[Diameter changes of epicardial coronary arteries and coronary stenoses after intracoronary application of SIN 1, a molsidomine metabolite]

Abstract

The vasodilating effects of intracoronary injections of 0.4 mg SIN 1, the active metabolite of molsidomine, on epicardial coronary arteries and coronary stenoses were evaluated in 14 patients with coronary artery disease in a double-blind randomized fashion versus placebo. 9 additional patients with well-definable coronary stenoses received 0.4 mg SIN 1 as well. Diameter changes of nonstenotic coronary arteries in proximal, medial and distal coronary segments as well as changes of the residual luminal diameters within coronary stenoses were determined before (K), immediately after (M1) and 10 minutes after (M2) intracoronary application of SIN 1; in addition, aortic pressure and heart rate were monitored continuously. Aortic pressure and heart rate did not change after SIN 1 or placebo. After SIN 1, the diameter of nonstenotic coronary arteries increased in proximal segments by + 9% (M1) and + 11.7% (M2), in medial segments by + 17.6% (M1) and + 17.6% (M2), in distal segments by + 26.4% (M1) and + 28.8% (M2). Within coronary stenoses, the residual luminal diameters showed a mean increase by 31.5% (M1) and 48.3% (M2). Placebo did not alter coronary diameters significantly. SIN 1 effectively dilates nonstenotic and especially stenotic epicardial coronary arteries, as it is already known for nitrates and calcium-channel blockers. By intracoronary injections, the direct effects on coronary vessels can be detected without interference with systemic effects. The increase in residual luminal diameters within dynamic coronary stenoses after SIN 1 is most likely an important antianginal mechanism also for molsidomine.