(Circulation. 1997;96:1378-1380.)
© 1997 American Heart Association, Inc.
Articles |
Catheter Ablation as an Adjunct to ICD Therapy
From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, Mass.
Correspondence to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail wgstevenso{at}bics.bwh.harvard.edu
Key Words: Editorials • ablation • myocardial infarction • tachyarrhythmias • catheter ablation
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Implantable cardioverter-defibrillators (ICDs) have become a mainstay of therapy for patients with life-threatening ventricular arrhythmias.1 2 3 These devices provide the best "safety net" available to prevent sudden death from sustained ventricular tachycardia (VT) and ventricular fibrillation. ICDs do not prevent attacks of VT. Rather, when tachycardia occurs, sinus rhythm is restored either by antitachycardia pacing or a high-voltage shock. Antitachycardia pacing is painless and well tolerated; often the patient is unaware that it has occurred. It is usually used for slower, hemodynamically tolerated tachycardias. For hemodynamically unstable tachycardias and when antitachycardia pacing is ineffective, high-voltage cardioversion or defibrillation shocks are required. Tolerance of ICD shocks varies. Although some tachycardias can be terminated by low-energy shocks, even these usually cause severe, although brief, discomfort. Some patients are not troubled by an occasional ICD shock; for others who experience severe discomfort from the shock, the anticipation of future shocks, even when episodes of tachycardia are rare, can cause considerable emotional distress. Frequent shocks are poorly tolerated by virtually all patients. Appropriate programming of ICDs and the use of adjunct therapies to reduce ICD shocks to a tolerable level are important aspects of caring for patients who have an ICD.1 4 5 6 Whenever an ICD delivers antitachycardia pacing or shocks, it should be interrogated to determine whether delivery of therapy might have been inappropriate, usually the result of a supraventricular tachycardia, such as atrial fibrillation or atrial flutter.1 2 4 Of 65 consecutive patients who received an ICD and were followed for a median of 19 months by Fahy and coworkers,5 5% required hospitalization for control of atrial fibrillation that had caused inappropriate shocks and 22% required hospitalization for therapy to control ventricular arrhythmias that caused appropriate shocks. When recurrent VT causes frequent ICD shocks, adjustments in antitachycardia pacing algorithms may increase the effectiveness of antitachycardia pacing for restoring sinus rhythm without shocks. However, identifying a pacing algorithm that works all the time has been surprisingly difficult, despite a multitude of programmable options. Many patients with episodes of VT terminated by antitachycardia pacing also receive ICD shocks at least occasionally.1
When antitachycardia pacing is not effective or when frequent episodes of VT are symptomatic despite antitachycardia pacing, antiarrhythmic drug therapy is usually added in an attempt to reduce episodes of VT or to make antitachycardia pacing more effective. In recent reports, 38% to 70% of patients with ICDs receive concomitant antiarrhythmic drugs for control of ventricular or supraventricular arrhythmias.5 7 Drug therapy introduces additional potential problems.5 6 7 Some drugs, notably amiodarone, may increase the energy required for defibrillation (the defibrillation threshold). When drug therapy is instituted, repeat defibrillation efficacy testing is warranted to be certain that the maximal ICD output provides an adequate safety margin for defibrillation. The effect of antiarrhythmic drugs on the efficacy of antitachycardia pacing is unpredictable. Occasionally, antiarrhythmic drugs render antitachycardia pacing less effective rather than more effective. Antiarrhythmic drugs can also increase the frequency of bradyarrhythmias, with consequent greater use of backup bradycardia pacing from the device. Perhaps the most difficult management problem occurs when antiarrhythmic drug therapy fails to prevent attacks of VT but slows the tachycardia to a rate equivalent to sinus tachycardia. In such circumstances, overlap of ventricular rates between sinus tachycardia and slow VT may result in spurious therapies, because current devices rely primarily on ventricular rate for detection of ventricular arrhythmias.
