Abstract
At least 50% of patients who received an ICD have been treated with antiarrhythmic drugs (AAD). The potential indications for combining antiarrhythmic drugs and ICD are generally the following: reduction of the number of episodes of ventricular tachycardia or ventricular fibrillation and therefore of the number of shocks, improving patient's quality of life and extending the battery life of the ICD, prevention of supraventricular arrhythmias and/or control of their rate, lengthening of the tachycardia cycle length to allow ventricular tachycardia conversion by antitachycardia pacing and reduction of the number of episodes of syncope.
Although previous papers reported conflicting results about pharmacologic therapy in reducing the frequency of iCD shocks, some recent randomized prospective studies showed the efficacy of pharmacologic therapy in reducing the frequency of ICD shocks.
The use of antiarrhythmic drugs can have also adverse effect: an increase in the defibrillation threshold, an increase in the pacing threshold and an increase in the VT cycle length leading to detection failure. We have also to consider that some advantages derived from antiarrhythmic drugs can be reached by the new devices with atrial sensing and pacing and/or the possibility of atrial defibrillation or by using catheter ablation as adjunctive therapy to ICD.
For these reasons, the concomitant use of antiarrhythmic drugs and ICD should be evaluated in each patient in relation to specific clinical and electrophysiologic features including: the frequency, the rate and the clinical presentation of the ventricular arrhythmia, the effect of the selected drug on the defibrillation threshold, the defibrillation threshold at the implant, the effect of the selected drug on the ventricular function and the likelihood of proarrhythmic events.
Similar content being viewed by others
References
Thomas AC, Moser SA, Smutka ML, Wilson PA. Implantable defibrillation: Eight years clinical experience. PACE 1998;11:2053–2058.
Winkle RA, Mead RH, Ruder MA, Gaudiani VA, Smith NA, Buch WS, Schmidt P, Shipman T. Long-term outcome with the automatic implantable cardioverter-defibrillator. J Am Coll Cardiol 1989;13:1353–1361.
Bardy GH, Troutman C, Poole JE, Kudenchuk PJ, Dolack GL, Johnson G, Hofer B. Clinical experience with a tieredtherapy, multiprogrammable antiarrhythmia device. Circulation 1992;85:1689–1698.
Estes NAM, Haugh CJ, Wang PJ, Manolis AS. Antitachicardia pacing and low-energy cardioversion for ventricular tachycardia termination a clinical perspective. Am Heart 1994;127:1038–1046.
Huang SKS, de Guzman WLT, Chenarides JG, Okike NO, Vander Salm TJ. Effects of long-term amiodarone therapy on the defibrillation threshold and the rate of shocks of the implantable cardioverter-defibrillator. Am Heart J 1991;122: 720–727.
Kou WH, Kirsh MM, Rolling SF, Stirling M, Kadish AH, De Buitler M, Calkins H, Lewis RR, Morady F. Effect of antiarrhythmic drug therapy on the incidence of shocks in patients who receive an implantable cardioverter defibrillator after a single episode of sustained ventricular tachycardia-fibrillation. PACE 1991;14:1586–1592.
Dolack GL, CASCADE Investigators. Clinical predictors of implantable cardioverter-defibrillator shocks/results of the CASCADE (Trial). Am J Cardiol 1994;73:237–241.
Podrid PJ, Lown B. Propafenone: a new agent for ventricular arrhythmia. J Am Coll Cardiol 1984;4:117–125.
Mahmarian JJ, Verani MS, Hohmann T, Hill R, Thornton BC, Bolli R, Young JB, Roberts R, Pratt CM. The hemodinamic effects of sotalol and quinidine: analysis by use of rest and exercise gated radionuclide angiography. Circulation 1987;76:324–331.
Kuhlkamp V, Mewis C, Mermi J. Suppression of sustained ventricular tachyarrhythmias. A comparison of d,l sotalol with no antiarrhythmic drug treatment.
Singer I, Guarnieri T, Kupersmith J. Implanted automatic defibrillators: effects of drugs and pacemakers. PACE 1988;11:2250–2262.
Jung W, Manz M, Luderitz B. Effects of antiarrhythmic drugs on defibrillation threshold in patient with the implantable cardioverter defibrillator. PACE 1992;15:645–648.
