Advertisement

Drugs

, Volume 29, Supplement 4, pp 33–44 | Cite as

Aggravation of Ventricular Arrhythmia

A Drug-induced Complication
  • Philip J. Podrid
Section 2: The ‘Risks’ Involved with the Clinical Use of Antiarrhythmic Agents

Summary

Each antiarrhythmic agent can cause side effects, but most of these are easily recognised by the patient or physician. However, one potentially serious side effect common to all of these drugs is aggravation of ventricular arrhythmia. Often this is without symptoms and goes unrecognised by the patient. It occurs in 11 to 16% of drug tests depending upon the method of drug evaluation employed. There are no ECG changes which predict its occurrence and blood concentrations of drug are usually within a therapeutic range. There are no clinical patient features which are associated with this toxic reaction and it does not correlate with the presence or extent of underlying heart disease, the nature of the presenting arrhythmia or the known electrophysiological properties of the antiarrhythmic drug. Careful evaluation of these drugs is therefore essential.

Keywords

Ventricular Tachycardia Ventricular Arrhythmia Ventricular Fibrillation Quinidine Disopyramide 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

Tous les medicaments antiarythmiques peuvent être source d’effets indésirables, mais la plupart de ceux-ci sont aisément reconnaissables par le malade ou par le médecin. L’aggravation de l’arythmie ventriculaire leur est un commun risque, souvent asymptomatique, et qui se développe â l’insu du malade. On l’observe dans 11 à 16% des évaluations des effets des médicaments, suivant les techniques utilisées. Il n’existe pas de modification prémonitoire de l’ECG et les concentrations sanguines du médicament sont habituellement dans les normes thérapeutiques définies. On ne retrouve pas de pathologie associée, ni de corrélation avec la présence ou l’aggravation de la maladie cardiaque, le type d’arythmie ou ce qu’on sait des propriétés électrophysiologiques de Vantiarythmique. Une évaluation soigneuse de ces médicaments est en conséquence d’intérêt capital.

