Wearable Cardioverter-Defibrillator Therapy for the Prevention of Sudden Cardiac Death: A Science Advisory From the American Heart Association.

Abstract

HomeCirculationVol. 133, No. 17Wearable Cardioverter-Defibrillator Therapy for the Prevention of Sudden Cardiac Death Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBWearable Cardioverter-Defibrillator Therapy for the Prevention of Sudden Cardiac DeathA Science Advisory From the American Heart Association Jonathan P. PicciniSr, MD, MHS, FAHA, Chair, Larry A. Allen, MD, MHS, FAHA, Peter J. Kudenchuk, MD, FAHA, Richard L. Page, MD, FAHA, Manesh R. Patel, MD, FAHA and Mintu P. Turakhia, MD, MAS, FAHAon behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology and Council on Cardiovascular and Stroke Nursing Jonathan P. PicciniSrJonathan P. PicciniSr Search for more papers by this author , Larry A. AllenLarry A. Allen Search for more papers by this author , Peter J. KudenchukPeter J. Kudenchuk Search for more papers by this author , Richard L. PageRichard L. Page Search for more papers by this author , Manesh R. PatelManesh R. Patel Search for more papers by this author and Mintu P. TurakhiaMintu P. Turakhia Search for more papers by this author and on behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology and Council on Cardiovascular and Stroke Nursing Originally published28 Mar 2016https://doi.org/10.1161/CIR.0000000000000394Circulation. 2016;133:1715–1727Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2016: Previous Version 1 Sudden cardiac death (SCD) accounts for >300 000 deaths in the United States annually.1 Although the majority of these deaths occur in low-risk populations2 in which aggressive interventions are not practical, some higher-risk populations have been established in whom intervention with an implantable cardioverter-defibrillator (ICD) has been shown in randomized trials to reduce mortality.3–7 Additionally, there is a population of patients who may benefit from automatic emergency cardioversion-defibrillation but are not deemed appropriate candidates for ICD implantation at the time of presentation. This group is defined by 2 populations. The first subgroup comprises those who are at perceived risk but for whom there may be optimism for clinical improvement (eg, patients soon after revascularization or those with a recent diagnosis of myocardial infarction [MI] or cardiomyopathy). Alternatively stated, the optimal management of these patients at risk (or perceived risk) during the waiting period before an ICD is indicated remains unknown. The second subgroup includes those who have a clear indication for ICD but also have a contraindication to immediate ICD placement (eg, active infection or unknown prognosis).The wearable cardioverter-defibrillator (WCD) is a device designed for patients at risk of SCD who are not immediate candidates for ICD therapy. By providing automatic therapy, the WCD does not depend on a second person to defibrillate, as required with a manual or automated external defibrillator (AED). Unlike the ICD (including both transvenous and subcutaneous devices), the WCD requires no surgical operation, can be provided for a short period of time, is temporary, and is easily removed. These characteristics of the WCD, along with safety and efficacy data presented to the US Food and Drug Administration (FDA), resulted in approval in the United States in 2002.8Because of the increasing use of the WCD and uncertainty of indications among practicing cardiovascular health professionals, this science advisory was prepared by the American Heart Association. In this advisory, we describe the WCD in the context of its unique technology, clinical niche, and alternative therapies. We review the available literature to support the efficacy and safety of WCDs and explore the possible indications for use of this technology. Finally, on the basis of our analysis and pending definitive trials, we provide relative guidance for use of the WCD in clinical practice according to the American Heart Association methods of classifying the consensus on their certainty and level (quality) of evidence available (Table 1). Table 2 provides a summary of the key concepts presented in this science advisory.Table 1. Applying Classification of Recommendations and Level of EvidenceTable 1. Applying Classification of Recommendations and Level of EvidenceTable 2. Key ConceptsSCD remains an important and preventable cause of death.Despite their obvious benefits, current defibrillator technologies have limitations and risks.Transient contraindications to implanted device therapy commonly arise in clinical practice.WCDs can serve as a temporary means of preventing arrhythmic death without the need for bystander response to cardiac arrest.WCDs use vector analysis of surface electrocardiographic signals to detect life-threatening ventricular arrhythmias.Patient compliance is an integral part of