Atrial rhythm after atrioventricular junctional ablation

Atrial

Rhythm After Atrioventricular Junctional Ablation

Mark A. Mitchell,

MD, Stephen J. Ackerman,

MD, Sunil Nath, MD, PhD

MD, David

E. Haines,

MD,

and John P. DiMarco, Atrioventricular (AV) junctional ablation followed by pacemaker implantation is an established treatment for patients with refractory paroxysmal atrial arrhythmias. The stability of the underlying atrial rhythm after AV junctional ablation is unknown. This study evaluates the atrial rhythm after AV junctional ablation in 49 patients with medically refractory atrial arrhythmias. The group included 25 men and 24 women, of whom 36 had known structural heart disease. Paroxysmal atrial fibrillation was the primary rhythm disturbance in 41 patients, whereas 8 manifested either atrial tachycardias or atrial flutter. All patients had failed therapy with 2 1 antiarrhythmic drug. Chronic pacing modes were DDIR or DDDR, with mode switching in 15 patients and WIR in 34 patients. After AV junctional ablation, chronic antiarrhythmic drug therapy was prescribed in only 4 patients (8%). Routine electrocardiograms (ECGs; 6.5 ?

6.1 /patient)

during long-term follow-up (18.6 k 15.6 months) showed that 7 patients (14%) had an atrial arrhythmia detected on all ECGs, 30 patients (61%) had sinus or atrial-paced rhythms on all recordings, and 12 patients (25%) had both atrial arrhythmias and sinus rhythm documented. Sinus or an atrial-paced rhythm was present on the last available ECG in 33 of 49 patients (67%). Pacing mode was not a predictor of continued sinus rhythm. In conclusion, most patients with a history of paroxysmal atrial tachyarrhythmias will not convert to chronic atrial arrhythmias after AV junctional ablation, even in the absence of antiarrhythmic drug therapy. Use of dual-chamber pacing modes will allow maintenance of at least intermittent atrial function in 0 I996 by Excerpta Medico, Inc. these patients. (Am J Cardiol 1996;78:1251-1254)

aroxysmal episodes of atria1 fibrillation and other tachyarrhythmias are common and often P defy pharmacologic approaches. Radiofrequency

fractory paroxysmal atria1 tachyarrhythmias at the University of Virginia Hospital between May 1989 and June 1994 were identified and evaluated by retablation of the atrioventricular (AV) junction fol- rospective chart review. The ablation technique conlowed by permanent pacemaker implantation has sisted of either high-voltage direct current (DC) shock become a valuable treatment strategy in these pa- (n = 3) or radiofrequency energy (n = 46).‘-7%9 tients.lm7 Initially, all patients who underwent this Early in the study period, all patients received sinprocedure received single-chamber ventricular gle-chamber VVIR pacemakers. Later in the study, pacemakers because atria1 tracking during parox- both single- and dual-chamber devices were imysmal episodes of tachycardia could not be pre- planted, with device selection made by the attendvented with the devices then available. More re- ing cardiologist based on the patient’s clinical hiscently, the DDIR pacing mode or pacemakers that tory. Follow-up information was obtained by automatically convert from DDDR to VVIR in re- reviewing the pacemaker clinic records and elecsponse to tachycardia have been introduced.* trocardiograms (ECGs) and the medical records These pacemaker modes would have limited value obtained from other physicians and hospitals. Each if most patients who underwent AV junctional ab- ECG thus obtained was analyzed, and atria1 lation for paroxysmal atria1 arrhythmias subse- rhythms were classified as either sinus rhythm, quently developed chronic atria1 fibrillation. Be- atrial-paced rhythm, or atria1 tachyarrhythmia. cause the progression of atria1 arrhythmias has not ECGs were grouped according to the postablation been studied in this population, we performed an time interval as follows: baseline, 1 to 3 months, observational study of the atria1 rhythm after AV 7 to 12 months, and 13 to 24 months. Patients with junctional ablation in patients with medically re- multiple ECGs during an interval were classified fractory paroxysmal atria1 tachyarrhythmias. as having an atria1 tachyarrhythmia if any tracing documented the arrhythmia during the respective METHODS interval. Patient population and follow-up: Forty-nine conStatistical analysis: Baseline data were compiled on secutive patients who underwent AV junctional ab- all patients. Patients were then classified according lation and permanent pacemaker implantation for re- to baseline rhythm, symptom duration, antiarrhythmic drug use, mode of pacing, age, left atria1 enlargement, and gender. Statistical comparisons of From the Cardiovascular Division, Department of Internal Medicine, Unwersity of Virginia Health Sciences Center, Charlottesville, Virginia follow-up data between subsets of patients were perManuscript received March 2 1, 1996: revised manuscrrat received formed using Fisher’s exact test or Student’s t test. and accepted June 12, 1996. Statistical significance was assumed when the null Address for reprints: John P. DiMarco, MD, PhD, Cardiovascular hypothesis could be rejected at a 95% confidence Division, Department of Internal Medicrne, Box 158, University of Virgrnia Health Sciences Center, Charlottesville, Virginia 22908. level (p <0.05). 01996 by Excerpta Medico, All rights reserved.

