Advanced vascular aging in patients with paroxysmal atrial fibrillation - Data from RACE V

Abstract

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dutch Heart Foundation, Medtronic Background The incidence of atrial fibrillation (AF) increases exponentially with age. To which extend vascular aging is part of this process is unknown. Pulse wave velocity and carotid intima-media thickness are established markers for vascular aging and have been combined in a vascular aging index as published before(1). Purpose We aim to investigate if vascular age exceeds chronological age in our cohort with paroxysmal AF and if yes to which extend. Methods In this substudy from RACE V we included 295 patients with paroxysmal AF in which carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (IMT) were measured. To calculate vascular aging we used a logarithmic formula derived from the Malmö-Cancer-and-Diet study which yields a vascular age index derived from cfPWV, cIMT and chronological age. This vascular aging index (VAI) is a strong predictor of cardiovascular events. (1). All patients underwent cardiac echocardiography and had a native cardiac CT scan in which fat around the heart and coronary calcium were quantified. In 121 patients Agatston scores from the ascending aortic artery were also measured. Results Patients in this study had a mean chronological age of 63.8 ± 10.1 years and a vascular age of 71.4 ± 11.7 years. Vascular age was on average 9.3 ± 10.2 years higher than chronological age. Vascular age correlated significantly with markers for diastolic dysfunction, vascular calcification in the coronary arteries as well as the aorta and the amount of epicardial and pericardial fat (table 1). Conclusions In patients with PAF vascular age was on average 9.3 years higher than chronological age in our cohort. Advanced vascular age is represented by vascular and myocardial remodeling related to fibrosis, calcification and fat accumulation. The results suggest that in patients with AF enhanced inflammation is leading to fibrosis and calcification. Whether AF is a marker, a mechanism or both in advanced vascular aging warrants further study.