Implantable Device Therapy of Atrial Tachyarrhythmias:Ready for Prime Time?

SERGIO L. PINSKI, M.D.

From the Section of Cardiology, Rush-Presbyterian–St. Luke’s Medical Center and Rush Medical College, Chicago, Illinois

Editorial Comment

Atrial � brillation (AF) is a ubiquitous arrhythmia asso-ciated with considerable morbidity and mortality that, dur-ing the last decade, has become the target of intensiveclinical research efforts.1 Dissatisfaction with the ef� cacyand safety of antiarrhythmic drugs (up to now the mainstayof therapy) has spurred interest in a variety of nonpharma-cologic approaches to AF therapy.2 The implantable cardio-verter de� brillator (ICD) now constitutes the gold standardfor treatment of ventricular tachyarrhythmias, but extrapo-lation of this paradigm to AF is not straightforward. Al-though low-energy internal cardioversion is highly effectivein terminating AF,3 there has been an understandable reluc-tance to rely on potentially painful shocks for primarytherapy of an (immediately) nonlethal arrhythmia. Theavailable evidence regarding the natural history of AF sug-gests that it tends to recur (despite antiarrhythmic drugtherapy) at a much higher rate than ventricular � brillation,making widespread acceptance of stand-alone atrial cardio-version therapy by patients and physicians unlikely.

Despite these limitations, several manufacturers havecontinued clinical development of devices for AF therapy.4Currently available devices incorporate not only cardiover-sion capability, but also two painless therapies: pacing al-gorithms to prevent tachyarrhythmia onset, and overdrivepacing for termination of organized tachycardias. Deviceprevention of AF is predicated on the concept that atrialpacing at speci� c sites, rates, and/or cadences (e.g., sup-pression of pauses, rate stabilization) can modify the acti-vation and recovery properties of the atrial myocardium ina way that will impede the onset of AF.

In this issue of the Journal, Gold et al.5 report an inter-national multicenter study on the use of an atrioventricularICD in patients with drug-refractory AF but no history ofventricular tachyarrhythmias. They conclude that the devicewas safe and ef� cacious in the population studied. Althoughthe absence of a control group makes it dif� cult to charac-terize the bene� t derived, indirect evidence is provided. Oneyear after implant, 94% of the patients remained in sinusrhythm, and 91% still had atrial therapies enabled. It isinteresting to note that although failure of drug therapy wasa requisite for patient enrollment, only 63% of the patientswere taking an antiarrhythmic drug at the time of implant,and the proportion did not change during follow-up. Thetherapy was well tolerated. Pacing terminated 40% of thedetected atrial tachyarrhythmia episodes, a proportion sim-ilar to that observed with the same device in patients with

history of ventricular tachyarrhythmias.6 Among patients inwhom atrial cardioversion therapy was programmed in thepatient-activated mode, the proportion of tachyarrhythmiaepisodes for which the activator was used increased overtime. In the patients with automatic therapy, programmingof shock delivery during night hours also may have con-tributed to acceptance of the device. The complication ratewas not excessive for the learning curve phase of a newtherapeutic modality. The high incidence of atrial lead dis-lodgment was due to the frequent use of a tripolar ventric-ular de� brillation electrode not designed for atrial applica-tion. Dislodgment should be much less common when astandard atrial pacing lead is used in combination with adual-coil ventricular de� brillation lead.

In a randomized cross-over substudy including 75 pa-tients, the authors found that enabling the two pacing pre-ventive algorithms available in the device did not decreasethe rate of recurrence of atrial tachyarrhythmias. The failureto demonstrate an effect could be due to a small sample sizewith low statistical power, the endpoint measured, the pre-ferred site of implantation of the atrial lead (not described inthe study), or true inef� cacy of the algorithms tested. In adifferent population treated with the same device, atrialpacing therapies signi� cantly decreased the total atrialtachyarrhythmia burden, but the relative contribution ofprevention versus termination algorithms was not clear.7The pacing site may be more important than the pacingalgorithm in preventing AF.8 Whereas a lateral location ofthe pacing lead often is recommended in patients withdual-chamber ICDs to reduce the incidence of far-� eld Rwave sensing,9 prevention of AF requires a septal loca-tion.1 0

The incidence of ventricular tachyarrhythmias was rela-tively high (7.5% of patients) in this study. Although thisobservation will further dwarf the prospects for a stand-alone atrial de� brillator, it may have arisen from selectionbias. It is plausible that Gold et al. included many patientsin whom a ventricular ICD was believed clinically valuabledespite the absence of formal implant indications. On theother hand, ventricular tachyarrhythmia or sudden deathwas not observed in clinical studies of the atrioverter devicein which patients with heart failure or severe left ventriculardysfunction were excluded from enrollment.1 1

