DOES THE BRADYCARDIAC EFFECT OF TEDISAMIL CAUSE INOTROPIC IMPAIRMENT IN PATIENTS WITH CORONARY-ARTERY DISEASE - PRESSURE-VOLUME ANALYSIS USING THE CONDUCTANCE (VOLUME) TECHNIQUE
J. Thormann et al., DOES THE BRADYCARDIAC EFFECT OF TEDISAMIL CAUSE INOTROPIC IMPAIRMENT IN PATIENTS WITH CORONARY-ARTERY DISEASE - PRESSURE-VOLUME ANALYSIS USING THE CONDUCTANCE (VOLUME) TECHNIQUE, Zeitschrift fur Kardiologie, 82(4), 1993, pp. 211-221
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.