Inc.

0002.9149/96/s 15.00 PII SOOO2.9149(96)00605-4

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to the VVIR mode. The dual-chamber pacers were programmed to the DDDR or DDIR &ode. Mode 70 2 9 switching was present in the 8 patients whose paceAge(yd 25/24 Men/women makers were in DDDR mode. None of these pace45 + 22 Symptom duration (mo) makers was capable of storing a mode switch history. Diagnosis Electrocardiographic follow-up: Baseline ECGs at 14 (29%) Coronary artery disease 12 (24%) the time of the AV junctional ablation revealed a Systemic hypertension 7 (14%) Obstructive lung disease sinus rhythm or an atrial-paced rhythm in 73% of 4 (8%) Valvular disease patients. The percentage of patients whose ECGs re2 (4%) idiopathic dilated cardiomyopathy vealed a sinus or atrial-paced rhythm at 1 to 3, 4 to 1 (2%) Sarcoidosis 6, 7 to 12, and 13 to 24 months is displayed in Fig9 (18%) No structural heart disease 17/39 (44%) Left atrial enlargement ure 1. Paroxysmal clinical rhythm Routine ECGs (n = 325; 6.5 + 6.1 ECGs/patient) 41 (84%) Atria1 fibrillation obtained during long-term follow-up (18.6 ? 15.6 6 (12%) Atrial flutter months) revealed that 30 patients (61%; 5.1 +_ 3.0 1 (2%) Atrial tachycardia 1 (2%) ECGs/patient) had a sinus or paced atria1 rhythm deMultifocal atrial tachycardia tected on all recordings (Figure 2). Twelve (25%; 10.4 + 9.5 ECGs/patient) had both sinus rhythm (or atrial-paced rhythm) and atria1 tachyarrhythmias documented. Only 7 (14%; 6.6 2 7.8 ECGs/patient) had an atria1 100 tachyarrhythmia detected on all tracings. Sinus or an a&l-paced N=49 N-40 N=35 rhythm was present on the last N-49 H 75 available ECG in 33 of 49 patients (67%). In the group of patients who had both sinus/ x atrial-paced rhythms and atria1 2 50 tachyarrhythmias during followup, 79 of 125 total tracings (63%) showed sinus/atrial-paced 6 rhythms. Of the 12 patients in ap 25 this group, 2 (17%) had only 1 atria1 tachyarrhythmia tracing during follow-up and 8 (67%) 0 had an atria1 tachyarrhythmia on 7-12 13-24 l-3 4-6 the last available tracing. 0 Follow-up atria1 rhythms MONTHS AFTER ABLATION were also tabulated according to chronic pacing mode and are disFIGURE 1. Prevalence of only sinus rhythm (SR) or atrial-paced rhythm (AP) during follow-u , Each bar represents the rcentage of Patients with electrocardiographic recordplayed in Figure 3. There were ings Buring the interval who ha F smus or atrial-paced rhythm on all electrocardiograms no statistically significant differ(ECG) from that interval. ences in rhythm prevalence between these groups during any interval, but the number of tracings at the later inRESULTS Baseline characteristics: The clinical characteristics tervals in patients with dual-chamber pacemakers of the patients are listed in Table I. The study pop- was small. ulation consisted of 49 patients aged 46 to 82 There was no correlation between gender, diagyears. Symptoms had been present for 45 ? 22 nosis, arrhythmia duration, left atria1 enlargement, or months, with 31 patients having symptoms for >2 age with the presence of sinus rhythm during followyears. Echocardiography had been performed in 39 up. Only baseline rhythm at the time of ablation was patients within the 3 months preceding the abla- significantly related to the follow-up rhythm. Among tion; left atria1 enlargement (left atria1 dimension 36 patients who had sinus rhythm at baseline, 69% ~4.5 cm in the parasternal long-axis view) was had sinus rhythm or a paced atria1 rhythm on every present in 17 of 39 patients (44%). Paroxysmal follow-up recording, whereas the remaining 31% atria1 fibrillation was the predominant clinical ar- demonstrated both atria1 tachyarrhythmias and sinus rhythmia in 41 patients. Only 4 patients took an- or paced atria1 rhythms on at least 1 follow-up retiarrhythmic drugs during follow-up. cording. No patient in this group had an atria1 tachySingle-chamber ventricular pacemakers were arrhythmia on all follow-up electrocardiographic reimplanted in 34 patients, and dual-chamber pace- cordings. Among the 13 patients who had an atria1 makers were used in 15 patients. All the single- tachyarrhythmia at baseline, 6 (46%) had an atria1 chamber ventricular pacemakers were programmed tachyarrhythmia on every follow-up recording, 2 TABLE I Clinical

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at every follow-up visit. These observations suggest that although most patients were not receiving antiarrhythmic drugs, the paroxysmal nature of the atria1 arrhythmias continued after AV junctional ablation and pacemaker implantation.

