High anxiety is associated with an increased risk of developing cardiovascular disease (CVD), in particular, atherosclerotic coronary artery disease. However, the mechanisms by which anxiety contributes to the development of CVD are unclear. Unlike other common psychiatric disorders such as depression, anxiety and its effects on CVD risk has not been studied extensively. Moreover, whether elevated anxiety is associated with arterial stiffness and vascular endothelial dysfunction, biomarkers of CVD risk, in healthy adults and whether a psychological intervention designed to lower anxiety levels in healthy adults with moderate to high baseline anxiety levels ameliorates vascular dysfunction remains unclear. The purpose of this study was twofold; first to determine the extent to which moderate to high anxiety levels are associated with vascular dysfunction including aortic stiffness as measured by carotid-femoral pulse wave velocity (cf-PWV), carotid artery stiffness via ultrasound-based β-stiffness index, and forearm resistance artery function measured as peak forearm blood flow using venous occlusion plethysmograph (VOP). Secondly, to determine whether the empirically validated Acceptance and Commitment Training (ACT) anxiety intervention improved vascular function after 12 weeks and if this was associated with reductions in anxiety in adults with moderate to high baseline anxiety levels.
Our results indicated that there was no association between increased anxiety levels and any of the three vascular outcomes of interest. Conversely, there was an association between the ACT intervention participation and improvement in forearm resistance artery function independent of age, sex, education, race/ethnicity, BMI and STAI Trait anxiety. Taken together, these data suggest that although higher State and Trait anxiety was not associated with aortic stiffness, carotid stiffness or forearm resistance artery function, and the ACT intervention was associated with improved peripheral resistance artery function. Additional studies are needed to determine whether this effect occurs earlier than 12 weeks and sustained longer that 12 weeks, and whether it occurs in adults with CVD risk factors (i.e. atherosclerosis), non-white racial/ethnic backgrounds and in resistance vessel function in response to intra-arterial vasoactive agonists such as acetylcholine.