Current concepts on ventricular fibrillation: A Vicious Circle of Cardiomyocyte Calcium Overload in the Initiation, Maintenance, and Termination of Ventricular Fibrillation

E. Zaugg, Christian (2004) Current concepts on ventricular fibrillation: A Vicious Circle of Cardiomyocyte Calcium Overload in the Initiation, Maintenance, and Termination of Ventricular Fibrillation. [Journal (Paginated)]

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Based on recent experimental studies, this review article introduces the novel concept that cardiomyocyte Ca2+ and ventricular fibrillation (VF) are mutually related, forming a self-maintaining vicious circle in the initiation, maintenance, and termination of VF. On the one hand, elevated myocyte Ca2+ can cause delayed afterdepolarizations, triggered activity, and consequently life-threatening ventricular tachyarrhythmias in various pathological conditions such as digitalis toxicity, myocardial ischemia, or heart failure. On the other hand, VF itself directly and rapidly causes progressive myocyte Ca2+ overload that maintains VF and renders termination of VF increasingly difficult. Accordingly, energy levels for successful electrical defibrillation (defibrillation thresholds) increase as both VF and Ca2+ overload progress. Furthermore, VF-induced myocyte Ca2+ overload can promote re-induction of VF after defibrillation and/or postfibrillatory myocardial dysfunction (postresuscitation stunning) due to reduced myofilament Ca2+ responsiveness. The probability of these adverse events is best reduced by early detection and rapid termination of VF to prevent or limit Ca2+ overload. Early additional therapy targeting transsarcolemmal Ca2+ entry, particularly during the first 2 min of VF, may partially prevent myocyte Ca2+ overload and thus, increase the likelihood of successful defibrillation as well as prevent postfibrillatory myocardial dysfunction.

Item Type:Journal (Paginated)
Keywords:calcium overload – ventricular fibrillation - defibrillation - myocardial stunning
Subjects:JOURNALS > Indian Pacing and Electrophysiology Journal
ID Code:4232
Deposited By: Indian Pacing and Electrophysiology, Journal
Deposited On:17 Apr 2005
Last Modified:11 Mar 2011 08:55

References in Article

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1. Kihara Y, Morgan JP. Intracellular calcium and ventricular fibrillation. Studies in the aequorinloaded isovolumic ferret heart. Circ Res. 1991;68:1378-1389.

2. Zaugg CE, Wu ST, Lee RJ, Buser PT, Parmley WW, Wikman-Coffelt J. Importance of calcium for the vulnerability to ventricular fibrillation detected by premature ventricular stimulation: Single pulse versus sequential pulse methods. J Mol Cell Cardiol. 1996;28:1059- 1072.

3. Lakatta EG, Guarnieri T. Spontaneous myocardial calcium oscillations: are they linked to ventricular fibrillation? J Cardiovasc Electrophysiol. 1993;4:473-489.

4. Kléber G. The potential role of Ca2+ for electrical cell-to-cell uncoupling and conduction block in myocardial tissue. Basic Res Cardiol. 1992;87 Suppl 2:131-43.

5. Aronson RS, Ming Z. Cellular mechanisms of arrhythmias in hypertrophied and failing myocardium. Circulation. 1993;87:VII-76-VII-83.

6. Thandroyen FT, Morris AC, Hagler HK, Ziman B, Pai L, Willerson JT, Buja LM. Intracellular

calcium transients and arrhythmia in isolated heart cells. Circ Res. 1991;69:810-9.

7. Viatchenko-Karpinski S, Terentyev D, Gyorke I, Terentyeva R, Volpe P, Priori SG, Napolitano C, Nori A, Williams SC, Gyorke S. Abnormal calcium signaling and sudden cardiac death associated with mutation of calsequestrin. Circ Res. 2004.

8. Terentyev D, Viatchenko-Karpinski S, Gyorke I, Volpe P, Williams SC, Gyorke S. Calsequestrin determines the functional size and stability of cardiac intracellular calcium stores: Mechanism for hereditary arrhythmia. Proc Natl Acad Sci U S A. 2003;100:11759-64.

9. Wehrens XH, Lehnart SE, Huang F, Vest JA, Reiken SR, Mohler PJ, Sun J, Guatimosim S, Song LS, Rosemblit N, D'Armiento JM, Napolitano C, Memmi M, Priori SG, Lederer WJ, Marks AR. FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death. Cell. 2003;113:829-40.

10. Zaugg CE, Wu ST, Barbosa V, Buser PT, Wikman-Coffelt J, Parmley WW, Lee RJ. Ventricular fibrillation-induced intracellular Ca2+ overload causes failed electrical defibrillation and post-shock reinitiation of fibrillation. J Mol Cell Cardiol. 1998;30:2183-92.

