Molsidomine improves flow-dependent vasodilation in brachial arteries of patients with coronary artery disease.

Flow-mediated vasodilation (FMD) of human blood vessels is essential to adaptation and regulation of peripheral blood flow, and is mediated by endogenously produced nitric oxide. Endothelial function is impaired in many pathologic states, especially in coronary heart disease. We questioned in this study whether exogenous nitric oxide (NO) would restore endothelial dysfunction in peripheral arteries of patients with coronary artery disease (CAD). In a randomized double-blinded case-control assay, we used computerized A-mode ultrasonography to measure diastolic diameters of the brachial artery before and after hyperemia in two groups of 10 patients with CAD. Each group received orally either placebo or 12 mg molsidomine a day for 48 h. In the molsidomine group, FMD was improved with a 60% increase after the first intake of molsidomine, and the same trend was observed after the last intake, although less pronounced. Significant increase in diastolic diameter was observed after the last molsidomine intake, but not after the first one. Thus molsidomine has an early positive effect on FMD in addition to a delayed vasodilator effect. Improvement of endothelial dysfunction by molsidomine in patients with CAD may uncover new therapeutic perceptive in the use of nitrovasodilators.