successful WCD therapy.Observational data suggest that the WCD can successfully identify and terminate ventricular arrhythmias.WCD use is reasonable when there is a clear indication for an ICD in the presence of a transient contraindication to an ICD.WCD use may be appropriate in clinical circumstances associated with transient increased arrhythmic risk.Risk counseling and discussion of patient preferences are integral parts of patient care and WCD therapy.ICD indicates implantable cardioverter-defibrillator; SCD, sudden cardiac death; and WCD, wearable cardioverter-defibrillator.Because there is a paucity of prospective data supporting the use of the WCD, particularly the absence of any published, randomized, clinical trials, the recommendations provided in this advisory are not intended to be prescriptive or to suggest an evidence-based approach to the management of patients with FDA-approved indications for use. Instead, these recommendations are offered to provide clinicians direction when discussing this therapy with patients. It is our opinion that the final decision on the use of the WCD should be based on shared decision making, which would include a frank risk-benefit discussion between the clinician and the patient that acknowledges the uncertainty surrounding the efficacy and safety of the WCD.Epidemiology and Prevention of SCDOne in 3 out-of-hospital cardiac arrests is attributable to ventricular tachycardia (VT) or ventricular fibrillation (VF).1 Despite the efficacy of rapid defibrillation, most patients with VT/VF arrest do not receive timely defibrillation. Although outcomes vary widely between communities in North America, on average, survival from VT/VF arrest averages <1 in 5.9 Thus, in recent years, efforts have become increasingly proactive and focused on protecting high-risk patient subgroups from arrhythmic death. The most obvious candidates are those with a history of cardiac arrest or sustained ventricular tachyarrhythmias, in whom ICDs are effective.6 ICDs are also beneficial for the primary prevention of SCD in patients with certain forms of structural heart disease associated with risk of malignant arrhythmias (such as hypertrophic cardiomyopathy) or primary electric disease (such as long-QT syndrome) and in those with significantly impaired left ventricular systolic function.10 The last group includes patients with ischemic or nonischemic heart disease and a persistently depressed left ventricular ejection fraction (LVEF) ≤0.35 combined with New York Heart Association (NYHA) functional class II to III heart failure despite long-term guideline-directed medical therapy or a prior MI and an ejection fraction ≤0.30 in the absence of severe (NYHA functional class IV) heart failure and who are >40 days from their MI.3–5 These FDA-approved indications are based on and supported by pivotal trials that confirmed a survival benefit from an ICD in these populations.3,4 Meta-analyses of the major trials suggest a net relative risk reduction of between 20% and 30%.11,12 Although these indications for ICD placement are widely accepted, the optimal management of patients who are perceived to be at high risk during the waiting period (before definitive ICD implantation is known to be beneficial) remains controversial.13,14 This waiting period is considered to be 90 days after diagnosis, while guideline-directed medical therapy is implemented and optimized.At the forefront of the debate are the merits of sudden death prevention in high-risk patients who are in the early phase of recovery from an acute MI (AMI) or with a newly diagnosed nonischemic cardiomyopathy. The rationale for postponing ICD placement under these circumstances is that a substantial portion of patients will experience significant myocardial recovery and improved ventricular function. Additionally, many patients experience improvement after the institution of optimal medical therapies or interventional therapies such that the need for ICD prophylaxis is obviated. For example, partial or complete recovery of LVEF has been observed in more than half of patients at 3 months after AMI after institution of heart failure therapies or revascularization.15–20 Guideline-directed medical therapy with β-blockade and renin-angiotensin-aldosterone system antagonism during the early period after diagnosis of nonischemic cardiomyopathy may result in improved ventricular function and decreased future risk of SCD; 50% of patients with newly diagnosed nonischemic cardiomyopathy will demonstrate a 10% improvement in LVEF with the initiation of medical therapy.21,22Although the rationale and reasons for postponing ICD implantation are sensible, the current evidence base is incomplete. For example, the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) excluded patients with a diagnosis of cardiomyopathy of <3 months and those who had not received guideline-directed medical therapy. No available