To determine the effect of verapamil in ventricular tachycardias, we p
erformed an experimental and clinical study. Experimental ventricular
tachycardias (VT) were produced in dog hearts with minute aconitine cr
ystal introduced into the periphery of a left ventricular area, damage
d by intramural injection of 1.0-1.5 ml phenol. The response of theses
tachycardias to 0.2 mg/kg verapamil was analyzed. Verapamil was infus
ed into the superior vena cava over 15-20 min. Leads II, aVL, intraven
tricular right and left unipolar records, as well as one of the superi
or vena cava, were registered under control conditions, in the presenc
e of VT, and after application of verapamil. Recordings were obtained
at constant intervals, waiting for the recovery of sinus rhythm (SR) a
nd the posterior reappearance of tachycardia. Experiments were perform
ed for 6 to 8 h under continuous infusion of Hartmann's solution. Thro
ughout these periods, variations in systemic systolic pressure were re
corded. From 75 animals submitted to this treatment, 30 (40%) recovere
d transiently the SR, whereas the drug exerted no antiarrhythmic effec
t in 19 (25%), and arterial systolic pressure fell importantly in 10 (
13%) animals. In two more groups, of 15 dogs each, the VT response to
verapamil was compared with the response to lidocaine and flecainide.
Endovenous verapamil (5-10 mg) was administered to 10 patients, coursi
ng with VT and having a structurally normal heart, after this arrhythm
ia was induced by electrical stimulation. The response to verapamil wa
s satisfactory in nine patients (90%), in which VT originated in the s
eptal and apical regions of the left ventricle. Verapamil seems to be
effective in experimental and clinical ventricular tachycardias relate
d to calcium-dependent potentials, in which the sustaining mechanism c
ould either be triggered activity or reentry.