Elsevier

Cardiology Clinics

Volume 18, Issue 1, 1 February 2000, Pages 25-36
Cardiology Clinics

PACING TO PREVENT ATRIAL FIBRILLATION

https://doi.org/10.1016/S0733-8651(05)70125-9Get rights and content

Atrial fibrillation(AF) is the most common sustained arrhythmia and is associated with substantial morbidity and mortality.26 Present pharmacologic treatment strategies are directed at heart rate control or prescription of class I/III antiarrhythmic drugs to prevent AF recurrence.45 Both strategies are frequently ineffective, or the drugs prescribed are not tolerated because of adverse effects, including ventricular proarrhythmia.9, 14, 45 Consequently, interest in the development of nonpharmacologic therapies for the prevention of AF has arisen.

Section snippets

MECHANISMS OF ATRIAL FIBRILLATION

The initiation of AF requires a trigger as well as an abnormal electrophysiologic substrate for maintenance of the arrhythmia. Most episodes of AF are believed to be due to a reentrant mechanism.1, 16, 25 A supraventricular premature beat (SVPB) usually initiates the arrhythmia, which is maintained if a region of slow conduction or heterogeneity of repolarization exists. Typically, multiple wavelets of reentry develop for AF to persist. Some episodes of AF may develop as a result of focal

FACTORS CONTRIBUTING TO INITIATION OF ATRIAL FIBRILLATION

Some clinical reports suggest that significant bradycardia may precede the initiation of AF. The concept of nocturnal vagally mediated AF was promoted by Coumel et al,10 who reported a series of patients with nocturnal bradycardia associated with AF onset, which was prevented by atrial pacing.3 It has been hypothesized that bradycardia exaggerates the dispersion of atrial repolarization, which might provide the substrate for AF.18, 20 Subsequent studies investigating the electrocardiographic

MECHANISMS OF PACING TO PREVENT ATRIAL FIBRILLATION

There are several mechanisms by which atrial pacing might prevent AF:

  • 1

    Atrial pacing may reduce bradycardia-induced dispersion of atrial repolarization, which contributes to the electrophysiologic substrate for AF.20, 43

  • 2

    Atrial overdrive suppression of SVPBs and runs of SVPBs would eliminate the trigger for AF.15, 18, 55

  • 3

    Some forms of atrial pacing may change atrial activation patterns, preventing the development of intra-atrial reentry should an SVPB occur.5, 28, 34 This concept is

SINGLE-SITE RIGHT ATRIAL PACING

A number of retrospective studies have reported that atrial-based pacing (AAI/R) or atrioventricular (AV) sequential pacing reduces the incidence of AF over time compared with ventricular pacing in patients with sinus node disease or complete heart block.8, 21, 38, 42, 44 Connolly et al8 reviewed 10 of these retrospective trials and calculated that the annual incidence of AF was 2.6% per year in patients receiving physiologic pacing compared with 6.8% per year in patients receiving a

PREVENTION OF ATRIAL FIBRILLATION WITH SINGLE-SITE PACING

Some clinical data suggest that single-site right atrial pacing is less effective in preventing AF in patients with right atrial conduction delays and in patients with increased dispersion of right atrial refractoriness.48 Some patients may benefit from site-specific pacing (e.g., atrial septum or Bachmann's bundle).4, 5, 31, 47 Preliminary data suggest that pacing from the septum or Bachmann's bundle may shorten overall atrial activation time and that this may play a role in preventing AF.