randomized trials have compared early ICD implantation (ie, within 3 months) with standard medical therapy in nonischemic cardiomyopathy. Furthermore, although clinical trials of ICD implantation early after MI have shown no benefit, these trials recruited highly selected patients who often had additional risk factors for increased all-cause mortality. For example, the Immediate Risk Stratification Improves Survival (IRIS) trial mandated an LVEF ≤40% and a resting heart rate >90 bpm or nonsustained VT >150 bpm on Holter monitoring. IRIS screened 62 944 unselected post-MI patients to enroll 898 (1.4% of the total screened). Thus, the generalizability of these trial findings is in question.An often-expressed concern about the current ICD criteria is the risk of fatal sustained VT/VF during the waiting period. In the Valsartan in Acute Myocardial Infarction Trial (VALIANT) trial, among patients with an ejection fraction of ≤0.30 after MI who were followed up for a median of 24.7 months, 21% of the sudden death or resuscitated cardiac arrest events occurred within the first 30 days after AMI.23 Although autopsy findings demonstrated that many of the sudden deaths were not arrhythmic in nature, a substantial portion (51%) were arrhythmic.24 Notably, the majority of the patients in VALIANT who died suddenly or were resuscitated within a month of AMI had also been judged to be in stable clinical condition on hospital discharge.In the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) Trial,25 a subgroup analysis of those with a recent diagnosis of cardiomyopathy, mortality was 48% lower in ICD recipients randomized within 9 months of initial diagnosis (9.2% versus 17.7%; P=0.058).26 Taken together, these findings suggest that benefit from a primary prevention ICD is not time dependent either in nonischemic cardiomyopathy or after AMI and that a comparable risk for life-threatening arrhythmias may exist for these patients at virtually all windows of time after their index event or diagnosis. Admittedly, most trials of primary prevention ICD therapy compared with guideline-directed medical therapy demonstrate that the survival benefits do not really emerge until ≈1 year after implantation, rendering it more difficult to identify an effect from treatment that is confined to an earlier and shorter time interval.3,4Although early ICD implantation appears to decrease SCD, the overall survival benefit from ICD placement early after MI or a new diagnosis of cardiomyopathy has not been substantiated. For example, the suggestion in DEFINITE of improved survival among ICD recipients with newly diagnosed cardiomyopathy was retrospective and statistically inconclusive. In the Cardiomyopathy Trial (CAT), patients with recently diagnosed dilated cardiomyopathy (LVEF <0.30) derived no measureable benefit from the ICD.27 The Defibrillator and Acute Myocardial Infarction (DINAMIT) and IRIS trials prospectively randomized patients with significantly impaired ventricular function (ejection fractions of <0.35 and <0.40, respectively), along with other risk factors, to receive an ICD shortly (mean, 18 and 13 days, respectively) after AMI.28,29 In both trials, the lower rates of sudden death in the ICD arms were paralleled by concomitant increases in nonarrhythmic mortality such that total mortality was ultimately no different in the ICD-treated and medically treated groups. Taken together, these findings do not support a survival benefit from early implanted/permanent defibrillator placement for primary prevention in otherwise high-risk patients.Defibrillator Technologies and LimitationsTime to defibrillation is crucial in the resuscitation of VT/VF arrest.30 The probability of survival during VT/VF arrest decreases by 7% to 10% for every minute that defibrillation is delayed without cardiopulmonary resuscitation and 3%/min to 4%/min with cardiopulmonary resuscitation. The development of the AED has been important to improving survival in cases of witnessed VT/VF arrest.31 An easily accessible AED obviates the need to wait for activation of the emergency medical response system and the arrival of advanced life support personnel (paramedics) with a manual defibrillator. The availability of an AED allows earlier defibrillation by first responder personnel or by laypeople if an AED is strategically located near the scene of the arrest (what has become known as public-access defibrillation).32 External defibrillators are highly efficacious in treating cardiac arrest resulting from ventricular tachyarrhythmias.33 However, their overall effectiveness in improving survival after cardiac arrest depends on the time required for their deployment on scene by emergency care providers or the availability of an AED and the presence of a bystander who is willing and able to administer the treatment when needed. A randomized, clinical trial of AED use in the home after AMI failed to identify a survival