Purpose: Heart failure (HF) is increasing in prevalence and a common cause of morbidity and mortality. We evaluated vascular structure and function in patients with HF.

Methods: Forearm flow-mediated dilatation (FMD) was used as a measure of endothelial nitric oxide (NO)-dependent vasodilation, and brachial artery dilation in response to sublingual glyceryl trinitrate (GTN 25 μg) was used to assess endothelial-independent dilation. Carotid intima media thickness (IMT) and pulse wave velocity (PWV), an index of arterial stiffness, was assessed using the Sphygmocor^® system. All data were expressed as mean±SEM. P < 0.05 (two tailed) was taken as indicating statistical significance.

Results: We studied 20 patients with HF (IHD-14 & DCM-6) and 24 controls of similar age and sex. Patients were studied on usual medication. FMD was impaired in patients with HF compared to controls (4.4±0.6% vs. 6.6±0.6%, p = 0.025), whereas GTN-induced dilatation was similar to controls (10.9±0.9% vs. 11.1±1.4%). IMT was higher in HF patients (1.19±0.09mm vs. 0.83±0.04 mm, p = 0.0008), and PWV was greater in patients with HF (10.7±1.1 m/s vs. 8.5±0.4m/s, p = 0.048). In subgroup analysis of the HF subjects, IMT was elevated specifically in the patients with IHD (1.16±0.03mm vs. 0.80±0.04mm in controls, p < 0.01) but not in those with DCM (0.96±0.11mm vs. 0.81±0.05mm in controls, p > 0.05); furthermore, the patients with IHD had higher PWV (11.5±1.3 m/s vs. 8.9±0.3 m/s in controls, p < 0.01), whereas those with DCM did not (8.1±0.6 m/s vs. 8.9±0.3 m/s in controls, p > 0.05). FMD impairment was similar in IHD and DCM subjects.

Conclusions: Patients with HF have endothelial dysfunction as well as elevated arterial stiffness and increased IMT, and that the latter two changes are seen specifically in patients whose HF is secondary to IHD.