11. Koretsune Y, Marban E. Cell calcium in the pathophysiology of ventricular fibrillation and in the pathogenesis of postarrhythmic contractile dysfunction. Circulation. 1989;80:369-379.

12. Kojima S, Wikman-Coffelt J, Wu ST, Parmley WW. Nature of intracellular calcium transients during ventricular fibrillation and quinidine treatment in perfused rat hearts. Am J Physiol. 1994;266:H1473-H1484.

13. Zaugg CE, Wu ST, Kojima S, Wikman-Coffelt J, Parmley WW, Buser PT. Role of intracellular calcium in the antiarrhythmic effect of procainamide during ventricular fibrillation in rat hearts. Am Heart J. 1995;130:351-358.

14. Kojima S, Wu ST, Wikman-Coffelt J, Parmley WW. Acute amiodarone terminates ventricular

fibrillation by modifying Ca++ homeostasis in isolated perfused rat hearts. J Pharm Exp Ther. 1995;275:254-262.

15. Zaugg CE, Ziegler A, Lee RJ, Barbosa V, Buser PT. Postresuscitation stunning: postfibrillatory myocardial dysfunction caused by reduced myofilament Ca2+ responsiveness after ventricular fibrillation-induced myocyte Ca2+ overload. J Cardiovasc Electrophysiol. 2002;13:1017-24.

16. Zaugg CE, Kojima S, Wu ST, Wikman-Coffelt J, Parmley WW, Buser PT. Intracellular calcium transients underlying interval-force relationship in whole rat hearts: effects of calcium antagonists. Cardiovasc Res. 1995;30:212-221.

17. Jones DL, Kim YH, Natale A, Klein GJ, Varin F. Bretylium decreases and verapamil increases defibrillation threshold in pigs. Pacing Clin Electrophysiol. 1994;17:1380-1390.

18. Jones DL, Irish WD, Klein GJ. Defibrillation efficacy. Comparison of defibrillation threshold versus dose-response curve determination. Circ Res. 1991;69:45-51.

19. Zaugg CE, Wu ST, Lee R, Wikman-Coffelt J, Parmley WW. Intracellular Ca2+ handling and vulnerability to ventricular fibrillation in spontaneously hypertensive rats. Hypertension. 1997;30:461-467.

20. Chen PS, Shibata N, Dixon EG, Martin RO, Ideker RE. Comparison of the defibrillation threshold and the upper limit of ventricular vulnerability. Circulation. 1986;73:1022-1028.

21. Bolli R, Marban E. Molecular and cellular mechanisms of myocardial stunning. Physiol Rev. 1999;79:609-34.

22. Kern KB, Hilwig RW, Rhee KH, Berg RA. Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning. J Am Coll Cardiol. 1996;28:232-40.

23. Tang W, Weil MH, Sun S, Gazmuri RJ, Bisera J. Progressive myocardial dysfunction after cardiac resuscitation. Crit Care Med. 1993;21:1046-50.

24. Kerber RE, Martins JB, Gascho JA, Marcus ML, Grayzel J. Effect of direct-current countershocks on regional myocardial contractility and perfusion. Experimental studies. Circulation. 1981;63:323-32.

25. Wijffels MC, Kirchhof CJ, Dorland R, Allessie MA. Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation. 1995;92:1954-1968.

26. Goette A, Honeycutt C, Langberg JJ. Electrical remodeling in atrial fibrillation. Time course and mechanisms. Circulation. 1996;94:2968-2974.

27. Tieleman RG, Van Gelder IC, Crijns HJ, De Kam PJ, Van Den Berg MP, Haaksma J, Van Der Woude HJ, Allessie MA. Early recurrences of atrial fibrillation after electrical cardioversion: a result of fibrillation-induced electrical remodeling of the atria? J Am Coll Cardiol. 1998;31:167-173.

28. Daoud EG, Knight BP, Weiss R, Bahu M, Paladino W, Goyal R, Man KC, Strickberger SA, Morady F. Effect of verapamil and procainamide on atrial fibrillation-induced electrical remodeling in humans. Circulation. 1997;96:1542-1550.

29. Burashnikov A, Antzelevitch C. Reinduction of atrial fibrillation immediately after termination of the arrhythmia is mediated by late phase 3 early afterdepolarization-induced triggered activity. Circulation. 2003;107:2355-60.

30. Leistad E, Aksnes G, Verburg E, Christensen G. Atrial contractile dysfunction after short-term atrial fibrillation is reduced by verapamil but increased by BAY K8644. Circulation. 1996;93:1747-54.

31. Bers DM. Excitation-contraction coupling and cardiac contractile force. 2nd ed. Dordrecht: Kluwers Academic Press; 2002.


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