benefit.34In the relatively small but important minority of patients in whom an increased risk of cardiac arrest is predictable on the basis of clinical risk factors, implantation of a prophylactic defibrillator offers distinct advantages. An ICD, which continuously monitors a patient’s rhythm, affords the benefit of minimal delay between the onset of a potentially fatal tachyarrhythmia and its automatically instituted treatment. To their disadvantage, ICDs require surgical placement, including vascular access, and long-term retention of hardware. Adverse event rates associated with implantation range from 1.3% to 11.0%, including bleeding, lead dislodgement, pneumothorax, cardiac perforation, acute infection, and death (0.4%–1.2%).35 ICDs also have potential for long-term morbidity resulting from component failure, lead dysfunction, inappropriate shocks, vascular occlusion, and infection. Lead longevity is ≈85% at 5 to 10 years after implantation, and removal often necessitates formal extraction with its attendant risks.36–38 The subcutaneous ICD recently approved by the FDA allays some but not all of these potential concerns.39 Although functionally analogous to a traditional ICD, the subcutaneous defibrillator system lacks intracardiac leads and thus avoids the need for vascular access and the potential long-term complications from indwelling intravascular hardware. Still, the subcutaneous ICD shares many of the same hazards as transvenous ICDs, including lead dislodgement (2.5%), skin erosion (1.7%), and infection (5.9%), along with a 13% incidence of inappropriate shocks during follow-up.40 Although subcutaneous ICDs have been shown to effectively terminate electrically induced VF, the effectiveness of the subcutaneous ICD compared with the transvenous ICD in improving survival from spontaneous VF has yet to be established.41External defibrillators and ICDs offer potential lifesaving therapy for malignant tachyarrhythmias. Determining whether and when to deploy such therapies in high-risk patients requires striking a critical balance among available clinical evidence, patient preference, and physician discretion.Technical Considerations of the WCDSensing and DefibrillationThe WCD has several unique sensing and energy delivery mechanisms that distinguish it from other forms of defibrillation. The WCD device consists of 2 primary components, a wearable garment and a battery-powered monitor-defibrillator. The garment is sized to the patient’s chest circumference and weight and is worn under clothes against the skin. The garment contains both sensing and defibrillation electrodes. A 4-electrode, 2-lead system, located in the belt of the garment, is used to record surface ECGs for morphology analysis and detection of arrhythmia. The monitor is usually worn on a belt or shoulder strap. WCD devices use analog and digital filters, as well as several algorithms to recognize electromagnetic interference and other sources of noise. The detection algorithms used by the WCD exhibit a sensitivity of 90% to 100% and a specificity of 98% to 99%.42,43 Inappropriate shock rates in early studies were ≈1% to 2%.43,44 WCD devices are programmable, with detection rates for both VT and VF zones.When a WCD detects a potential arrhythmia, a detection and treatment algorithm is initiated. The process incorporates patient interaction. Once an arrhythmia has met the morphology and rate criteria, formal detection occurs, and the device initiates patient responsiveness testing. This testing incorporates vibratory, audible, and visual alerts. If the patient presses a response button, the episode is aborted. If no patient response is recorded, the defibrillation electrodes discharge gel onto the skin and ultimately deliver a shock via an apex-posterior vector. Depending on the type of arrhythmia (VT or VF) and the device programming, the overall response time (detection to shock) can take between 25 and 60 seconds.45 WCD shock energies range between 75 and 150 J biphasic, and shock efficacy rates between 69% and 99% have been reported.42,46–48 WCD devices are capable of delivering up to 5 shocks; however, once the device has treated an episode of arrhythmia, the garment and electrodes must be replaced. Although the vast majority of observational data are from adults, small series have reported WCD use in pediatric populations, including patients 9 to 17 years of age.49,50 A key challenge in pediatric use is appropriate fitting given the smaller torso of children and adolescents.Use of the WCD is approved by the FDA in selected patients at risk for sudden cardiac arrest. However, there are several important relative contraindications. Patients with unipolar pacing (atrial or ventricular) cannot use a WCD because the large-amplitude pacing stimuli can interfere with arrhythmia detection.51 Additionally, patients who cannot detect or respond to patient responsiveness testing stimuli are not