The Effects of Propranolol on Induction of A-V Nodal Reentrant Paroxysmal Tachycardia

Abstract

Twelve patients with paroxysmal supraventricular tachycardia (PSVT) were studied before and after administration of 0.1 mg/kg i.v. propranolol. Echo zones for inducing atrioventricular (A-V) nodal reentry were determined using His bundle recording and the atrial extrastimulus technique. After propranolol the echo zone was abolished in two patients, decreased in one, unchanged in five, increased in two. In two patients echo zones appeared only after propranolol. Nine patients had episodes of sustained PSVT prior to propranolol. Following propranolol PSVT persisted in only five. In these five patients propranolol slowed the rate of PSVT. The data were analyzed by plotting A 1 -A 2 and H 1 -H 2 interval curves. On the basis of these curves the patients were separated into those with "dual pathways" and those with "reflection." The effects of propranolol on both conduction patterns are discussed. In summary, the actions of propranolol in PSVT patients were variable. Potentially beneficial effects included slowing of induced PSVT, loss of the ability to sustain PSVT, and decrease or total elimination of echo zones. Potentially deleterious effects included potentiation of the echo phenomenon with either increase or development of echo zones.

Pirmenol in termination of paroxysmal supraventricular tachycardia

“…Therefore, termination of SVT via an antegrade block in the AV node will be unlikely. This contrasts the effects of digitalis, beta-blocking agents, and calcium antagonists which mainly affect the antegrade re-entrant limb both in AV intranodal tachycardia and AVRT (Wellens et al, 1975(Wellens et al, , 1977Wu et al, 1974). The effects of pirmenol resemble those of quinidine, procainamide, disopyramide, and the newer drugs, propafenone and flecainide (Brugada and Wellens, 1984;Garcia-Civera et al, 1984;Hellestrand et al, 1983, Wu et al, 1978b, 1981.…”

Salutary effects of intravenous ajmaline in patients with paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways: blockade of the retrograde fast pathway.

“…The efficacy of other drugs in preventing induction of atrioventricular nodal reentrant PSVT has been reported to be as follows: intravenous propranolol 41 % to 44%,12 22 intravenous ouabain 44% to 54%,12. 23 intravenous ouabain plus propranolol 58% ,2 intravenous procainamide 65%,"1 oral quinidine 78%,2 13 oral disopyramide 67%,"' and intravenous disopyramide 60%.6 Intravenous verapamil converts 80% to 100% of episodes of PSVT into sinus rhythm,24, 25 but is less effective in preventing induction of PSVT after oral administration.26 One peculiar feature observed in dual atrioventricular nodal pathways has been that drugs like procainamide,4 27 quinidine,27 and disopyramide, 14 which inhibit the accessory pathway in WolffParkinson-White syndrome, prevent atrioventricular nodal reentry by selective inhibition of the retrograde fast pathway.…”

Demonstration of sustained sinus and atrial re-entry as a mechanism of paroxysmal supraventricular tachycardia.

“…Both A-V nodal reentrant and sinus or atrial re-entrant PSVT could also be induced with ventricular pacing; however, the former would be dependent upon induction of A-V nodal retrograde Wenckebach sequences,34 35 while the latter would be dependent upon intact 1:1 retrograde V-A conduction. Heart rates during induced sinus or atrial re-entrant PSVT appeared to be slower than those described for A-V nodal re-entrant PSVT.1 2,6 Organic heart disease was present in our five patients with sinus or atrial re-entrant PSVT. Whether organic heart disease is a prerequisite for the occurrence of sustained sinus or atrial re-entrance in man cannot be determined with the small number of patients studied.…”

“…[5][6][7]. In all the patients, the lowest pacing rate inducing PSVT was slower than the pacing rate inducing A-V nodal Wenckebach periods ( In all of the patients, multiple A-H1 intervals were noted during the study.…”

“…Most cases of PSVT appear to reflect sustained atrioventricular (A-V) nodal re-entrance. [1][2][3][4][5][6] Recent animal and human studies have demonstrated that re-entry can also occur in the sinus node and atrium, implying that reentrance in these latter structures could produce clinical PSVT.7"12 In this study, we describe sustained sinus and atrial re-entry as the probable mechanism of clinical tachycardia in five patients with organic heart disease. The electrophysiological behavior of sinus or Abbreviations: PSVT = paroxysmal supraventricular tachycardia; ASHD = arteriosclerotic heart disease; fuHiD = hypertensive heart disease; RBBB = right bundle branch block; LASH = left anterior superior hemiblock; L = left atrium.…”