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Electrophysiological effects of disopyramide in patients with bundle branch block.

Jessica Desai, Melvin M. Scheinman, Robert W. Peters, Judy O'Young

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Abstract

Electrophysiological studies were performed in 22 patients with intraventricular conduction delay before and after intravenous infusion of disopyramide (Norpace), 2 mg/kg. Mean control maximal sinus node recovery time (1039 +/- 187 msec), atrioventricular nodal conduction time (113 +/- 28 msec), and atrioventricular nodal effective refractory periods (349 +/- 67 msec) did not change significantly after administration of disopyramide (1073 +/- 284 msec, 112 +/- 31 msec, and 342 +/- 42 msec, respectively). Mean spontaneous cycle length (756 +/- 146 msec) decreased significantly 5 minutes after disopyramide (717 +/- 124 msec) (p less than 0.05), but not after 30 minutes (734 +/- 142 msec). A small but statistically significant (p less than 0.05) increase occurred after disopyramide in the mean atrial effective refractory period (259 +/- 51 to 280 +/- 53 msec), ventricular effective refractory period (253 +/- 23 to 275 +/- 33 msec), as well as the relative refractory period of the ventricular specialized conduction system (six patients) 433 +/- 78 to 479 +/- 62 msec). Although mean control infranodal conduction time (67 +/- 35 msec) increased 5 minutes after disopyramide (79 +/- 41 msec) (p less than 0.001) (18%), no spontaneous episodes of second-degree or third-degree atrioventricular block were observed. In six patients with premature ventricular depolarizations (greater than or equal to 1/min), the arrhythmia was totally abolished in four, markedly reduced in one, and remained unchanged in one. Disopyramide resulted in significant prolongation of infranodal conduction time as well as in atrial and ventricular refractoriness, but nevertheless appears to be safe in patients with bundle branch block.

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What this paper is about

Electrophysiological studies were performed in 22 patients with intraventricular conduction delay before and after intravenous infusion of disopyramide (Norpace), 2 mg/kg. Mean control maximal sinus node recovery time (1039 +/- 187 msec), atrioventricular nodal conduction time (113 +/- 28 msec), and atrioventricular nodal effective refractory periods (349 +/- 67 msec) did not change significantly after administration of disopyramide (1073 +/- 284 msec, 112 +/- 31 msec, and 342 +/- 42 msec, respectively). Mean spontaneous cycle length (756 +/- 146 msec) decreased significantly 5 minutes after disopyramide (717 +/- 124 msec) (p less than 0.05), but not after 30 minutes (734 +/- 142 msec). A small but statistically significant (p less than 0.05) increase occurred after disopyramide in the mean atrial effective refractory period (259 +/- 51 to 280 +/- 53 msec), ventricular effective refractory period (253 +/- 23 to 275 +/- 33 msec), as well as the relative refractory period of the ventricular specialized conduction system (six patients) 433 +/- 78 to 479 +/- 62 msec). Although mean control infranodal conduction time (67 +/- 35 msec) increased 5 minutes after disopyramide (79 +/- 41 msec) (p less than 0.001) (18%), no spontaneous episodes of second-degree or third-degree atrioventricular block were observed. In six patients with premature ventricular depolarizations (greater than or equal to 1/min), the arrhythmia was totally abolished in four, markedly reduced in one, and remained unchanged in one. Disopyramide resulted in significant prolongation of infranodal conduction time as well as in atrial and ventricular refractoriness, but nevertheless appears to be safe in patients with bundle branch block.

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Available abstract

Electrophysiological studies were performed in 22 patients with intraventricular conduction delay before and after intravenous infusion of disopyramide (Norpace), 2 mg/kg. Mean control maximal sinus node recovery time (1039 +/- 187 msec), atrioventricular nodal conduction time (113 +/- 28 msec), and atrioventricular nodal effective refractory periods (349 +/- 67 msec) did not change significantly after administration of disopyramide (1073 +/- 284 msec, 112 +/- 31 msec, and 342 +/- 42 msec, respectively). Mean spontaneous cycle length (756 +/- 146 msec) decreased significantly 5 minutes after disopyramide (717 +/- 124 msec) (p less than 0.05), but not after 30 minutes (734 +/- 142 msec). A small but statistically significant (p less than 0.05) increase occurred after disopyramide in the mean atrial effective refractory period (259 +/- 51 to 280 +/- 53 msec), ventricular effective refractory period (253 +/- 23 to 275 +/- 33 msec), as well as the relative refractory period of the ventricular specialized conduction system (six patients) 433 +/- 78 to 479 +/- 62 msec). Although mean control infranodal conduction time (67 +/- 35 msec) increased 5 minutes after disopyramide (79 +/- 41 msec) (p less than 0.001) (18%), no spontaneous episodes of second-degree or third-degree atrioventricular block were observed. In six patients with premature ventricular depolarizations (greater than or equal to 1/min), the arrhythmia was totally abolished in four, markedly reduced in one, and remained unchanged in one. Disopyramide resulted in significant prolongation of infranodal conduction time as well as in atrial and ventricular refractoriness, but nevertheless appears to be safe in patients with bundle branch block.

Key concepts: Disopyramide, Medicine, Refractory period, Effective refractory period, Cardiology, Internal medicine, Anesthesia, Electrophysiology

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