TEDISAMIL (KC 8857) IS A NEW SPECIFIC BRADYCARDIAC DRUG - DOES IT ALSO INFLUENCE MYOCARDIAL-CONTRACTILITY - ANALYSIS BY THE CONDUCTANCE (VOLUME) TECHNIQUE IN CORONARY-ARTERY DISEASE
J. Thormann et al., TEDISAMIL (KC 8857) IS A NEW SPECIFIC BRADYCARDIAC DRUG - DOES IT ALSO INFLUENCE MYOCARDIAL-CONTRACTILITY - ANALYSIS BY THE CONDUCTANCE (VOLUME) TECHNIQUE IN CORONARY-ARTERY DISEASE, The American heart journal, 125(5), 1993, pp. 1233-1246
To determine whether inotropism influences the bradycardic action of t
edisamil, hemodynamic assessment was performed in 13 patients with isc
hemic coronary artery disease including analysis of end-systolic press
ure-volume relationships after an infusion of tedisamil, 0.3 mg/kg, at
rest, and during paced tachycardia stress. Slope E(max) fell by 14% a
t rest (13 patients) and by 10% during tachycardia (6/13 patients), wh
ereas loops of end-systolic pressure-volume relationships moved rightw
ard; all parameter changes indicated a lack of significant inotropism
loss with tedisamil (p > 0.05). Although the mean heart rate decreased
from 77.5 to 64.7 beats/min and QT(c) duration increased by 14% (p <
0.05), filling pressure and dp/dt(min) remained unchanged and vascular
resistance increased by 30%. Parameters of left ventricular pump func
tion (ejection fraction, stroke volume, left ventricular efficiency) d
ecreased slightly (between 3% and 13%), whereas left ventricular volum
es increased (end-diastolic volume by 6%, end-systolic volume by 23%).
The respective parameter changes during tachycardia were comparable i
n tendency, and angina could no longer be induced during postdrug paci
ng stress. We concluded that the bradycardic effects of tedisamil are
selectively generated without impairing either ventricular pump functi
on or contractility in a clinically relevant fashion, whereas the post
drug anginal threshold appears elevated. Thus tedisamil can be used sa
fely in ischemic coronary artery disease.