Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation: Insight into the maintenance of fibrillation wave fronts

Young Hoon Kim, Masaaki Yashima, Tsu Juey Wu, Rahul Doshi, Peng Sheng Chen, Hrayr S. Karagueuzian

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Background - Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break. Methods and Results - The endocardial surfaces of 7 isolated, perfused swine right ventricles were mapped with a 3.2 x 3.8 cm plaque with 477 bipolar electrodes. Activation pattern during VF was visualized dynamically while simultaneously recording epicardial action potentials with a glass microelectrode. APD restitution curves were constructed during VF (dynamic) and during S1S2 protocols. At baseline, VF was maintained by 5.3 ± 1 wavelets. Procainamide (PA) at 10 μg/mL decreased the number of wavelets to 3.5 ± 1 (P < 0.05). At baseline VF was maintained by spontaneous wave break and by new reentrant wave front formation. PA eliminated spontaneous wave break during VF while having no effect on reentry formation. PA increased the cycle length of the VF (148.5 ± 41.2 ms vs 81 ± 10 ms, P < 0.01) and the core area of the reentry from 5.8 to 14.5 mm2 (P < 0.05). Dynamic APD restitution curve during VF showed that PA eliminated the initiation of activation with APDs shorter than 30 ms. The effects of PA on cellular properties and wave front dynamics were reversed during 60 minutes of drug- free perfusion. Conclusions - Critically short APDs during VF promote spontaneous wave break. Their elimination with PA, however, maintains VF by generating new reentrant wave front.

Original languageEnglish
Pages (from-to)666-674
Number of pages9
JournalCirculation
Volume100
Issue number6
DOIs
Publication statusPublished - 1999 Aug 10

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Procainamide
Ventricular Fibrillation
Maintenance
pamidronate
Action Potentials
Microelectrodes
Heart Ventricles
Glass
Electrodes
Swine
Perfusion

Keywords

  • Action potentials
  • Fibrillation
  • Reentry
  • Waves

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation : Insight into the maintenance of fibrillation wave fronts. / Kim, Young Hoon; Yashima, Masaaki; Wu, Tsu Juey; Doshi, Rahul; Chen, Peng Sheng; Karagueuzian, Hrayr S.

In: Circulation, Vol. 100, No. 6, 10.08.1999, p. 666-674.

Research output: Contribution to journalArticle

Kim, Young Hoon ; Yashima, Masaaki ; Wu, Tsu Juey ; Doshi, Rahul ; Chen, Peng Sheng ; Karagueuzian, Hrayr S. / Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation : Insight into the maintenance of fibrillation wave fronts. In: Circulation. 1999 ; Vol. 100, No. 6. pp. 666-674.
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T1 - Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation

T2 - Insight into the maintenance of fibrillation wave fronts

AU - Kim, Young Hoon

AU - Yashima, Masaaki

AU - Wu, Tsu Juey

AU - Doshi, Rahul

AU - Chen, Peng Sheng

AU - Karagueuzian, Hrayr S.

PY - 1999/8/10

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N2 - Background - Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break. Methods and Results - The endocardial surfaces of 7 isolated, perfused swine right ventricles were mapped with a 3.2 x 3.8 cm plaque with 477 bipolar electrodes. Activation pattern during VF was visualized dynamically while simultaneously recording epicardial action potentials with a glass microelectrode. APD restitution curves were constructed during VF (dynamic) and during S1S2 protocols. At baseline, VF was maintained by 5.3 ± 1 wavelets. Procainamide (PA) at 10 μg/mL decreased the number of wavelets to 3.5 ± 1 (P < 0.05). At baseline VF was maintained by spontaneous wave break and by new reentrant wave front formation. PA eliminated spontaneous wave break during VF while having no effect on reentry formation. PA increased the cycle length of the VF (148.5 ± 41.2 ms vs 81 ± 10 ms, P < 0.01) and the core area of the reentry from 5.8 to 14.5 mm2 (P < 0.05). Dynamic APD restitution curve during VF showed that PA eliminated the initiation of activation with APDs shorter than 30 ms. The effects of PA on cellular properties and wave front dynamics were reversed during 60 minutes of drug- free perfusion. Conclusions - Critically short APDs during VF promote spontaneous wave break. Their elimination with PA, however, maintains VF by generating new reentrant wave front.

AB - Background - Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break. Methods and Results - The endocardial surfaces of 7 isolated, perfused swine right ventricles were mapped with a 3.2 x 3.8 cm plaque with 477 bipolar electrodes. Activation pattern during VF was visualized dynamically while simultaneously recording epicardial action potentials with a glass microelectrode. APD restitution curves were constructed during VF (dynamic) and during S1S2 protocols. At baseline, VF was maintained by 5.3 ± 1 wavelets. Procainamide (PA) at 10 μg/mL decreased the number of wavelets to 3.5 ± 1 (P < 0.05). At baseline VF was maintained by spontaneous wave break and by new reentrant wave front formation. PA eliminated spontaneous wave break during VF while having no effect on reentry formation. PA increased the cycle length of the VF (148.5 ± 41.2 ms vs 81 ± 10 ms, P < 0.01) and the core area of the reentry from 5.8 to 14.5 mm2 (P < 0.05). Dynamic APD restitution curve during VF showed that PA eliminated the initiation of activation with APDs shorter than 30 ms. The effects of PA on cellular properties and wave front dynamics were reversed during 60 minutes of drug- free perfusion. Conclusions - Critically short APDs during VF promote spontaneous wave break. Their elimination with PA, however, maintains VF by generating new reentrant wave front.

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