In this issue of Circulation, Strickberger and colleagues8 report the use of ablation therapy for reducing episodes of VT in patients with ICDs. In a series of 21 patients who had been receiving an average of 134 ICD therapies (shocks and antitachycardia pacing) per month, ablation was judged to be successful in 16 patients (76%). In these patients, the average number of ICD therapies per month fell from 59 to 0.6 (P=.01). As expected, quality of life, as assessed by a questionnaire, improved. However, the reliability of the quality of life assessment is diminished by the fact that the questionnaire for both the preablation and postablation periods was administered only after the ablation procedure.
These results are encouraging and consistent with previous studies of catheter ablation in selected patients at experienced centers.6 9 10 11 12 13 Gonska et al9 reported successful ablation in 74% of 72 patients; during a mean follow-up of 24 months, 80% remained free of recurrent VT. Dramatic reductions in the frequency of VT episodes are achieved in some patients. However, the present study also serves to illustrate some of the problems with catheter ablation and difficulties faced in the postinfarct patient population.
Although catheter ablation has become a first-line therapy for many
types of supraventricular tachycardia, progress
in ablation of VT due to previous myocardial infarction has been
slower.10 The reentry circuits that give rise to VT can be
large and complex. Surgical ablation, which was effective in 
90% of
selected cases, achieved this efficacy by removal of large segments of
subendocardium, often >30 cm2 in area.14
Current catheter ablation methods produce substantially smaller
lesions, 5 to 10 mm in diameter. To achieve success with
catheter ablation, the critical region of the infarct that is causing
VT must be identified with a degree of precision greater than is
required for surgical ablation. At present, optimal localization
requires that the VT be induced in the electrophysiology laboratory and
that the patient remain hemodynamically stable during
tachycardia, ideally for several minutes, while a mapping
catheter explores the ventricle in search of the reentry circuit. In
some cases, tachycardia that is poorly tolerated can be
mapped if the tachycardia can be repeatedly initiated and
quickly terminated by pacing before hemodynamic
collapse. When hemodynamic stability cannot be
achieved, identification of target sites for ablation may be attempted
by searching for abnormalities that are present during sinus
rhythm, such as abnormal electrograms, or pacing at suspected
tachycardia sites during sinus rhythm and comparing the
paced QRS morphology with that of the tachycardia (pace
mapping). Methods of mapping during sinus rhythm, which are sufficient
in some cases to guide surgical ablation, are not sufficiently precise
to guide present methods of catheter ablation, because abnormal
sites that could potentially be in the reentry circuit are observed
over relatively large areas. In two patients in the present series,
ablation was not successful when guided by pace mapping during sinus
rhythm. Thus, ablation can be optimally performed only in selected
patients who have hemodynamically tolerated
tachycardias. This is an important and difficult group of
patients to manage, but one that comprises the minority of patients
with VT after myocardial infarction. The average rate of
tachycardias in this study was 140 bpm.
Second, in patients with VT due to prior myocardial infarction, more than one morphology of VT can usually be induced by programmed electrical stimulation.8 10 11 12 13 14 Multiple tachycardias often indicate the presence of multiple reentry circuits that may form in the same general region or in disparate regions of the ventricle. The best approach to ablation when multiple morphologies of VT are present is controversial. Many centers attempt to limit VT ablation to patients with a single VT that has been observed to occur spontaneously.9 This VT is referred to as the "clinical" VT, and any other VTs provoked at electrophysiology study are designated "nonclinical." Ablation then targets only the clinical VT, simplifying the mapping and ablation procedure and reducing the size of the regions ablated. One problem with this approach is the difficulty in determining whether a VT is nonclinical. VTs labeled as nonclinical occasionally occur spontaneously. In the present report, 26 VTs were thought to have occurred spontaneously, 46 were targeted for ablation, and 36 of these were thought to have been successfully ablated because they were no longer inducible at the end of the ablation procedure. During follow-up, however, 5 of the 16 patients who had an ablation that was judged to be successful received either antitachycardia pacing or ICD shocks, although at a substantially reduced frequency compared with that observed before ablation. It appears that at least some of the tachycardias that occurred during follow-up were not the previously identified clinical tachycardias. Gonska and coworkers9 observed a 20% recurrence rate of VT after apparently successful ablation of a clinical tachycardia. Identification of clinical tachycardias that have occurred spontaneously can be a difficult problem in patients with ICDs because VT is terminated by the device before 12-lead ECG recordings can be obtained. Interrogation of the ICD does provide the rate of the tachycardia and the morphology of a local electrogram. From analysis of these features, Sweeney and coworkers15 observed that in the vast majority of patients with ICDs, more than one type of VT occurred spontaneously during long-term follow-up and that new tachycardias emerged progressively over time, even years later. Thus, targeting a single tachycardia when multiple tachycardias are inducible is unlikely to abolish all spontaneous episodes of VT.
