doi: 10.1161/CIRCULATIONAHA.106.670075
(Circulation. 2007;116:1196-1203.)
© 2007 American Heart Association, Inc.
Controversies in Cardiovascular Medicine |
Do patients with hemodynamically tolerated ventricular tachycardia require implantable cardioverter-defibrillators?
Patients With Hemodynamically Tolerated Ventricular Tachycardia Require Implantable Cardioverter–Defibrillators
From the Division of Cardiovascular Medicine, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia.
Correspondence to David J. Callans, MD, 9 Founders Pavilion, 3400 Spruce St, Philadelphia, PA 19104. E-mail david.callans{at}uphs.upenn.edu
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Introduction |
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 Top Introduction Tolerated VT Signals a...The Benefit of Secondary...Successful Catheter Ablation...SummaryReferences |
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Conventional wisdom has long held that patients with tolerated ventricular tachycardia (VT) in the setting of chronic coronary heart disease are at low risk of arrhythmic death. This logic held that arrhythmia recurrence, although reasonably likely, could be predicted to be well tolerated. As with all truisms, it is good to reexamine this belief periodically. Disease states change; more information becomes available; and the general context of medical care improves. Expectations and capacity to tolerate risk, which are essentially societal rather than medical considerations, continue to evolve. Situations exist such as the present case in which this process of reexamination rather than the results of well-constructed randomized trials will determine the correct course.
Response by Almendral and Josephson p 1203
Many past studies have looked at this question at least tangentially. Despite this experience, no study directly answers this question in the present day. Our contemporary strategies for treating patients with advanced structural heart disease, including more aggressive revascularization and prevention of remodeling in heart failure, were not available during the time when these studies were performed. These strategies certainly have antiarrhythmic effects but more profoundly influence the natural history of progressive heart failure. There also have been marked changes in strategies for specific antiarrhythmic therapy. For all of these reasons, the data from trials performed in the 1980s and 1990s are reviewed for themes rather than direct answers.
Despite these disclaimers, critical review of the evidence demonstrates that patients with structural heart disease (primarily healed myocardial infarction) who present with tolerated VT require implantable cardioverter-defibrillator (ICD) therapy. The foundations for this conclusion are as follows. First, tolerated VT is not a benign condition but signals a risk of life-threatening ventricular arrhythmias. Second, the benefit of secondary-prevention ICD therapy is difficult to challenge. Finally, successful catheter ablation does not sufficiently reduce residual risk. These considerations in the context of our current societal expectations for medical care make ICD therapy difficult if not impossible to avoid.
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Tolerated VT Signals a Risk of Life-Threatening Arrhythmias |
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TopIntroductionTolerated VT Signals a...The Benefit of Secondary...Successful Catheter Ablation...SummaryReferences |
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The logical bases for many ideas widely accepted in the "oral history" of electrophysiology are often difficult to determine. In my mind, the foundation of the idea that patients with tolerated VT will do well is formed by a series of early studies comparing patients who present with resuscitated cardiac arrest and tolerated VT.1–3 These studies demonstrated that presentation with cardiac arrest was a major risk for sudden and total mortality; however, given the lack of appropriate treatment for this condition at this time, these data are not surprising. The study by Saxon and coworkers3 presents data to support that the sudden and total mortality rates in patients with tolerated VT (presenting with palpitations and/or dizziness) are significantly better than those with cardiac arrest (4-year survival from sudden death and total mortality, 87±6% versus 59±11% and 67±8% versus 45±10%; P<0.05 for both comparisons). These early studies identified other predictors for mortality such as presentation with VT/ventricular fibrillation early after myocardial infarction, severe left ventricular (LV) dysfunction, and symptomatic heart failure. A study by Waller et al4 provides some basis for the idea that patients with tolerated VT have a good prognosis, if only tangentially. In this study, 258 patients with a variety of arrhythmia presentations underwent serial electrophysiologically guided drug testing. Group 1 patients (n=103) were noninducible on the final regimen; group 2 patients (n=51) were inducible, but a drug regimen conferred a beneficial response (VT cycle length increased by >100 ms and no severe symptoms during VT); and group 3 patients (n=52) had no response to antiarrhythmic drugs. Although group 2 patients had a 39% incidence of recurrent sustained VT over 19.9 months, the total and sudden death mortality rates were substantially reduced compared with group 3 (12% and 4% compared with 39% and 34%) and were not different from group 1. However, patients in this study were censored at the time of VT recurrence if changes in antiarrhythmic therapy were made, artificially making them "immune" from mortality end points.
