Flosequinan induces hemodynamic improvement in heart failure complicating acute myocardial infarction.

The hemodynamic effects of a single dose of flosequinan, a new balanced vasodilator, were studied in twelve patients with severe acute onset heart failure complicating acute myocardial infarction. Flosequinan was added to conventional therapy within 3.8 +/- 0.5 days of the infarction, in the form of a single oral dose of 100 mg in ten of the patients. In the remaining two, reinfarction developed on the sixth day and they received flosequinan immediately thereafter. Hemodynamic monitoring was performed for four hours after the administration, without any other drug being given. Flosequinan produced hemodynamic improvement in all patients. The effect peaked at one to two hours and remained at this level at four hours. Pulmonary capillary wedge pressure decreased from 27.4 +/- 5.0 to 16.5 +/- 2.9 mm Hg and cardiac output increased from 3.5 +/- 0.3 to 4.1 +/- 0.4 l/min (p less than 0.001 for both). Pulmonary arterial and right atrial pressures and systemic and pulmonary vascular resistances were also significantly reduced. Heart rate was not significantly altered (from 84.0 +/- 4.5 to 87.4 +/- 4.6). Mean systemic arterial pressure was slightly reduced. Administration of flosequinan was not associated with any adverse effects and the hemodynamic effect was not related to the pre-treatment serum sodium concentration. We concluded that flosequinan can produce acute hemodynamic improvement in patients with heart failure, complicating acute myocardial infarction. The drug is well tolerated.