1986Clinical CardiologyRequires access

Effects of atenolol in patients with reciprocating supraventricular tachycardia

João Pimenta, Carlos Britto Pereira

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Abstract

We studied 12 patients with crisis of paroxysmal reciprocating supraventricular tachycardia before and after intravenous injection of 5 mg of atenolol. The patients were then followed for periods ranging from 6 to 50 months (median 34 months). During this time, they received oral atenolol therapy, at 200 mg for the first two weeks, and 100 mg daily thereafter. Tachycardia was due to reciprocation within the atrioventricular node in 9 patients, and to pre-excitation in 3 patients. Atenolol slowed the sinus rate, prolonged the atrioventricular conduction time, and increased the atrial cycle length at which atrioventricular nodal Wenckebach phenomenon occurred. During the tachycardia, atenolol increased the tachycardia During the tachycardia, atenolol increased the tachycardia cycle length, due to prolongation of the intranodal atrioventricular conduction time. Of the 11 patients who were observed for the full period, 7 had no further episodes of arrhythmia. One patient (with left-sided pre-excitation) failed to respond to any antiarrhythmic medication, one patient remained free of symptoms for two years, but received an atrial pacemaker for control of the tachycardia at the end of this period. Two patients (one with dual atrioventricular nodal pathways, and one with concealed left-sided pre-excitation) await other treatment for their tachycardia, after remaining free of symptoms for one and two years, respectively. These findings suggest that atenolol is an effective beta blocker for use in controlling arrhythmias in patients with reciprocating supraventricular tachycardia, for use in once daily dosage, and is a medication largely free of side effects.

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What this paper is about

We studied 12 patients with crisis of paroxysmal reciprocating supraventricular tachycardia before and after intravenous injection of 5 mg of atenolol. The patients were then followed for periods ranging from 6 to 50 months (median 34 months). During this time, they received oral atenolol therapy, at 200 mg for the first two weeks, and 100 mg daily thereafter. Tachycardia was due to reciprocation within the atrioventricular node in 9 patients, and to pre-excitation in 3 patients. Atenolol slowed the sinus rate, prolonged the atrioventricular conduction time, and increased the atrial cycle length at which atrioventricular nodal Wenckebach phenomenon occurred. During the tachycardia, atenolol increased the tachycardia During the tachycardia, atenolol increased the tachycardia cycle length, due to prolongation of the intranodal atrioventricular conduction time. Of the 11 patients who were observed for the full period, 7 had no further episodes of arrhythmia. One patient (with left-sided pre-excitation) failed to respond to any antiarrhythmic medication, one patient remained free of symptoms for two years, but received an atrial pacemaker for control of the tachycardia at the end of this period. Two patients (one with dual atrioventricular nodal pathways, and one with concealed left-sided pre-excitation) await other treatment for their tachycardia, after remaining free of symptoms for one and two years, respectively. These findings suggest that atenolol is an effective beta blocker for use in controlling arrhythmias in patients with reciprocating supraventricular tachycardia, for use in once daily dosage, and is a medication largely free of side effects.

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Available abstract

We studied 12 patients with crisis of paroxysmal reciprocating supraventricular tachycardia before and after intravenous injection of 5 mg of atenolol. The patients were then followed for periods ranging from 6 to 50 months (median 34 months). During this time, they received oral atenolol therapy, at 200 mg for the first two weeks, and 100 mg daily thereafter. Tachycardia was due to reciprocation within the atrioventricular node in 9 patients, and to pre-excitation in 3 patients. Atenolol slowed the sinus rate, prolonged the atrioventricular conduction time, and increased the atrial cycle length at which atrioventricular nodal Wenckebach phenomenon occurred. During the tachycardia, atenolol increased the tachycardia During the tachycardia, atenolol increased the tachycardia cycle length, due to prolongation of the intranodal atrioventricular conduction time. Of the 11 patients who were observed for the full period, 7 had no further episodes of arrhythmia. One patient (with left-sided pre-excitation) failed to respond to any antiarrhythmic medication, one patient remained free of symptoms for two years, but received an atrial pacemaker for control of the tachycardia at the end of this period. Two patients (one with dual atrioventricular nodal pathways, and one with concealed left-sided pre-excitation) await other treatment for their tachycardia, after remaining free of symptoms for one and two years, respectively. These findings suggest that atenolol is an effective beta blocker for use in controlling arrhythmias in patients with reciprocating supraventricular tachycardia, for use in once daily dosage, and is a medication largely free of side effects.

Key concepts: Medicine, Atenolol, Tachycardia, Supraventricular tachycardia, Cardiology, Anesthesia, Internal medicine, Atrioventricular node

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