Author + information
- Received May 26, 1989
- Revision received September 20, 1989
- Accepted October 3, 1989
- Published online March 1, 1990.
- Pablo A. Chiale, MD,
- Julio D. Pastori, MD,
- Ruben A. Sanchez, MD,
- Marcelo V. Elizari, MD, FACC∗ and
- Mauricio B. Rosenbaum, MD, FACC
- ↵∗Address for reprints: Marcelo V. Elizari, MD, Service of Cardiology, Ramos Mejia Hospital, Urquiza 609, 1st Floor, 1221 Buenos Aires, Argentina.
The mechanisms responsible for intermittent bundle branch block are still under debate. The role of the time-dependent behavior of the slow calcium channel has recently been emphasized. To test this hypothesis and ascertain the possible involvement of the fast sodium channel, the effects of the slow calcium channel blocker verapamil and the fast sodium channel blocker procainamide were compared in 10 patients with intermittent bundle branch block. All 10 patients showed bundle branch block during spontaneous sinus rhythm. Maneuvers to slow cardiac rate (that is, carotid sinus massage, Valsalva maneuver) were performed to identify normal conduction as well as phase 4 bundle branch block.
Thus, the ranges of diastolic intervals (RR) resulting in phase 3 (tachycardia-dependent) bundle branch block, phase 4 (bradycardia-dependent) bundle branch block and normal conduction were measured in two control studies performed before intravenous administration of verapamil (control 1) and procainamide (control 2) and at the peak effect of both drugs. In the control studies, all 10 patients showed phase 3 bundle branch block, whereas phase 4 bundle branch block occurred in only 4 patients. The ranges of phase 3 bundle branch block, phase 4 bundle branch block and normal conduction were very similar in control studies 1 and 2. The phase 3 bundle branch block range was slightly shortened by verapamil (983 ±83.5 ms in control 1; 930 ±69.4 ms at the peak effect of verapamil), whereas phase 4 bundle branch block remained unchanged. In contrast, conduction was systematically worsened by procainamide. The phase 3 bundle branch block range was prolonged 80 to 1,770 ms in five of the six patients with apparently isolated phase 3 bundle branch block, and rate-independent bundle branch block occurred in all four patients with both phase 3 and phase 4 bundle branch block as well as in one patient showing an isolated phase 3 bundle branch block.
The absence of any depressing action of verapamil and the marked effects induced by procainamide strongly support the view that clinical intermittent bundle branch block is related to depressed fast responses and not to slow calcium-mediated responses. Hence, these conduction disturbances probably occur in tissues operating at a subnormal but still relatively high level of membrane potential.
☆ This work was supported in part by the Fundacion de Investigaciones Cardiologicas Einthoven, Buenos Aires, Argentina. Dr. Pastori was a research fellow of the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
- Received May 26, 1989.
- Revision received September 20, 1989.
- Accepted October 3, 1989.