appropriate candidates for the WCD.Beyond the contraindications to WCD therapy, there are also several important limitations. Again, it is important to note that there are no pacing capabilities with the WCD. Patient comfort remains a challenge with WCD therapy, particularly over longer periods of time. Additional patient characteristics make the WCD less than ideal, including extreme body habitus (eg, obesity) and open or healing chest wounds. Given the use of external shocks, patients may also experience adverse events, including but not limited to diminished quality of life secondary to pain and even cutaneous burns. Finally, at the time of this writing, there are no completed randomized trials of WCD therapy. Thus, no definitive data are available on comparative efficacy versus alternative (or no) treatment.Patient AdherenceCompliance is an important component of effective WCD therapy. Patients are instructed to wear their device at all times except when showering or bathing. Discontinuation rates as high as 22% have been reported, resulting primarily from patient comfort and lifestyle concerns.46 In the largest observational series to date, daily use was >90% in more than half of the cohort, and the device discontinuation rate was 14%.48 Some concerns have been expressed about compliance rates in pediatric populations. However, data are limited. A cohort of 4 children with anthracycline-induced cardiomyopathy found limited compliance in half of the patients.50 A second, larger study found that there was no difference in compliance between young adults (age, 19–21 years; n=103) and those ≤18 years of age (n=81); both groups had an average compliance of 19 h/d (80% compliance).49Clinical Experience With WCDsA summary of the available clinical studies of WCD therapy is shown in Table 3. After demonstration of shock efficacy in controlled settings,42 the first systematic, clinical evaluation of the WCD occurred in the companion Wearable Defibrillator Investigative Trial (WEARIT) and Bridge to ICD in Patients at Risk of Arrhythmic Death (BIROAD) study.46 The WEARIT study enrolled patients with symptomatic heart failure (NYHA class III–IV) and LVEF <0.30 who were considered high risk but did not meet eligibility requirements for an ICD. Similarly, the BIROAD study enrolled patients who were perceived to be at high risk for sudden death and within 4 months of an MI or surgical revascularization. Specific reasons for consideration of the WCD in the BIROAD cohort included but were not limited to ventricular arrhythmias within 48 hours of coronary artery bypass grafting (CABG), LVEF <0.30 after CABG, syncope after CABG, and patient refusal of an ICD. In these 2 prospective studies, which enrolled 289 patients, 6 of 8 WCD defibrillation attempts (75%) were successful. There were 12 deaths, half of which were sudden and occurred in patients who were not wearing the WCD as instructed. Approximately one quarter of the study population (n=68 of 289) discontinued the study as a result of device-related discomfort or adverse reactions. These studies were the first to demonstrate the feasibility of the WCD in patients at high risk for SCD. Moreover, they demonstrated reasonable efficacy in those patients who complied with wearing the device.Table 3. Clinical Studies of WCDs*ReferencePatient PopulationSample Size, nAdherence, h/dDuration of Therapy, dAppropriate Shock Rate, %Inappropriate Shock Rate, %Survival, %Epstein et al,52 2013Patients 0–3 mo after AMI845321.8 (median)69±611.61.393Mitrani et al,53 2013Newly diagnosed cardiomyopathy or recent revascularization13414±872±550098Zishiri et al,54 2013Recent revascularization with left ventricular dysfunction809NR79±69 (CABG) 81±183 (PCI)1.31.698Kao et al,55 2012HF patients listed for transplantation, with a new diagnosis, or receiving inotropes8220±580±5800100Saltzberg et al,56 2012Peripartum10718±575±810097Nonischemic cardiomyopathy15917±656±540.6085Rao et al,57 2011Congenital structural heart disease4319 (12–21)27 (10–55)0087Inherited arrhythmias11919 (10–22)29 (7–68)2.55.997Chung et al,48 2010Aggregate US experience356920±553±701.71.999Collins et al,49 2010Age ≤18 y8120 (1–24)29 (0–531)01.289Age 19–21 y10319 (1–24)35 (0–499)1.90.991Klein et al,43 2010Nationwide experience in Germany354211063.10.8NRFeldman et al,46 2004WEARIT/BIROAD clinical studies (HF patients or bridge to ICD for other indications)289NR931.02.196Shock rates are given as percentages (n patients with shock/n WCD patients). AMI indicates acute myocardial infarction; BIROAD, Bridge to ICD in Patients at Risk of Arrhythmic Death; CABG, coronary artery bypass grafting; HF, heart failure; ICD, implantable cardioverter-defibrillator; NR, not relevant; PCI, percutaneous coronary intervention; WCD, wearable cardioverter-defibrillator; and WEARIT, Wearable Defibrillator Investigative Trial.