Kasanuki H, Ohnishi S, Hosoda S
Department of Internal Medicine, Tokyo Women's Medical College, Japan.
Am J Cardiol. 1989 Dec 5;64(20):46J-49J. doi: 10.1016/0002-9149(89)91198-3.
The purpose of this study was to differentiate by means of electrophysiologic study, a drug's ability to terminate or to prevent ventricular tachycardia (VT). Differences between the 2 effects were examined in patients with VT and the underlying mechanisms were studied in verapamil-responsive idiopathic sustained VT. The clinical significance of the distinction for chronic oral drug therapy is discussed. Thirty-five cases of inducible sustained VT were studied. A drug was considered "preventive" if it prevented VT induction and repetitive ventricular response, and "terminating" if it stopped induced VT within 15 complexes or could stop VT after its intravenous administration. Prevention and termination occurred together in 13 of 19 cases (68%) with disopyramide, in 10 of 19 cases (53%) with procainamide, in 8 of 12 cases (67%) with lidocaine, in 11 of 15 cases (73%) with mexiletine, and in 10 of 16 cases (63%) with verapamil. In the 16 in which verapamil terminated VT, VT rate immediately before termination slowed markedly from 167 +/- 33 to 134 +/- 28 beats/min. In the 6 cases without preventative effects, minimal and maximal premature intervals for VT induction increased significantly, from 291 +/- 70 to 335 +/- 85 ms and 323 +/- 68 to 423 +/- 109 ms, respectively, after verapamil administration. In 2 cases in which verapamil had a terminating effect, 5 mg of verapamil restored sinus rhythm but 10 mg caused premature beats resembling VT complexes. In another 2, 5 mg of verapamil lengthened the minimal premature interval; 10 mg increased both minimal and maximal premature intervals and lengthened the VT cycle.(ABSTRACT TRUNCATED AT 250 WORDS)
