INTRAVENOUS MOLSIDOMINE IS HEART-FAILURE - PART-I - DOSE-RESPONSE RELATIONSHIP WITH REGARD TO HEMODYNAMIC PARAMETERS

In 20 patients (9 women, 11 men, median age 62 Sears) with chronic hea rt failure (NYHA II-III) the dose response relationship of intravenous molsidomine was investigated. Bolus application of 5 mg molsidomine i .v. led to a reduction of mean pulmonary capillary wedge pressure (PCm ) from 27 to 19 mmHg, of mean pulmonary artery pressure (PAm) from 38 to 29 mmHg and of mean right atrial pressure (RAm) from 10 to 8 mmHg ( medians, p < 0.05 each). After disappearance of the primary effect a c ontinuous i.v. molsidomine infusion with increasing doses from 2 to 10 mg/h resulted in a further reduction of PCm to 16 mmHg, of PAm to 27 mmHg and of RAm to 7 mmHg (medians, p < 0.05 each). The median dose of i.v. molsidomine being necessary to reach the peak hemodynamic effect was 6 mg/h, ranging from 2 to 10 mg/h. The values of heart rate and b lood pressure did not change significantly. Cardiac output remained co nstant after bolus application but increased from 4.1 to 4.7 l/min (me dians, p < 0.05) during maximal continuous i.v. infusion with molsidom ine. Conclusions: Molsidomine provokes, independently of bolus applica tion or continuous infusion, a significant decrease of PCm, PAm and RA m without leading, as do nitrates, to reflex tachycardia or systemic h ypotension. The dose response relationship to reach the peak hemodynam ic effect differs substantially in each individual patient, but can be assessed by continous i.v. infusion of molsidomine with increasing do ses.