffness on multivariable linear regression analysis (final model; 95% CI, ß = 0.025, 0.009 - 0.042). Arterial stiffness measured by cfPWV is increased in individuals with PRISm independent from CV disease and risk factors. The pathobiological mechanisms underlying this association deserve further research.