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Unloading Effects of Molsidomine on Peripheral Circulation and Cardiac Hemodynamics in Patients with Acute Myocardial Infarction

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

John K. Vyden

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

Harold B. Rose

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

Teruo Takano

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

Kanji Obayashi

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

Hirokazu Hayakawa

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

Eiichi Kimura

Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Nippon Medical School, Tokyo, Japan

The unloading mechanisms and site of peripheral action of the new antian ginal 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) in creased calf venous capacitance (CVC) (0.42 ± 0.18 to 0.64 ± 0.09 ml/100 ml, p<0.05) from 30 to 240 minutes, while simultaneously lowering of PCWP (25.9 ± 4.9 to 15.8 ± 7.3 mmHg, p<0.05) and CVP (9.3 ± 3.7 to 5.8 ± 3.5 cmH₂O, p<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<0.05) and CVC from 5 to 60 minutes (0.42 ± 0.19 to 0.68 ± 0.24 ml/100ml p<0.01) while simultaneously lowering PCWP (24.3 ± 2.2 to 14.6 ± 4.5 mmHg, p<0.01) and CVP (9.0 ± 2.8 to 5.5 ± 3.5 cmH₂O, p<0.05). Neither drug affected cardiac index, blood pressure or systemic vascular resistance. These data suggest that molsidomine significantly lowered elevated preload (PCWP/CVP) 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 uncompli cated by forward failure in whom continued preload reduction is necessary. (Results are expressed as the mean ± standard deviation).

Angiology, Vol. 34, No. 8, 535-545 (1983)
DOI: 10.1177/000331978303400805


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