An important pre-ICD study that directly evaluated this question was presented by Sarter et al.5 This study retrospectively analyzed the outcome of 124 patients who presented with hemodynamically tolerated VT and were treated with arrhythmia surgery (46 patients) or antiarrhythmic drugs (78 patients) between 1981 and 1990. The duration of follow-up was 36±30 months. Most patients had multivessel coronary artery disease and depressed LV ejection fraction (mean, 31%); 60% had an LV aneurysm. Total mortality was 29%, including a discouraging 20% operative mortality. Sudden death mortality was 7% at 3 years (2.4% per year), although it was higher in medically treated (9.1%) than surgically treated (5.4%) patients.
Although not necessarily flawed in terms of construction, the information provided by these studies may be less applicable to present-day patients. Background cardiovascular care has improved dramatically, with infarct revascularization and aggressive treatment of LV remodeling. LV aneurysms are unusual. Arrhythmia surgery is seldom used, largely owing to concerns over operative mortality. The number of patients included in these single-center studies was small, and follow-up was limited in duration. Many have questioned the accuracy of cause-of-death assessment in single-center, retrospective trials; this is essentially why major ICD trials have focused on the end point of total mortality. Finally, the widespread applicability of ICD therapy has changed expectations about residual risk considerably.
In this context, the first observation that weakened the status quo was by Bocker et al.6 These investigators reported a 22% incidence of rapid VT (<250-ms cycle length) in 17 months documented by ICD interrogation in a group of 50 patients who received ICDs after presenting with tolerated VT (Figure 1). Furthermore, the results of programmed stimulation were not helpful in predicting patients at risk. Glickson et al7 reported that 12% of 82 patients treated with ICDs for hemodynamically well-tolerated VT developed unstable ventricular arrhythmias over 23.6±21.5 months. No one would contend that ICD shocks are equivalent to arrhythmic death had the ICD not been present (see below); however, these observations imply that patients with stable VT are at risk for poorly tolerated arrhythmia recurrence.
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Several large and more current albeit observational studies appear to advance this same point. Caruso and coworkers8 analyzed the predictors of sudden cardiac death in patients enrolled in the Electrophysiology Study Versus Electrocardiographic Monitoring (ESVEM) over a 6-year follow-up period. This study included 381 patients who presented with sustained VT and 105 cardiac arrest survivors. The mean LV ejection fraction was 32%, and 84% had coronary artery disease. Although univariate analysis suggested a relationship between presentation and outcome, the multivariable analysis did not, implying that LV function has a stronger influence than presentation on outcome. Comparison between the groups aside, 18% of patients who presented with VT suffered arrhythmic death or cardiac arrest in the short-term follow-up; however, it must be acknowledged that the use of potentially harmful, type I antiarrhythmic agents may have contributed to this result. Raitt et al9 compared total mortality in 440 patients with tolerated VT and 1029 patients with unstable VT in the Antiarrhythmics Versus Implantable Defibrillator (AVID) Registry. It is important to realize that this analysis was retrospective and that patients in the registry were not randomized in terms of treatment strategy; in the tolerated VT group, treatment included ICDs with or without antiarrhythmic drugs (32%), antiarrhythmic drugs (52%), and catheter ablation (14%) as determined by physician preference. Significant differences existed between the groups in incidence of heart failure and the use of ICD therapy, but no difference existed in ejection fraction or the number with coronary disease. Total mortality at 3 years was 33.6% in the tolerated VT group, higher than the 27.6% of the unstable VT group (Figure 2). Multivariable analysis identified that treatment with antiarrhythmic drugs was associated with an increased risk and that ICD therapy was protective. In a similar manner, a retrospective multivariable analysis of the entire AVID Registry (3559 patients) demonstrated that prognosis was determined predominantly by the severity of structural heart disease and the presence of heart failure.10 Arrhythmia presentation had no impact on survival, and ICD therapy was protective (hazard ratio, 0.51; P<0.001). The potential confounding influence of selection bias for prescription of ICDs notwithstanding, these studies support the hypothesis that tolerated VT is not a benign condition and that arrhythmic death contributes to total mortality.
