DOES THE BRADYCARDIAC EFFECT OF TEDISAMIL CAUSE INOTROPIC IMPAIRMENT IN PATIENTS WITH CORONARY-ARTERY DISEASE - PRESSURE-VOLUME ANALYSIS USING THE CONDUCTANCE (VOLUME) TECHNIQUE

To exclude or prove potential inotropic influences from tedisamil's br adycardic effects, our hemodynamic evaluation in 13 patients (pat.) wi th coronary artery disease (CAD) included analyses of endsystolic pres sure-volume relationships (ESPVR) after tedisamil, 0.3 mg/kg infusion at rest and during tachycardia induced by atrial pacing. Slope Emax [m m HG/ml] fell by 14% at rest (13 pat.) and by 10% during paced tachyca rdia (6/13 pat.) while loops of ESPVR tended to move rightward towards larger volumes (p > 0.05): all parameter changes indicated lack of si gnificant inotropy loss with tedisamil. While mean heart rate decrease d from 77.5 to 64.7 b/min and QTc duration increased by 14% (p < 0.05) , filling pressure as well as dP/dtmin remained unchanged and vascular resistance rose by 30%. Parameters of LV-pump function (ejecton fract ion, stroke volume) decreased slightly (between 3 and 13%), while LV-v olumes increased (end-diastolic by 6%, endsystolic by 23%). The respec tive parameter changes during paced tachycardia were comparable in ten dency. Conclusion: Tedisamil's bradycardic effects are selectively gen erated without impairing either ventricular pump function or contracti lity in a clinically relevant fashion. Thus, tedisamil can be used saf ely in CAD.