Reiffel JA. Coromilas JM, Zimmermann JM. Drug device interactions: Clinical considerations. PACE 1985;8:369–373.
Peters W, Gang ES, Okazaki H. Acute effects of intravenous propafenone on the internal ventricular defibrillation threshold in the anesthetized dog. Am Heart J 1991;122: 1355–1360.
Stevens SK, Haffajee CI, Naccarelli G. Effects of oral propafenone on defibrillation and pacing thresholds in patients receiving implantable cardioverter-defibrillators. J Am Coll Cardiol 1996;28:418–422.
Marchlinski FE, Flores B. Effect of procainamide on the defibrillation threshold in man. Circulation 1988;78:II-154 (Abstract).
Dorian P, Fain ES, Davy JM. Lidocaine causes a reversible, concentration-dependent increase in defibrillation energy requirements. J Am Coll Cardiol 1986;8:327–332.
Marinchak RA, Friehling TD, Kline RA. Effect of antiarrhythmic drugs on de~brillation threshold: Case report of an adverse effect of mexiletine and review of literature. PACE 1988;11:7–12.
Wang M, Dorian P. Dl and D sotalol decrease defibrillation energy requirements. PACE 1989;12:1522–1529.
Fain ES, Lee JT, Winkle RA. Effects of acute intravenous and chronic oral amiodarone on defibrillation energy requirements. Am Heart J 1987;114:839–842.
Fogoros RN. Amiodarone-induced refractoriness to cardioversion. Ann Intern Med 1984;100:699–700.
Jung, W, Manz M, Pizzulli L, Luderitz B. Effects of chronic amiodarone therapy on defibrillation threshold, Am J Cardiol 1992;70:1023–1027.
Cornacchia D, Fabbri M, Maresta A, Puglisi A, Ricci R, Azzolini P, Nigro P, Sorrentino F, Sestu P, Sanna A, Villani GQ, Dieci G, Capucci A, De Seta F. Steroid-eluting electrodes prevent chronic pacing threshold rise in the atrial chamber after oral propafenone administration. PACE 1997;20:240–244.
Cornacchia D, Fabbri M, Maresta A, Nigro P, Sorrentino F, Puglisi A, Ricci R, Peraldo C, Fazzari M, Pistis G, Sestu P, Mereu D, De Seta F. Effect of steroid eluting versus conventional electrodes on propafenone induced rise in chronic ventricular pacing threshold. PACE 1993;16:2279–2284.
Niazi I, Kadri N, Mahmud R. Absence of post defibrillation bradyarrhythmias in patients with automatic implantable defibrillators. Am Heart J 1988;115:830–836.
Levick CE, Mizgala HF, Kerr CR. Failure to pace followinghigh dose antiarrhythmic therapy-reversal with isoproterenolo. PACE 1984;7:252–256.
Platia EF, Griffith LSC, Reid PR. Post-defibrillation bradycardia following implantable defibrillator discharge. J Am Coll Cardiol 1986;7:144A.
Guarnieri T, Datorre SD, Bondke H. Increased pacing threshold after an automatic de~brillator shock in dogs: Effects of class I and class II antiarrhythmic drugs. PACE 1988;11:1324–1330.
Khastger T, Lattuca J, Aarons D. Ventricular pacing threshold and time to capture postdefibrillation in patients undergoing implantable cardioverter-defibrillator implantation. PACE 1991;14:768–772.
Jung W, Manz M, Luderitz B. The use of antiarrhythmic drugs in implantable cardioverter-defibrillator patients, In: Camm AJ, ed. Transvenous Defibrillation and Radiofrequency Ablation. Armonk, NY: Futura Publishing Company, Inc, 1995:137–147.
Greene HL. Interactions between pharmacologic and nonpharmacologic antiarrhythmic therapy. Am J Cardiol 1996;78(Suppl 4A):61–66.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Santini, M., Pandozi, C. & Ricci, R. Combining Antiarrhythmic Drugs and Implantable Devices Therapy: Benefits and Outcome. J Interv Card Electrophysiol 4 (Suppl 1), 65–68 (2000). https://doi.org/10.1023/A:1009874330416
Issue Date:
DOI: https://doi.org/10.1023/A:1009874330416