Abstract 12610: Vascular Function and Vascular Structure are impaired in Patients With Heart Failure With Preserved Ejection Fraction

Abstract

Background: Endothelial dysfunction and abnormal vascular structure may be involved in the pathogenesis of chronic heart failure. The purpose of this study was to evaluate simultaneously the vascular dysfunction and structure in patients with heart failure with preserved ejection fraction (HFpEF). Methods and Results: We measured flow-mediated vasodilatation (FMD) and nitroglycerine-induced vasodilation as indices of vascular function and intima-media thickness (IMT) as an index of vascular structure of brachial artery in 116 patients with HFpEF (66 men and 50 women; mean age, 61±14 yr) and 64 patients without HF (48 men and 16 women; mean age, 50±17 yr). There were significant differences in age, sex, blood pressure, N-terminal pro-brain natriuretic peptide, estimated glomerular filtration and prevalence of diabetes mellitus between the 2 groups. FMD was significantly smaller in patients with HFpEF than in patients without HF (3.6±2.5% versus 5.2±3.1%, P<0.001). Nitroglycerin-induced vasodilation was significantly smaller in the patients with HFpEF than in patients without HF (11.3±5.0% versus 13.3±4.9%, P=0.015). Brachial artery IMT were significantly larger in the patients with HFpEF than in patients without HF (0.34±0.07 mm versus 0.29±0.08 mm, P<0.001). After adjustment for age and sex, hypertension, diabetes mellitus, the associations remained significant between HFpEF and FMD (hazard ratio, 1.18; 95% confidence interval, 1.02-1.37: P=0.025) and brachial artery IMT (hazard ratio, 0.93; 95% confidence interval, 0.88-0.99: P=0.031) but not nitroglycerine-induced vasodilation (hazard ratio, 1.05; 95% confidence interval, 0.98-1.13: P=0.17). Conclusions: These findings suggest that both endothelial dysfunction and abnormal vascular structure contribute to the pathogenesis of HFpEF. Endothelial function and vascular structure may be potential therapeutic targets for HFpEF.