Efficacy and safety of ajmaline in patients with electrical storm.

POSTER PRESENTATIONS

Electrical storm (ES) is a rare and life-threatening cardiac emergency characterized by recurrent ventricular arrhythmias, posing unique challenges when it occurs during pregnancy. We report the case of a 28-year-old woman presenting with refractory ES in the late stages of a dichorionic-diamniotic twin pregnancy. Initial management included emergent cesarean delivery under general anesthesia due to maternal hemodynamic instability and fetal bradycardia. Despite pharmacological stabilization and multiple synchronized cardioversions, the arrhythmia persisted, necessitating catheter ablation to restore sinus rhythm. Multidisciplinary collaboration involving anesthesiology, obstetrics, cardiology, and electrophysiology ensured a favorable outcome for both mother and neonates, with no long-term complications. This case highlights the critical importance of tailored, interdisciplinary approaches in managing ES during pregnancy and underscores the need for resource optimization and rapid decision-making to balance maternal and fetal safety. Future investigations should focus on identifying potential triggers and improving protocols for the management of ES in high-risk pregnancies.

Natural history of potentially lethal ventricular arrhythmias in patients treated with long-term antiarrhythmic drug therapy

ORAL PRESENTATION

IntroductionWhen electrical storm (ES) is amenable to neither antiarrhythmic drugs, nor deep sedation or catheter ablation, autonomic modulation may be considered. We report our experience with percutaneous left stellate ganglion block (PSGB) to temporarily suppress refractory ventricular arrhythmia (VA) in patients with structural heart disease.MethodsA retrospective analysis was performed at our institution of patients with structural heart disease and an implantable cardioverter defibrillator (ICD) who had undergone PSGB for refractory VA between January 2018 and October 2021. The number of times antitachycardia pacing (ATP) was delivered and the number of ICD shocks/external cardioversions performed in the week before and after PSGB were evaluated. Charts were checked for potential complications.ResultsTwelve patients were identified who underwent a combined total of 15 PSGB and 5 surgical left cardiac sympathetic denervation procedures. Mean age was 73 ± 5.8 years and all patients were male. Nine of 12 (75%) had ischaemic cardiomyopathy, with the remainder having non-ischaemic dilated cardiomyopathy. Mean left ventricular ejection fraction was 35% (± 12.2%). Eight of 12 (66.7%) patients were already being treated with both amiodarone and beta-blockers. The reduction in ATP did not reach statistical significance (p = 0.066); however, ICD shocks (p = 0.028) and ATP/shocks combined were significantly reduced (p = 0.04). At our follow-up electrophysiology meetings PSGB was deemed ineffective in 4 of 12 patients (33%). Temporary anisocoria was seen in 2 of 12 (17%) patients, and temporary hypotension and hoarseness were reported in a single patient.DiscussionIn this limited series, PSGB showed promise as a method for temporarily stabilising refractory VA and ES in a cohort of male patients with structural heart disease. The side effects observed were mild and temporary.

Background: Electrical storm (ES) is a life‑threatening cardiac emergency characterized by recurrent, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) episodes that are often refractory to standard therapies. It predominantly affects patients with structural heart disease - most notably those with ischemic cardiomyopathy and chronic heart failure with reduced ejection fraction (HFrEF). Case Presentation: We describe a 75‑year‑old man with ischemic cardiomyopathy and HFrEF admitted for sustained VT unresponsive to conventional management. His history included multiple catheter ablations, prior myocardial infarction, and an implanted ICD placed for recurrent ventricular arrhythmias. Despite additional ablations and antiarrhythmic medication, he continued to experience electrical storms. Definitive rhythm control was achieved via a multidisciplinary strategy comprising left stellate ganglion block, upgrade to cardiac resynchronization therapy‑defibrillator (CRT‑D), personalized ICD reprogramming, and initiation of flecainide in combination with propranolol. Device interrogation at follow‑up confirmed effective biventricular pacing and complete suppression of sustained ventricular arrhythmias. Conclusion: This case underscores the complexity of managing ES in patients with advanced structural heart disease and multiple comorbidities. Individualized device programming, innovative pharmacological regimens, and targeted interventional techniques can stabilize patients refractory to standard approaches. A holistic, team‑based model of care is essential to optimize outcomes and improve quality of life in this high‑risk population.