ALL ATRIAL ARRHYTHMIA

ALL SINUS OR A-PACED

Comparison

with

previous

re-

ports: In 1930, Parkinson and Campbell” described a group of 200 patients with paroxysmal atria1 fibrillation in which 24% had hypertension, 22.5% had BOTH 1 myocardial disease (including I ’ coronary artery disease), 22% FIGURE 2. Distribution of rhythms documented by electrocardiogram during follow-up. Ahad rheumatic valvular disease, paced = atrial-paced rhythm. 14% had hyperthyroidism, and 15% had no structural heart dis(15%) had both sinus rhythm and atria1 fibrillation, ease. The mean age of the population was 50 years. and the remaining 5 (38%) had only sinus or atrial- During follow-up, 25% progressed to stable, chronic paced rhythms. This distribution was significantly atria1 fibrillation. A more recent description of the different from that seen in the patients with sinus natural history of paroxysmal atria1 fibrillation and rhythm at baseline (p 12 months, the underlying cardiopulmonary disDISCUSSION ease prevalence was 40.5% hypertension, 38% corParoxysmal atria1 fibrillation and other atria1 tachyarrhythmias are often refractory to pharmaco- onary heart disease, 3.2% rheumatic valvular dislogic therapy.rO,” Although ventricular rates are of- ease, and 2.1% hyperthyroidism; 25% had no ten rapid and difficult to control during paroxysms, structural heart disease. The mean age of the popumost patients spend most of the time in sinus rhythm. lation was 60 years. During 1 year of follow-up, 25% Our data document the course of atria1 rhythm progressed to continuous atria1 fibrillation. Although changes in patients with a history of highly symp- the patients in the present report differ with regard tomatic paroxysmal atria1 tachyarrhythmias who un- to age and underlying disease prevalence, we obderwent AV junctional ablation and permanent pace- served a similar low rate of progression (14%) to maker implantation. Only 14% of the population had continuous atria1 fibrillation. Role of atrial fxtcing: Whether a specific type of atria1 arrhythmia at every follow-up interval, sugpacemaker (single-chamber ventricular vs dualgesting that even in the absence of ant&rhythmic therapy, conversion to permanent atria1 fibrillation is chamber) offers an advantage in the setting of paruncommon. More than 60% had stable atria1 rhythms oxysmal atria1 tachyarrhythmias is a matter of 100

c

m

FIGURE 3. Influence of pacing mode on the percentage of sinus rhythm (SR) or atrial-paced rhythm (AP) during follow-up. Patients are grouped according to pacing modality, which was not randomly selected. ECG = electrocardiogram.

VVI-R DDD/I-R

0

l-3

MONTHS ARRHYTHMIAS AND CONDUCTION

4-6

AFTER

7-12

13-24

ABLATION

DISTURBANCES/ATRIA1 RHYTHM AFTER ABLATION

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debate.13-27The present study demonstrated no significant difference between VVI-paced and DDD/ DDI-paced patients with regard to the percentage of patients who had atria1 arrhythmias during followup. This difference may be explained in part by the relatively small population in the present study, but consideration must also be given to the possibility that AV junctional ablation, which disrupts both AV and ventriculoatrial conduction, may eliminate the negative effects of ventriculoatrial conduction on the development of atria1 fibrillation. Our data, however, do demonstrate that AV synchrony frequently can be maintained long term in patients after AV junctional ablation for paroxysmal atria1 fibrillation and other atria1 tachyarrhythmias. Furthermore, among patients who had an atria1 tachyarrhythmia at the time of pacemaker implantation, only 46% had this rhythm on all follow-up tracings. This observation implies that implantation of a dual-chamber pacemaker would allow maintenance of at least intermittent atria1 function even in this subgroup. Study limitations: This report has several limitations, which may influence the accuracy of the estimates provided. Patients were not randomized either to AV junctional ablation versus pharmacologic therapy or to single- versus dual-chamber pacing. The end points (rhythm on a routine ECG) used in this study occurred at discrete points in time, and the recordings represent only a small fraction of the total follow-up interval; therefore, they may not accurately reflect the proportion of time that patients spent in each rhythm. In addition, more electocardiographic tracings were available in those patients with the most frequent medical contact, implying that ECGs were more likely to be obtained during periods of illness. Newer pacemaker models may have memory for time spent in mode switch, which will provide a measurement of the total time spent in atria1 fibrillation. Finally, 4 patients took antiarrhythmic drugs during follow-up, which may have altered the prevalence of atria1 arrhythmias. Despite these limitations, we believe that our observations provide a qualitatively accurate picture of the progression of atria1 rhythm in patients with refractory tachyarrhythmias. Conclusions: Most patients with paroxysmal atria1 tachyarrhythmias will not convert to chronic atria1 arrhythmias after AV junctional ablation, even in the absence of antiarrhythmic drug use. Dual-chamber pacing (either DDIR or DDDR with mode switching) should be encouraged for maintenance of at least intermittent AV synchrony.

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