Zusammenfassung

Jedes Antiarrhythmikum kann Nebenwirkungen verursachen, aber die meisten von ihnen werden vom Patienten oder Arzt leicht erkannt. Eine allen diesen Substanzen gemeinsame potentiell ernste Nebenwirkung ist jedoch die Verstärkung der ventrikuläre Arrhythmie. Oft erfolgt dies ohne Symptome und wird vom Patienten nicht erkannt. In Abhängigkeit der angewandten Erfassungsmelhode tritt sie bei11bis 16% der Pharmakaprüfungen auf. Es gibt keine EKG-Veränderungen, die das Auftreten vorhersagen, und die Blukonzentrationen der An:tiarrhythmika befinden sich meist im therapeutischen Bereich. Es existieren keine mit der toxischen Reaktion assoziierte Patientenmerkmale noch Korrelationen mit dem Vorhandensein oder Ausmaβ von zugrundeliegenden Herzkrankheiten, der Art der vorliegenden Arrhythmie oder den bekannten elektrophysiologischen Eigenschaften des Antiarrhythmikums. Eine sorgfältige Beurteilung dieser Pharmaka ist daher notwendig.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Castellanos, A. and Salhanick, L.: Electrocardiographic patterns of procainamide cardiotoxicity. American Journal of the Medical Sciences 253: 52 (1967).PubMedCrossRefGoogle Scholar
  2. Cocco, G.; Stozzi, C; Chu, D. and Pansini, R.: Torsade de pointes as a manifestation of mexiletine toxicity. American Heart Journal 100: 878–880 (1980).PubMedCrossRefGoogle Scholar
  3. Chung, E.K.: Beta blockers in the treatment of disturbances in cardiac rhythm; in Schweizer (Ed.) Beta Biockers —Present Status and Future Prospects, p.221 (University Park Press, Baltimore 1974).Google Scholar
  4. Davies, P.; Leak, D. and Oram, S.: Quinidine induced syncope-British Medical Journal 2: 517 (1965).Google Scholar
  5. Davis, D. and Sprague, H.B.: Ventricular fibrillation: Its relation to heart block. Report of a case in which syncopal attacks and death occurred in the course of quinidine therapy. American Heart Journal 4: 559 (1929).Google Scholar
  6. Dhurandhar, R.W.; Nademanee, K. and Goldman, A.W.: Ventricular tachycardia — flutter associated with disopyramide therapy — report of 3 cases. Heart and Lung 7: 783 (1978).PubMedGoogle Scholar
  7. DiBianco, R.; Fletcher, R.D.; Cohen, A.Z.; Gottdienec, J.S.; Singh, S.; Katz, R.J.; Bates, H.R. and Sauerbrunn, B.: Treatment of frequent ventricular arrhythmia with encainide — assessment using serial ambulatory electrocardiograms, intracardiac electrophysiologic studies, treadmill exercise tests and radio-nuclide cineangiographic studies. Circulation 65: 1134(1982).PubMedCrossRefGoogle Scholar
  8. Engler, R.L. and LeWinter, M.: Tocainide induced ventricular fibrillation. American Heart Journal 101: 494–496 (1981).PubMedCrossRefGoogle Scholar
  9. Epstein, M.A.: Ventricular standstill during the intravenous procainamide treatment of ventricular tachycardia. American Heart Journal 45: 890 (1953).CrossRefGoogle Scholar
  10. Frieden, J.: Quinidine effects due to disopyramide. New England Journal of Medicine 298: 975 (1978).PubMedGoogle Scholar
  11. Gaughan, C.E.; Lown, B.; Lanigan, J.; Voukydes, P. and Besser, W.: Acute oral testing for determining antiarrhythmic drug efficacy. 1. Quinidine. American Journal of Cardiology 38: 677 (1976).CrossRefGoogle Scholar
  12. Graboys, T.B.; Lown, B.; Podrid, P.J. and DeSilva, R.A.: Long term survival of patients with malignant ventricular arrhythmias treated with antiarrhythmic drugs. American Journal of Cardiology 50: 437–443 (1982).PubMedCrossRefGoogle Scholar
  13. Jelinek. M.V. and Lown, B.: Exercise stress testing for exposure of cardiac arrhythmia. Progress in Cardiovascular Diseases 16: 497–522 (1974).PubMedCrossRefGoogle Scholar
  14. Keren, A.: Tzivoni, D.; Gavish, D.; Levi, J.; Gottlieb, S.; Benhorin, J. and Stern, S.: Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients. Circulation 64: 1167 (1981).PubMedCrossRefGoogle Scholar
  15. Kerr, W.J. and Bender, W.L.: Paroxysmal ventricular fibrillation with cardiac recovery in a case of auricular fibrillation and complete heart block while under quinidine sulfate therapy. Heart 9: 269 (1971).Google Scholar
  16. Khan, MM.; Logan, K.R.; McComb, J.M. and Adgey, A.A.J.: Management of recurrent ventricular tachyarrhythmias associated with QT prolongation. American Journal of Cardiology 47: 1301 (1981).PubMedCrossRefGoogle Scholar
