This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, Y.-H. Articles by Karagueuzian, H. S. Search for Related Content PubMed PubMed Citation Articles by Kim, Y.-H. Articles by Karagueuzian, H. S.

(Circulation. 1999;100:666-674.)
© 1999 American Heart Association, Inc.

Basic Science Reports

Mechanism of Procainamide-Induced Prevention of Spontaneous Wave Break During Ventricular Fibrillation

Insight Into the Maintenance of Fibrillation Wave Fronts

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

From the Divisions of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, Calif (M.Y., T.-J.W., R.D., P.-S.C., H.S.K.), and the Division of Cardiology, Korea University, Seoul, Korea (Y.-H.K.).

Correspondence to Hrayr S. Karagueuzian, PhD, Division of Cardiology, Cedars-Sinai Medical Center, Davis Research Bldg, Room 6066, 8700 Beverly Blvd, Los Angeles, CA 90048. E-mail karagueuzian{at}csmc.edu

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 3.2x3.8 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.

Key Words: fibrillation • waves • reentry • action potentials

This article has been cited by other articles:

				Z. Y. Lim, B. Maskara, F. Aguel, R. Emokpae Jr, and L. Tung Spiral Wave Attachment to Millimeter-Sized Obstacles Circulation, November 14, 2006; 114(20): 2113 - 2121. [Abstract] [Full Text] [PDF]

				J. Kneller*, J. Kalifa*, R. Zou, A. V. Zaitsev, M. Warren, O. Berenfeld, E. J. Vigmond, L. J. Leon, S. Nattel, and J. Jalife Mechanisms of Atrial Fibrillation Termination by Pure Sodium Channel Blockade in an Ionically-Realistic Mathematical Model Circ. Res., March 18, 2005; 96(5): e35 - e47. [Abstract] [Full Text] [PDF]

				T. Ohara, Z. Qu, M.-H. Lee, K. Ohara, C. Omichi, W. J. Mandel, P.-S. Chen, and H. S. Karagueuzian Increased vulnerability to inducible atrial fibrillation caused by partial cellular uncoupling with heptanol Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1116 - H1122. [Abstract] [Full Text] [PDF]

				B.-S. Kim, Y.-H. Kim, G.-S. Hwang, H.-N. Pak, S. C. Lee, W. J. Shim, D. J. Oh, and Y. M. Ro Action potential duration restitution kinetics in human atrial fibrillation J. Am. Coll. Cardiol., April 17, 2002; 39(8): 1329 - 1336. [Abstract] [Full Text] [PDF]

				T. Ohara, K. Ohara, J.-M. Cao, M.-H. Lee, M. C. Fishbein, W. J. Mandel, P.-S. Chen, and H. S. Karagueuzian Increased Wave Break During Ventricular Fibrillation in the Epicardial Border Zone of Hearts With Healed Myocardial Infarction Circulation, March 13, 2001; 103(10): 1465 - 1472. [Abstract] [Full Text] [PDF]

				F. H. Samie, O. Berenfeld, J. Anumonwo, S. F. Mironov, S. Udassi, J. Beaumont, S. Taffet, A. M. Pertsov, and J. Jalife Rectification of the Background Potassium Current: A Determinant of Rotor Dynamics in Ventricular Fibrillation Circ. Res., December 7, 2001; 89(12): 1216 - 1223. [Abstract] [Full Text] [PDF]