*Based on a Medline search on July 1, 2013, and updated on December 2, 2013. Studies with ≥50 subjects were included.On the basis of data from a manufacturer registry, in the United States between 2002 and 2006, a total of 3569 patients wore a WCD for at least 1 day (mean duration, 53±70 days).48 WCD discontinuation because of discomfort or adverse reactions occurred in 14%. Longer duration of use was associated with higher rates of compliance. Indications for WCD use included ICD explantation (23%), ventricular arrhythmia before planned ICD implantation (16%), recent MI (16%), post-CABG status (9%), and recent diagnosis of cardiomyopathy with an LVEF ≤0.35 (28%). During a total of 143 643 patient-years, there were 80 sustained VT/VF events in 59 patients (1.7%/patient-year). Most of these sustained VT/VF events occurred in patients with an explanted device (event rate, 5.2%). First-shock efficacy was 99% (n=79 of 80), and post-VT/VF survival was 90% (n=72 of 80). Consistent with other studies of sudden death events,58 a substantial number of sudden cardiac arrests were attributable to non-VT/VF events (25%), including 23 asystole events.Compared with a single-center cohort of patients receiving ICDs (1996–2004) for traditional indications, survival was similar in the WCD cohort (3.6% mortality rate versus 4.4% at 3 months; P=0.256).48 However, the comparison of event rates between these WCD and ICD cohorts was complicated by limited demographic and clinical data. Overall, 2% of the WCD patients received an inappropriate shock (rate, 1.4%/mo), which was similar to the rate of appropriate shocks (Table 3). Reasons for inappropriate WCD shocks included signal noise (68%), supraventricular tachycardia (27%), nonsustained VT (6%), oversensing of normal cardiac signals (4%), ECG signal loss (4%), and failure to activate the response button. Other data suggest that the inappropriate shock rate in patients treated with the WCD can reach 1.9% to 5.9% within 2 to 3 months.46,48,57 In contrast, ICD shock rates have been demonstrated to be 13% over 41 months.59In addition to the overall published national experience,48 several observational studies in selected patient groups and single centers have been reported. In a manufacturer’s database of WCD use in 8453 patients within 90 days of MI (median time from AMI to WCD, 16 days; 62% of patients revascularized; 77% with LVEF ≤0.30), 1.6% of the patients received appropriate shocks.52The WCD has been used as a bridge until either myocardial recovery or ICD implantation in patients with newly diagnosed cardiomyopathy, patients with NYHA functional class IV heart failure, and those listed for transplantation. In a multicenter prospective WCD registry of 89 patients with idiopathic dilated cardiomyopathy, 42% experienced myocardial recovery and did not develop an indication for permanent ICD.55 Furthermore, none of the patients had SCD or required WCD therapy. Event rates appear to be lower in patients with newly diagnosed cardiomyopathy (<1%) compared with patients who meet current ICD guideline indications.48,53 Event rates are also lower in patients with recent revascularization, although there appears to be greater variation in these event rates across WCD studies (0%–1.6%; Table 3) Although overall event rates are lower in patients with newly diagnosed cardiomyopathy or recent coronary revascularization, retrospective observational data suggest that the WCD may confer a survival benefit. In a comparison of 4149 patients with recent revascularization and LVEF ≤0.35 who did not receive an ICD at hospital discharge with 809 patients who received a WCD at discharge, propensity-adjusted survival was greater in those treated with a WCD after CABG (7% versus 3%; adjusted hazard ratio, 0.42; 95% confidence interval, 0.31–0.55) or percutaneous coronary intervention (PCI; 10% versus 2%; adjusted hazard ratio, 0.33; 95% confidence interval, 0.21–0.52). Consistent with prior data, however, only 1.3% of those treated with a WCD received appropriate therapy for VT/VF.54 WCD therapy may also be a reasonable treatment option in appropriate pediatric patients at high risk of SCD.44,50Although there is an accumulating series of observational data of WCD use in clinical practice, questions about device efficacy will ultimately require randomized studies. The Vest Prevention of Early Sudden Death Trial (VEST) and Registry60 (NCT01446965) is currently evaluating the use of the WCD after MI. The study is randomizing patients within 7 days of an MI who have an LVEF ≤0.35. The study will test the hypothesis that WCD use improves 12-month survival after MI.Potential Indications for WCD TherapyWith the recognition that a WCD might be advocated in a wide variety of clinical circumstances, the following recommendations are derived from the accrued clinical experience, available observational data, and prospective evidence. The recommendations are aggregated and summarized in Table 4.Table 4. Indications and Recommendations fo