Unloading effects of molsidomine on peripheral circulation and cardiac hemodynamics in patients with acute myocardial infarction.

The unloading mechanisms and side of peripheral action of the new antianginal drug molsidomine was compared with isosorbide dinitrate (ISDN) in 14 patients with acute myocardial infarction using a Swan-Ganz catheter and venous occlusion plethysmography. Sublingual molsidomine (2-4 mg) increased calf venous capacitance (CVC) (0.42 +/- 0.18 to 0.64 +/- 0.09 ml/100 ml, p less than 0.05) from 30 to 240 minutes, while simultaneously lowering of PCWP (25.9 +/- 4.9 to 15.8 +/- 7.3 mmHg, p less than 0.05) and CVP (9.3 +/- 3.7 to 5.8 +/- 3.5 cmH2O, p less than 0.05). Calf blood flow (CBF), calf vascular resistance (CVR), CI, TSPR and SWI were not affected significantly. Molsidomine reduced preload more than 240 minutes after its administration. Sublingual ISDN increased CBF into the initial 15 minutes (1.19 +/- 0.49 to 1.83 +/- 0.98 ml/100ml/min, p less than 0.05) and CVC from 5 to 60 minutes (0.42 +/- 0.19 to 0.68 +/- 0.24 ml/100ml p less than 0.01) while simultaneously lowering PCWP (24.3 +/- 2.2 to 14.6 +/- 4.5 mmHg, p less than 0.01) and CVP (9.0 +/- 2.8 to 5.5 +/- 3.5 cmH2O, p less than 0.05). Neither drug affected cardiac index, blood pressure or systemic vascular resistance. These data suggest that molsidomine significantly lowered elevated preload (PCWP/PCP) by dilating venous capacitance vessels. Its length of action was 240 minutes compared with 60 minutes obtained with ISDN, which suggests this new agent may be of marked benefit in the AMI patients suffering from backward failure uncomplicated by forward failure in whom continued preload reduction is necessary. (Results are expressed as the mean +/- standard deviation).