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The Benefit of Secondary-Prevention ICD Therapy Is Difficult to Challenge |
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TopIntroductionTolerated VT Signals a...The Benefit of Secondary...Successful Catheter Ablation...SummaryReferences |
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ICD therapy has been demonstrated to result in a reduction in total mortality in patients with hemodynamically unstable arrhythmias in well-designed, randomized clinical trials.11–13 The logic in assuming that this benefit would extend to patients with tolerated VT may be questioned. However, because the total mortality is higher in patients with tolerated VT than unstable VT and because ICD therapy reduces total mortality in patients with unstable VT, this "leap of faith" does not seem farfetched. Whether the magnitude of this ICD benefit is worth the cost—to society, in terms of resource allocation, or to individual patients, in terms of enduring potential adverse consequences of ICD therapy—remains worth examining. To this end, what arguments have been raised against secondary-prevention ICD therapy?
The foundation of secondary-prevention therapy was the AVID study, which demonstrated that ICD therapy reduced total mortality by 26% at 2 years compared with antiarrhythmic drug therapy (primarily amiodarone) in patients with aborted cardiac arrest or VT with severe symptoms.13 Detractors often focus on the small increase in life expectancy afforded by ICD therapy (2.7 months at 3 years) and marginal cost efficacy based on this calculation ($66 677 per life-year saved).14 However, it is important to consider how the limitations of randomized clinical trials in general dilute the benefit of ICD therapy. Although intention to treat is the scientifically correct analysis, 18.4% of the antiarrhythmic drug group crossed over to receive ICDs. In addition, particularly in light of subsequent, longer-term ICD trials, the duration of follow-up was too short to realize the greatest portion of the benefit of ICD therapy.
To this last point, a recent report about longer-term follow-up in the Canadian Implantable Defibrillator Study (CIDS) is illustrative.15 In the main trial, follow-up of 659 patients for a mean of 3 years demonstrated that ICD therapy resulted in a nonsignificant reduction in total mortality (8.3% versus 10.2% per year; P=0.142) compared with amiodarone. However, in a single enrolling center, follow-up was maintained in 120 patients (60 in each treatment assignment) for a mean of 5.6±2.6 years. This experience showed a more dramatic benefit of ICD therapy compared with amiodarone (total mortality, 27% versus 47%; P=0.0213), which appeared to increase over time (Figure 3). The time dependence of the ICD benefit also was demonstrated in an analysis of 8 landmark ICD trials by Salukhi and coworkers.16 This study demonstrated that the marginal effectiveness (in life-years gained) with ICD therapy increased in a nonlinear fashion, at least over the amount of time provided by clinical trial data (maximum, 3 years). Although longer-term time frames are not economically feasible in randomized controlled trials, the time-weighted benefit of ICD therapy also has been observed in primary prevention trials such as the Second Multicenter Automated Defibrillator Implantation Trial (MADIT II) and the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT).17,18
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From a patient standpoint, one of the biggest problems associated with ICD therapy is inappropriate shocks. Traditionally, inappropriate shocks occur in approximately one third of ICD patients18; the chance of these shocks occurring can be reduced with improved diagnostic algorithms and proper attention to programming.19 A new twist on this issue is the concept that appropriate therapy delivery may be "inappropriate" in that the device itself may be somehow proarrhythmic. In a compelling analysis of the major ICD trials, Germano et al20 raise the point that the frequency of appropriate ICD therapy exceeds the control group sudden death rate by a factor of 2 to 3. They propose that several factors may be responsible, including treatment of VT that would have been nonsustained and actual ICD proarrhythmia (caused by right ventricular pacing, lead-induced tricuspid regurgitation, and other factors). It is important to recognize that the majority of "excess" therapy delivered took the form of antitachycardia pacing as opposed to high-energy shocks. Recent research has demonstrated that the delivery of appropriate shocks is a significant risk for subsequent development of heart failure and death.21,22 However, the substantial benefit of ICD therapy demonstrated in most major trials persisted despite the concern over potential device proarrhythmia.
As discussed above, the vast majority of the therapy delivered by ICDs is in the form of antitachycardia pacing. This therapy is highly effective; even in nonselected patients with VT (faster VTs are less amenable to successful antitachycardia pacing), antitachycardia pacing terminates 78% to 94% of episodes,19 typically before patients even develop symptoms. Although this is too self-evident to submit to formal study, antitachycardia pacing is helpful in preventing symptoms and repeat hospitalization in patients who are bound to have recurrent VT.
