The electrophysiological effects of intramuscular quinidine on the atrioventricular conducting system in man

Josephson, Mark E.; Seides, Stuart F.; Batsford, William P.; Weisfogel, Gerald M.; Akhtar, Masood; Caracta, Anthony R.; Lau, Sun H.; Damato, Anthony N.

doi:10.1016/0002-8703(74)90391-3

Cited by 86 publications

(29 citation statements)

References 34 publications

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“…As reported by other authors (Hirschfeld et al, 1977;Josephson et al. 1974) the QRS duration also increased significantly in our study.…”

Section: Effect Of Quinidinesupporting

confidence: 92%

“…In transplanted and therefore no longer autonomously innervated hearts, on the other hand, the AH interval increased significantly (Mason et al, 1977). The accelerated conduction in the AV node is therefore probably due to the anticholinergic effect of quinidine, whereas the direct membrane effect results in a conduction delay in the AV node (Josephson et al, 1974;Mason et al, 1977).…”

Section: Effect Of Quinidinementioning

confidence: 99%

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Electrophysiological effects of quinidine alone and of the combination quinidine‐verapamil on av conduction in humans

Theisen

Scheininger

1983

Clinical Cardiology

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Summary:The influence of 320 mg quinidine administered intravenously (i.v.), as well as subsequent administration of 5 mg verapamil i.v. on atrioventricular conduction was studied in 8 patients during sinus rhythm and atrial stimulation with the aid of His bundle electrography. Among the electrophysiologic parameters of the atrium the sinus rate increased significantly after quinidine and again increased slightly after subsequent administration of verapamil. During sinus rhythm the PA interval was not influenced by either substance. Conversely, during atrial stimulation the STA interval increased significantly under the effect of quinidine, while verapamil had no further influence. As an indicator of conduction time in the AV node, the AH interval was decreased significantly by quinidine during sinus rhythm and atrial stimulation. This effect was significantly counteracted by the additional administration of verapamil. The HV interval as a measure of the His-Purkinje conduction was not significantly affected. The QRS duration was increased significantly by quinidine and was not further influenced by verapamil. The QT, and QT intervals increased significantly after administration .of quinidine and were again slightly, but significantly shortened by verapamil. Our investigations show that the combination of quinidine and verapamil, which has clinically been found to have a higher conversion rate than quinidine alone, is well justified from an electrophysiologic point of view and that undesirable quinidine-related effects, such as rapid AV conduction in cases of atrial fibrillation and flutter, can be avoided by the subsequent administration of verapamil.

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“…As reported by other authors (Hirschfeld et al, 1977;Josephson et al. 1974) the QRS duration also increased significantly in our study.…”

Section: Effect Of Quinidinesupporting

confidence: 92%

Section: Effect Of Quinidinementioning

confidence: 99%

Electrophysiological effects of quinidine alone and of the combination quinidine‐verapamil on av conduction in humans

Theisen

Scheininger

1983

Clinical Cardiology

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“…The refractory period decreased in five cases with procainamide and two cases with quinidine. These results are consistent with the results previously recorded in the literature.9-1, 23,24 It was possible to determine and compare antegrade and retrograde refractory periods of the accessory pathway at any cycle length in only 11/33 patients because in others the atrium and/or ventricle became refractory. The greatest comparable numbers were obtained at a basic cycle length of 400 msec ( Abbreviations: PA = procainamide; Q = quinidine; AF = atrial fibrillation; BL = blood level; nl = normal; TDIV = total dose, intravenously; P Q46 = oral dose, every six hours; TD total dose; Fib = fibrillation; RT = reciprocating tachycardia; S = septal accessory atrioventricular pathway; R = right free-wall accessory atrioventricular pathway; L -left free-wall accessory atrioventricular pathway; LGL = Lown-Ganong-Levine.…”

Section: Methodssupporting

confidence: 89%

Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome.

Sellers¹,

Campbell²,

Bashore³

et al. 1977

Circulation

118

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Thirty-three patients with Wolff-Parkinson-White syndrome were studied electrophysiologically before and after administration of intravenous procainamide and oral quinidine sulfate. Procainamide prolonged the shortest R-R (SRR) interval between two consecutive pre-excited beats during atrial fibrillation 20-70 msec in 15 of 21 patients with no change observed in 6 of 21 patients. Quinidine sulfate prolonged the SRR 20-170 msec in all 16. In 14 of 18 patients where procainamide and quinidine were comparable, quinidine prolonged the SRR 30-100 msec more than procainamide.

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“…Slowing of phase zero (upstroke) and delays of phase two (plateau) and phase three (rapid repolarization) of the action potential are seen (16 (6). The quinidine levels which Josephson et al.…”

Section: Discussionmentioning

confidence: 98%

The electrophysiologic effects of quinidine in the transplanted human heart.

Mason¹,

Winkle²,

Rider³

et al. 1977

J. Clin. Invest.

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A B S T R A C T Using His btundle recording techniq(utes, we examined direct and auitonomically mediated condtuction system effects of (qtiinidine in five cardiac transplant recipients who have anatomically denervated hearts. We made control conduction interval and refractory period measurements, and then inftused 10 mg/kg quiinidine gltuconate over a 20-min period. At 30 min, we determined the electrophysiologic changes indtuced by quiinidine. Quiinidine significantly increased the atrial-His (AH) interval (from 97±9 [SEM] to 1083+7 ms,P < 0.001), the His-ventricular (HV) interval (from 43.9± Ito 52.8±3 ms, P < 0.01), the donor heart sintus cycle length (from 599±38 to 630 ±56 ms, P < 0.08), and the atrial effective refractory period (from 214 ± 14 to 241 ± 11 ms, P < 0.01). Qtuinidine significantly decreased the innervated, remnant atrial sintus cycle length (from 847±104 to 660±96 ms, P < 0.01) and the blood pressure. The mean plasma concentration of qutiinidine at the time that electrophysiologic measturements were repeated was 4.37+0.449 ,ug/ml. We concltude that quiinidine's predominant sintus nodal and atrioventrictular nodal effects in man are auitonomically mediated and opposite to its direct actions upon these structures. On the other hand, quinidine's prevailing effect on atrial refractoriness and His-Purkinje conduction in man is direct.

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The electrophysiological effects of intramuscular quinidine on the atrioventricular conducting system in man

Cited by 86 publications

References 34 publications

Electrophysiological effects of quinidine alone and of the combination quinidine‐verapamil on av conduction in humans

Electrophysiological effects of quinidine alone and of the combination quinidine‐verapamil on av conduction in humans

Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome.

The electrophysiologic effects of quinidine in the transplanted human heart.

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