In 5 of 21 patients (24%), ablation of the inducible, targeted tachycardia was unsuccessful. The reasons for failure are often difficult to ascertain. The reentry circuits may have been located deep to the subendocardium, inaccessible to present mapping and ablation techniques, or the reentry circuit paths may have been broad and difficult to interrupt with focal ablation lesions. In two patients, mapping during the tachycardia was limited by hemodynamic intolerance.
Interestingly, the frequency of ICD therapies decreased after unsuccessful ablation. Alterations in antiarrhythmic drug therapy may have been responsible, raising the question of whether some of the patients in the successful group could have been managed in a similar way or whether spontaneous variability in frequency of arrhythmia events could account for the apparent success of ablation during follow-up. However, chronic antiarrhythmic drug therapy was not altered after successful ablation, and the extremely high frequency of spontaneous VTs before ablation makes spontaneous variability an unlikely cause of the dramatic reduction that was observed during follow-up. The absence of a control group is a problem in assessing the magnitude of benefit. However, as the authors point out, it would have been difficult to recruit a control group of patients to be followed with no alteration in therapy, given the frequency of symptomatic VT. It should also be noted that this study did not address whether ablation could be used to withdraw antiarrhythmic drug therapy; antiarrhythmic drugs were continued during follow-up to avoid introducing another confounding influence on frequency of VT episodes after ablation. Whether antiarrhythmic drugs could be withdrawn after ablation without increasing VT episodes is an important question that will require further study.
It should be pointed out that catheter ablation of postinfarction VT remains a technically challenging procedure. In contrast to patients with supraventricular tachycardia, the induced arrhythmia is often not well tolerated for long periods. The patients are older and subject to a greater incidence of complications. The procedure-related mortality may be in the 2% range.9 10 13 In the present study, 1 patient developed heart block as a consequence of ablation of a reentry circuit close to the His bundle. Pericardial tamponade, myocardial infarction, stroke, and femoral arterial occlusion are recognized risks that appear to be infrequent; larger series are required to establish their incidence.9 10 16 Importantly, radiofrequency catheter ablation has not been observed to damage the ICD, which is programmed off during the procedure.
The ICD has dramatically reduced sudden cardiac death from rapid VTs. This is creating a novel population of patients who, having survived rapid tachycardias, suffer recurrences of slower tachycardias during antiarrhythmic drug therapy. These tachycardias, although not life-threatening, can be a difficult management problem and have an important impact on quality of life. Catheter ablation shows promise for reducing episodes of VT in patients with recurrent, relatively slow VTs. When ICD reprogramming and antiarrhythmic drug therapy fail to achieve adequate arrhythmic control, radiofrequency catheter ablation should be considered. However, catheter ablation is a technically demanding procedure that will likely have a somewhat greater risk of complications than that observed for ablation of supraventricular tachycardias. It should be attempted as a compassionate or investigational therapy in an experienced center. The ease and efficacy of VT ablation may potentially be enhanced by newer mapping and ablation technologies that are now entering clinical trials. Further investigation is required to determine whether ablation should become the major adjunctive therapy to the ICD safety net.
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Footnotes |
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The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
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References |
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TopIntroductionReferences |
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