Ventricular preexcitation occurs when a supraventricular impulse activates the whole or a part of the ventricular myocardium earlier than would be expected because of the presence of an accessory conduction pathway. This accessory AV pathway may connect the atrium with the distal part of the AV node (James fiber), the atrium with the His bundle (Brechenmacher fiber), the AV node or the His bundle with the ventricular myocardium (Mahaim fiber), or the atrium with the ventricular myocardium (Kent bundle). In the Lown-Ganong-Levine syndrome, our recent electrophysiologic studies have demonstrated that the occurrence of atrial flutter-fibrillation is related to atrial vulnerability, and the genesis of supraventricular tachycardia can be accounted for by the presence of dual AV nodal pathways or a concealed accessory AV pathway (Kent bundle). The ventricular rate during both supraventricular tachycardia and atrial flutter-fibrillation in patients with the Lown-Ganong-Levine syndrome is significantly higher than in those with a normal P-R interval. The Wolff-Parkinson-White syndrome constitutes the most common variety of preexcitation syndrome. In AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome, the AV node is part of the tachycardia circuit. Therefore, vagal maneuvers and medications used to slow conduction and increase refractoriness in the AV node are useful for terminating AV reciprocating tachycardia. In addition, lidocaine and procainamide given intravenously may be effective in interrupting the tachycardia circuit by increasing refractoriness in the accessory AV pathway. For long-term prophylaxis, digitalis, propranolol, and verapamil, either alone or in various combinations, can be administered orally to prevent recurrence of AV reciprocating tachycardia.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Dec 1 1980|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine