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J Am Coll Cardiol, 1983; 2:894-903
© 1983 by the American College of Cardiology Foundation
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Nadolol and supraventricular tachycardia: an electrophysiologic study

MS Chang, RJ Sung, TY Tai, SL Lin, PH Liu, and BN Chiang

To assess antiarrhythmic efficacy of oral nadolol, 15 patients with recurrent supraventricular tachycardia were studied. Eight patients had atrioventricular (AV) nodal reentrant tachycardia and seven had AV reciprocating tachycardia involving an accessory AV pathway. Electrophysiologic studies were performed before and after intravenous infusion of propranolol (0.20 mg/kg), and were repeated 5 to 8 days after oral nadolol therapy at a daily dose of 80 to 160 mg. Both intravenous propranolol and oral nadolol induced significant prolongation of the sinus cycle length from 741 +/- 73 ms to 834 +/- 97 and 1,029 +/- 95 ms, respectively (p less than 0.001 and p less than 0.0001, respectively). Both intravenous propranolol and oral nadolol depressed AV nodal but not accessory AV pathway conduction, and shifted the dual AV nodal pathway conduction curves (A1A2, A2H2; A1A2, H1H2) upward and to the right by prolonging the conduction time and increasing the refractory period. Ten patients (seven with AV nodal reentry and three with AV reciprocation) who responded to intravenous propranolol also responded to oral nadolol with loss of the inducibility of sustained tachycardia; the remaining five patients (one with AV nodal reentry and four with AV reciprocation) who did not respond to intravenous propranolol also failed to respond to oral nadolol with persistence of the inducibility of sustained tachycardia. Thus, in conclusion, intravenous propranolol testing predicts the therapeutic efficacy of oral nadolol therapy and oral nadolol in once-daily doses may be used for long-term prophylaxis of recurrent supraventricular tachycardia.




 
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