APPROPRIATE PACING MODALITY AFTER ATRIOVENTRICULAR NODE ABLATION

The PA3 Investigators compared the effects of DDDR versus VDD pacing after total AV node ablation for prevention of persistent AF in 67 patients with antiarrhythmic drug–refractory AF.7, 17 The time to first recurrence of AF after AV node ablation was similar in the DDDR group compared with the VDD group. As well, the AF burden increased over time in both groups. A substantial number of patients (28%) developed persistent AF 6 months postablation, and 48% of patients were in persistent AF 12

MULTISITE ATRIAL PACING

Multisite atrial pacing has been evaluated for prevention of atrial flutter and AF. Daubert et al11 described biatrial pacing using the high right atrium and distal coronary sinus. Saksena et al12, 40, 41 have described dual-site right atrial pacing using the high right atrium and the coronary sinus os. Preliminary studies suggest that these approaches may have an incremental benefit for prevention of AF compared with high right atrial pacing if used in conjunction with antiarrhythmic drug

PACING THERAPIES TO TERMINATE ATRIAL FIBRILLATION

Newer pulse generators will include antitachycardia pacing therapies for termination of atrial tachycardias, atrial flutter, and AF. Studies in patients receiving a dual-chamber implantable cardioverter defibrillator with atrial tachycardia detection features have revealed that atrial tachycardias, atrial flutter, and AF occur frequently in this patient population, particularly in patients with a prior history of AF.49 Sixty-seven percent of episodes of atrial tachycardias were terminated by

PREVENTIVE THERAPIES AFTER TERMINATION OF ATRIAL FIBRILLATION

AF frequently recurs after termination of an episode of AF. Some DDDR devices now have rate smoothing features designed to eliminate cyclical variation of the heart rate that might predispose to recurrent AF. Likewise, overdrive pacing at higher rates for periods after termination of AF might prevent recurrence if overdrive pacing suppresses SVPBs. Studies are presently underway evaluating such features for prevention of AF.

IDEAL STUDY OUTCOME EVENT IN ATRIAL FIBRILLATION PACING STUDIES

Some investigators have used the time to first recurrence of any episode of AF18 and others have used the time to first recurrence of symptomatic AF as the primary study outcome event.13, 27 The time to first recurrence of AF assumes that AF is a random event. It has been shown that the time course of PAF recurrence is not random and that other mathematical models (e.g., a Weibull distribution or a biexponential distribution) may better describe the temporal patterns of AF.37 This type of

VENTRICULAR PACING MAY BE PROARRHYTHMIC

It is possible that atrial pacing per se does not prevent AF, but rather ventricular pacing alters the electrophysiologic substrate in the atria because of the loss of AV synchrony and resulting retrograde conduction, causing left atrial stretch because of atrial contraction against a closed AV valve or increased valvular regurgitation associated with the asynchronous activation pattern, which predisposes to AF (Fig. 8).29, 39, 43, 50 AF may contribute to contractile dysfunction because of an

CONCLUSIONS

Atrial and dual-chamber pacing prevents the development of AF in some pacemaker patients. There is no evidence the single-site right atrial pacing prevents PAF or chronic AF in patients without symptomatic bradycardia. In conjunction with antiarrhythmic drugs, site-specific or dual-site and biatrial pacing may prevent AF recurrences in selected patients. Promising new pacing therapies for early termination of atrial tachyarrhythmias or overdrive suppression of SVPBs may prove to be beneficial

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      Citation Excerpt :

      Whether these episodes indicate true pace termination will need further investigation. Although we are skeptical that atrial fibrillation can be reliably pace-terminated, arrhythmias that trigger atrial fibriallation (such as atrial flutter or tachycardia) can be readily pace-terminated.90,97 Two small studies98,99 have suggested that DDD pacing with a short atrioventricular delay might benefit patients with dilated cardiomyopathy and a prolonged baseline PR interval.

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    Address reprint requests to Anne M. Gillis, MD, FRCPC, Division of Cardiology, Faculty of Medicine, The University of Calgary, 3330 Hospital Drive NW, Room 1634, HSC, Calgary, Alberta T2N 4N1, CANADA, email:[email protected]

    Supported by the Heart and Stroke Foundation of Alberta and the Medical Research Foundation of Canada (PG 11188). Dr. Gillis is a Senior Scholar of the Alberta Heritage Foundation for Medical Research

    *

    Department of Pacing and Electrophysiology, Division of Cardiology, Foothills Hospital and the Cardiovascular Research Group, The University of Calgary, Calgary, Alberta, Canada

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