  17. Koster, R.W. and Wellens, H.J.J.: Quinidine induced ventricular flutter and fibrillation without digitalis therapy. American Journal of Cardiology 38: 519 (1976).PubMedCrossRefGoogle Scholar
  18. Lown. B.; Calvert, A.F. and Armington, R.: Monitoring for serious arrhythmias and high risk of sudden death. Circulation (Suppl. III): I89-198 (1975).Google Scholar
  19. Lown, B.; Matta, R.J. and Besser, H.W.: Programmed ‘trend-scription.’ A new approach to electrocardiographic monitoring. Journal of the American Medical Association 232: 34–36 (1978).Google Scholar
  20. Lown, B.; Podrid, P.J.; DeSilva, R.A. and Graboys, T.B.: Sudden cardiac death management of the patient at risk. Current Problems in Cardiology 14: 12 (1980).Google Scholar
  21. McCord, ML. and Taguchi, J.T.: A study of the effect of procainamide hydrochloride in supraventricular arrhythmia. Circulation 4: 387(1951).PubMedCrossRefGoogle Scholar
  22. Meltzer, R.S.; Robert, E.W.; McMorrow, M. and Martin, R.P.: Atypical ventricular tachycardia as a manifestation of diso-pyramide toxicity. American Journal of Cardiology 42: 1044 (1978).CrossRefGoogle Scholar
  23. Morganroth, J. and Horowitz, L.N.: Flecainide — its proar-rhythmic effect and expected changes in the surface electrocardiogram. American Journal of Cardiology 53: 89B–94B (1984).PubMedCrossRefGoogle Scholar
  24. Nicholson, J.J.; Martin, L.E.; Gracey, J.G. and Knock, H.R.: Disopyramide induced ventricular fibrillation. American Journal of Cardiology 43: 1053(1979).PubMedCrossRefGoogle Scholar
  25. Oravitz, J. and Slodki, S.J.: Recurrent ventricular fibrillation precipitated by quinidine. Archives of Internal Medicine 122: 63 (1968).CrossRefGoogle Scholar
  26. Poser, R.; Lombardí, F.; Podrid, P.J. and Lown, B.: Aggravation of arrhythmia during electrophysiologic testing (abstract). Journal of American College of Cardiology 1: 708 (1983).Google Scholar
  27. Reid, P.R.; Griffith, L.S.C.; Platia, E.V. and Ord, S.E.: Evaluation of flecainide acetate in the management of patients at high risk of sudden cardiac death. American Journal of Cardiology 53: 108B–111B (1984).PubMedCrossRefGoogle Scholar
  28. Reynolds, E.W. and VanderArk, C.R.: Quinidine syncope and the delayed repolarization syndromes. Modern Concepts of Cardiovascular Disease 54: 117–122 (1976).Google Scholar
  29. Rinkenberger, R.L.; Prystowsky, E.N.; Jackman, W.M.; Naccarelli, G.V.; Heger, J.J. and Zipes, D.P.: Drug conversion of non-sustained ventricular tachycardia and sustained ventricular tachycardia during serial electrophysiologic studies. Identification of drugs that exacerbate tachycardia and potential mechanisms. American Heart Journal 103: 177 (1982).PubMedCrossRefGoogle Scholar
  30. Rokseth, R. and Storstein, O.: Quinidine therapy of chronic auricular fibrillation: Occurrence and mechanisms of syncope. Archives of Internal Medicine 111: 102(1963).CrossRefGoogle Scholar
  31. Ruskin, J.N.; McGovern, B.; Garan, H.; DiMarco, J.P. and Kelly, E.: Antiarrhythmic drugs. A possible cause of out of hospital cardiac arrest. New England Journal of Medicine 309: 1302–1306 (1983).Google Scholar
  32. Selzer, A. and Wray, H.W.: Quinidine syncope. Circulation 30: 17(1964).PubMedCrossRefGoogle Scholar
  33. Strasberg, B.; Sclarovsky, J.; Erdberg, A.; Duffy, C.E.; Lam, W.; Swiryn, S.; Agmon, J. and Rosen, K.M.: Procainamide induced polymorphous ventricular tachycardia. American Journal of Cardiology 47: 1309 (1981).PubMedCrossRefGoogle Scholar
  34. Velebit, V.; Podrid, P.J.; Lown, B.; Cohen, B.H. and Graboys, T.B.: Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs. Circulation 65: 886 (1982).PubMedCrossRefGoogle Scholar
  35. Winkle, R.A.; Mason, J.W.; Griffen, J.C. and Ross, D.: Malignant ventricular tachycardia associated with the use of encainide. American Heart Journal 102: 857 (1981).PubMedCrossRefGoogle Scholar
  36. Zipes, DP. and Troup, P.J.: New antiarrhythmic agents — amio-darone, aprindine, disopyramide, ethmozine, mexiletine, tocainide. verapamil. American Journal of Cardiology 41: 1005 (1978).CrossRefGoogle Scholar

Copyright information

© ADIS Press Limited 1985

Authors and Affiliations

  • Philip J. Podrid
    • 1
  1. 1.Cardiovascular Laboratories, Department of NutritionHarvard School of Public HealthBostonUSA

Personalised recommendations