To evaluate cordiodepressive risks of antiarrhythmic treatment with
diprafenone, we monitored, in addition to conventional hemodynamic parameters, end-systolic pressure-volume relations to assess potential negative inotropic effects. Thirteen patients underwent hemodynamic analysis with and without the influence of
diprafenone 1.5 mg/kg, both a) at rest (paced heart rate of 90 beats/min and b) during
tachycardia (paced
tachycardia of 160 beats/min). Left ventricular volumes increased under the influence of
diprafenone, both at rest (end-diastolic volume by an average of 12%, end-systolic volume by 21%) and during
tachycardia (by 15% and by 47%, respectively).
Diprafenone induced a depression of left ventricular function during
tachycardia only: Ejection fraction fell by an average of 25% and
stroke work by 19%, while end-diastolic pressure increased by an average of 28% and systemic vascular resistance by 34%.
Diprafenone caused the loops of the end-systolic pressure-volume relationship to move rightward and decreased the slope k, indicating negative entropy, both at rest and during
tachycardia. Thus, since under the influence of
diprafenone negative inotropic effects and depressed left ventricular function were found (while determinants of preload and afterload increased),
diprafenone should not be used as an antiarrhythmic agent in patients with advanced
cardiac failure.