No one would argue that ICDs have been conclusively demonstrated to be effective in reducing arrhythmic death. Observations available from the trials discussed above suggest that arrhythmic death contributes to the high total mortality in patients with tolerated VT (although the extent of this contribution has not been determined accurately). No compelling medical reason exists to not want to protect patients from this residual risk.
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Successful Catheter Ablation Does Not Sufficiently Reduce Residual Risk |
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TopIntroductionTolerated VT Signals a...The Benefit of Secondary...Successful Catheter Ablation...SummaryReferences |
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Other nonpharmacological therapy strategies for the treatment of patients with tolerated VT have not consistently eliminated the risk of death. Although technically not restricted to patients with tolerated VT, most ablation trials have focused on such patients, at least before the development of substrate-based ablation for unmappable VT. Many of these studies were focused on the evaluation of mapping/ablation strategy or end point (eg, evaluation of whether ablation of all inducible VT morphologies influenced outcome), but some provide insight into prognosis in patients with tolerated VT. Independently of procedural strategy, these studies typically demonstrate a high incidence of recurrent VT, some rapid, and a high total mortality, even in short-term follow-up (Table 1). Two studies that are often presented as supporting the idea that successful ablation procedures and the absence of inducible VT predict a good outcome in fact are not convincing. Rothman et al23 studied 35 patients with hemodynamically well tolerated VT after myocardial infarction. In a "complete success" subgroup of 11 patients, the clinical VT was successfully ablated, and no VT was inducible at the conclusion of the procedure and at a predischarge electrophysiological study; in addition, programmed stimulation was repeated late (4.2 months) after the procedure in 8 of the 11 patients. One patient who had no inducible VT after the procedure and only polymorphic VT at late follow-up died suddenly at 18 months after ablation. Della Bella and coworkers24 evaluated the strategy of catheter ablation often followed by treatment with amiodarone and β-blockers (86%) in 124 patients who presented with hemodynamically tolerated VT. These investigators estimated that this represented 30% of the total VT/ventricular fibrillation population treated at 4 participating referral centers over the time period of interest (1992 to 1997). Over a 41.5-month follow-up period (range, 1 to 86 months), low sudden and total mortality rates were observed (2.4% and 12%, respectively), perhaps reflecting the exclusion of patients with active coronary disease and the small number of patients with severely reduced LV ejection fraction. The authors conclude that catheter ablation (if successful) is appropriate treatment for this group of patients and that ICD therapy is not required. However, 24 patients were treated with ICDs in this study, 11 before study entry and 13 after less than completely successful ablation procedures or VT recurrence.
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Despite increasing use of optimal therapy for heart failure and coronary heart disease, most contemporary studies of catheter ablation for VT are more sobering. In a multicenter evaluation of internally cooled RF ablation,25 124 patients with healed infarction and spontaneous sustained VT were followed up after ablation for 243±153 days. All patients had ICDs with electrogram storage capabilities. Despite successful elimination of all mappable VTs in 75% of patients, recurrent VT was observed in 46%. Furthermore, total mortality at 1 year was 25%, mostly because of progressive heart failure. A recent study by Segal and coworkers26 investigating a noncontact mapping strategy in 40 patients is of interest because they distinguished between arrhythmia recurrence (ie, of targeted VT morphologies) and the development of new arrhythmias. Of the 140 VTs induced, 81 were targeted; "rapid and nonclinical" VT morphologies were not targeted, and patients in whom these arrhythmias were induced received an ICD (n=13; in addition, 13 had a preexisting ICD). Ablation was successful in 33 patients. Programmed stimulation after ablation demonstrated no inducible VT in 24 patients, and only rapid, nonclinical VT was induced in 9 patients. At 36±21 months, recurrence of an ablated VT was observed in 7.5%, a new or nontargeted VT in 37.5%, and ventricular fibrillation in 7.5% of patients. Total mortality was 32.5%, and although the suggestion existed that the presence of an ICD curtailed mortality (hazard ratio, 0.54), it did not reach statistical significance (Figure 4). The frequency of ICD therapy was markedly reduced after ablation in this study.
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Catheter ablation for VT does not appear to be sufficiently protective against VT recurrence or risk of total mortality even in short-term follow-up. In general, programmed stimulation after ablation has not proved helpful in assessment of subsequent arrhythmia risk. Given the complexity of the arrhythmia substrate (Figure 5) and the typically inexorable progression of severe structural heart disease, the outlook over the longer term is certainly even less favorable.