The fact that most episodes (75%) of ventricular tachy-arrhythmia occurred during an ongoing episode of atrialtachyarrhythmia has therapeutic implications. Other inves-tigators have reported similar � ndings. In a study of 250ICD recipients, the presence of permanent AF was an inde-pendent predictor of appropriate device therapy for ventric-ular tachyarrhythmias.12 It was proposed that long-shortsequences during AF can amplify the dispersion of repolar-ization in the ventricular myocardium and, therefore, pro-mote ventricular arrhythmogenesis. Rapid conduction of

J Cardiovasc Electrophysiol, Vol. 12, pp. 1254-1255, November 2001.

Address for correspondence: Sergio L. Pinski, M.D., Rush-Presbyterian–St. Luke’s Medical Center, 1750 W. Harrison Street, JS-1091, Chicago, IL60612. Fax: 312-942-5862; E-mail: spinski@rush.edu

1254 Reprinted with permission fromJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 12, No. 11, November 2001

Copyright ©2001 by Futura Publishing Company, Inc., Armonk, NY 10504-0418

atrial tachyarrhythmias to the ventricle also can induceelectrophysiologic and metabolic derangements that canlead to ventricular � brillation. This sequence is best docu-mented in hypertrophic cardiomyopathy,13 but can be ex-pected in other forms of heart disease. Thus, prompt termi-nation of AF can decrease the incidence of ventriculartachyarrhythmia. To our knowledge, ventricular proarrhyth-mia secondary to automatic atrial therapies has not beenreported. Shocks are synchronized to the R wave and onlydelivered after a relatively long R-R interval (nominal $500msec in this device) to prevent encroachment of the vulner-able period of ventricular repolarization. As the vast major-ity of these patients receive drugs that block AV nodalconduction, rapid conducted ventricular rates during atrialpacing bursts are unlikely. However, induction of ventric-ular � brillation due to far-� eld ventricular capture duringmanual, high-output 50-Hz atrial bursts has been observedin a patient with an atrial antitachycardia pacemaker and anatrial lead implanted in the ostium of the coronary sinus(Andrina Houghman, personal communication).

It is likely that the ECG de� nition of AF encompasses aseries of entities with different pathophysiology, naturalhistory, and response to treatment. Future research shouldbe aimed at better de� ning these entities.14 Prima facie,ablation strategies should be most suitable for patients inwhom focal mechanisms predominate. Pharmacologic ther-apy, supplemented by devices capable of pacing and car-dioversion, would be most useful in patients in whom AFresults mainly from generalized abnormalities in the struc-ture and function of the atrial myocardium. On the basis ofcurrent nonrandomized evidence, devices like those used inthe study by Gold et al. appear most valuable in patientswith an indication for conventional ICD therapy who alsohave a history of AF. In patients with AF without a separateindication for ICD, these devices should be considered onlyafter failure of at least one of the most effective drugs(amiodarone, dofetilide) and (probably) of attempted focalablation, including pulmonary vein isolation. In conclusion,the answer to the question posed in the title of this editorialis “no.” However, the therapy certainly deserves a covetedslot in the late-night schedule. We should continue moni-toring the ratings to see if a change in programming iswarranted in the future.

References

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9. Weretka S, Becker R, Hilbel T, Karle C, Osswald BR, Kuebler W,Schoels W: Far-� eld R wave oversensing in a dual chamber arrhyth-mia management device: Predisposing factors and practical implica-tions. PACE 2001;24:1240-1246.

10. Bailin SJ, Adler S, Giudici M: Prevention of chronic atrial � brillationby pacing in the region of Bachmann’s bundle: Results of a multicenterrandomized trial. J Cardiovasc Electrophysiol 2001;12:912-917.

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12. Gronefeld GC, Mauss O, Li YG, Klingenheben T, Hohnloser SH:Association between atrial � brillation and appropriate implantablecardioverter de� brillator therapy: Results from a prospective study.J Cardiovasc Electrophysiol 2000;11:1208-1214.

13. Lopez Gil M, Arribas F, Cosio FG: Ventricular � brillation induced byrapid atrial rates in patients with hypertrophic cardiomyopathy. Eu-ropace 2000;2:327-332.

14. Allessie MA, Boyden PA, Camm AJ, Kleber AG, Lab MJ, Legato MJ,Rosen MR, Schwartz PJ, Spooner PM, Van Wagoner DR, Waldo AL:Pathophysiologyand prevention of atrial � brillation. Circulation 2001;103:769-777.

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