Endothelium-dependent vasodilatation is not selectively impaired in patients with chronic heart failure secondary to valvular heart disease and congenital heart disease.

Abstract

This study examined possible selective impairment of endothelial dysfunction in the peripheral vascular bed in patients with chronic heart failure in the absence of confounding factors influencing endothelial function (i.e. hypertension, hypercholesterolaemia and diabetes mellitus). Several recent studies have suggested that endothelium-dependent peripheral vasodilation is impaired but endothelium-independent vasodilation is preserved in patients with chronic heart failure. However, a classical paper has demonstrated that sodium nitrite-mediated calf blood flow is clearly depressed in patients with valvular heart disease and cardiomyopathy. We examined forearm blood flow changes mediated by acetylcholine and nitroprusside in patients with valvular heart disease (n = 55) or congenital heart disease (n = 13), and a comparison was made with healthy volunteers (n = 21). The blood flow changes mediated by acetylcholine and nitroprusside were significantly impaired in both patient groups (P < 0.01). When blood flow responses were collected from all patients, two types of vasodilatory capacity were found to have decreased significantly with increasing clinical severity of heart failure (New York Heart Association functional class; P < 0.01). This suggests that the peripheral vasodilatory responses mediated by endothelium-dependent and endothelium-independent vasodilators are significantly impaired in patients with symptomatic chronic heart failure due to non-ischaemic heart disease.