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Summary |
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TopIntroductionTolerated VT Signals a...The Benefit of Secondary...Successful Catheter Ablation...SummaryReferences |
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Patients who present with tolerated VT in the setting of structural heart disease should be treated with ICD therapy independently of the other strategies used to care for them. The points that lead to this conclusion are summarized in Table 2. One of the most compelling concepts that I hope is clear from the discussion above is the influence of the duration of follow-up on our expectations for patient well-being. Over the short term, patients with tolerated VT do well, and ICD therapy appears less necessary; with passing years, disease processes progress, risk escalates, and the benefit of ICD therapy increases. These factors are unlikely to be captured in the framework of randomized controlled studies.
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Patients who present with tolerated VT in the setting of structural heart disease with relatively preserved ejection fractions (
40%) represent a special, although rather unusual, circumstance in which more thought is required. Even fewer data exist to guide this specific decision, although the powerful effect of ejection fraction on arrhythmic and cardiac mortality is well understood. In this setting, it is my opinion and practice that primary catheter ablation without ICD therapy may be the most reasonable approach. As mentioned in the prior paragraph, it is important to consider the possibility of progressive structural heart disease complicating the course of this initial therapy.
Although intellectually interesting, this exercise of comparing one therapy with another is distinctly different from how physicians practice. The question is not which therapy in isolation is best for the patient but rather which of these potentially complementary strategies will provide some possibility of improved outcome, both now and in the future. In my own practice, patients with tolerated VT receive an ICD. If they have symptoms from frequently recurrent VT, most patients benefit from concomitant VT ablation.
Many of us began practicing electrophysiology before its interventional era, when this field was intensely intellectual but less successful at protecting patients from future harm. The unappealing part of this exciting present era is the fact that many problems are approached exactly the same way in all patients (ie, all patients with structural heart disease and ventricular arrhythmias receive ICDs). I look forward to the time when our understanding is sufficient to offer ICD therapy to only those specific patients who will benefit. That time is not now. Our present focus should not be on wishing that things were different but instead on working to improve all applicable strategies that are useful in caring for patients with this complex, dynamic, and high-risk condition.
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Acknowledgments |
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Disclosures
Dr Callans has received honoraria from Boston Scientific, Medtronic, and St Jude Medical and is on an advisory board for St Jude Medical. His program receives fellowship support from Boston Scientific, Medtronic, and St Jude Medical.
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References |
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TopIntroductionTolerated VT Signals a...The Benefit of Secondary...Successful Catheter Ablation...SummaryReferences |
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Response to Callans
Jesús Almendral, MD, PhD; Mark E. Josephson, MDAlthough conventional wisdom might be against the use of implantable cardioverter-defibrillators (ICDs) for well-tolerated ventricular tachycardia (VT), the reverse (ie, implantation of ICDs) is intuitively more likely. The logic would be as follows: If we are implanting ICDs for primary prevention because patients are at risk of malignant ventricular arrhythmias, how could we not implant in patients who have already had a sustained VT (ie, the paradigm of a malignant arrhythmia)? Such a dilemma needs the discourse of scientific information that demonstrates that tolerated VT, adequately treated, is truly a malignant arrhythmia. Despite Dr Callans’ convincing discussion of secondary-prevention ICD trials, these trials do not help scientifically simply because patients with tolerated VT were explicitly excluded from them. The most important information derives from observational studies on catheter ablation, including almost 800 patients altogether. It is claimed that ablation does not "appear sufficiently protective" on the basis of a high rate of recurrent VT and total mortality. However, recurrent tolerated VT is overestimated by the ICD and is not a catastrophic event; it allows further therapy. Total mortality is high, but sudden death is low (2.5% after procedures considered successful). One of the series quoted as having high mortality (that of Calkins et al) is the series with the highest ICD implantation rate (79% had ICDs), suggesting that most deaths were nonarrhythmic and/or that the ICD contributed to the outcome. Thus, catheter ablation series are consistent with observational series from the 1980s and perhaps with the Antiarrhythmics Versus Implantable Defibrillator Registry, pointing toward a high total mortality but a low sudden death risk if the VT substrate can be substantially modified with catheter ablation or surgery. Why should we add the risks and complications of ICDs to all of these patients?
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Footnotes |
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The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
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