Radio frequency ablation for VT – A cost-effective tool to combat SCD in developing countries

Patients with implanted cardioverter-defibrillator (ICD) often have justified ICD activations no matter if the indication for implantation was primary or secondary prophylaxis of sudden death. First line therapy in the prevention of recidivate ventricular arrhythmia in these patients is antiarrhythmic therapy, but if this is inefficient, arrhythmic substrate radiofrequency (RF) ablation is recommended. Ablation treatment is an accepted procedure in patients with ischemic heart disease, but it has rarely been used in patients with idiopathic and particularly polymorphic ventricular tachycardia (VT). It must be emphasized that acute ablation is relatively successful, but because of substrates progression, relapses of VTs are very frequent (35%) (1). Therefore, antiarrhythmic therapy remains an important therapy after the ICD implantation, before, and often after RF ablation (2). We present the cases of five patients in whom the prevention of recidivate VTs was achieved only by an old nonselective beta-blocker propranolol (dose 20 × 40 or 2 × 80mg). Patient 1: a 52 years old woman with ICD implanted as a secondary prevention after out-of-hospital cardiac arrest caused by ventricular fibrillation. There was no structural heart disease, coronarography was normal, and there was only arterial hypertension in patient's history. QTc interval was within the reference range, there were no Brugada syndrome elements, and no sudden death in family history. During the first year after the implantation, ICD was activated for more than 10 times because of polymorphic VT in spite of medicaments therapy. On one occasion even an electrical storm occurred. After the implantation, bisoprolol maximum dose was given, and later in combination with mexiletine, which was stopped as a result of intolerance. Combination with amiodarone was used for a short period of time but with no effects. Only after bisoprolol had been replaced with propranolol, there were no tachycardias and ICD stopped activating. Since then the patient has been followed-up for 5 years. Patient 2: a 56 years old man with no family or individual heart disease history, or any other serious disease. ICD was implanted as secondary prophylaxis after relapsing syncopes caused by VTs. The first therapy with amiodarone had not prevented multiple ICD activations, so it was replaced by a combination of bisoprolol and mexiletine. Despite the new therapy, ICD continued to activate for several justified occasions (5 times). Only after bisoprolol had been replaced with propranolol, ICD stopped activating. Since then the patient has been followed-up for 3 years. In the meantime, mexiletine therapy has been stopped (it is unavailable in Croatia), so now he takes propranolol only. Patient 3: a 69 years old man with ICD implanted after relapsing sustained VTs. The patient had no structural heart disease or any signs of ischemia. Coronarography was normal. In spite of the maximum dose of bisoprolol in combination with amiodarone, ICD was reasonably activated on over 20 occasions. On 3 occasions, an electrical storm was detected. Arrhythmia could not have been controlled even by the combination of bisoprolol and mexiletine. Only the replacement of bisoprolol by propranolol led to a complete VT suppression. In the last 3 years, the patient has not had any ICD activation. In the meantime, mexiletine therapy has been stopped. Patient 4: a 86 years old man. Two years ago, he had inferioposterior myocardial infarction with ST-elevation (STEMI) and a year after he was hospitalized for hemodynamically unstable VT. Slightly reduced ejection fraction (EF 45%-50%) was determined, caused by inferioposterior hypokinesia. Coronarography showed an old collateralized occlusion of the right coronary artery (RCA) and irrelevant changes on other coronary arteries. Sustained VTs repeated daily, despite the use of different antiarrhythmics: bisoprolol, lidocaine, amiodarone, and magnesium. After the temporary electrode had been placed, conversion was achieved by overdrive electrostimulation, but only occasionally. However, electrical cardioversion had to be done in most cases (6 times). Only the combination of propranolol and lidocaine in high doses managed to suppress VT. The patient had a successful RF ablation of VT with propranolol therapy only. During the 2 years of follow-up, he has had no arrhythmia. ICD has not been implanted. Patient 5: a 60 years old man. After anteroseptal STEMI with severely reduced left ventricular systolic function, the patient developed frequent VTs that responded neither to combination of bisoprolol and lidocaine nor to overdrive stimulation. The use of amiodarone induced a remarkable extension of the QTc interval without suppressing arrhythmia. On most occasions, arrhythmia had to be stopped by electrical cardioversion (5 times). Only after using propranolol instead of bisoprolol, arrhythmia was completely suppressed. When propranolol had been cancelled, because of septic shock, VT relapsed. After the septic shock had been stabilized, ICD was implanted and propranolol was included to the therapy again. Further follow-up (1 year) has not recorded any ICD activation. In our cases, non-selective propranolol was more effective in suppressing severe VTs than newer selective beta blocker bisoprolol. Unlike bisoprolol, propranolol blocks both beta 1 and beta 2 receptors (20% of beta adrenergic receptors in the heart) and owing to liposolubility also penetrates into the brain (3). Thereby, it can also result in the central inhibition of the sympathetic nervous system. The unique stability effect on the membrane of myocytes has also been described (4). Previous studies showed that propranolol in combination with amiodarone offered the best prevention of VT relapses (5). The reason why propranolol is not widely used in patients with cardiomyopathy is the lack of evidence-based data for these indications. Studies in patients with cardiomyopathy have recently been conducted using only newer beta-blockers (carvedilol, metoprolol, bisoprolol) (6). We believe it could be useful to conduct a study on propranolol, because propranolol possibly has more beneficial effect on the survival of patients with cardiomyopathy than selective beta blockers.

Relation of the Severity of Obstructive Sleep Apnea in Response to Anti-Arrhythmic Drugs in Patients With Atrial Fibrillation or Atrial Flutter

Heart transplantation (HT) can be proposed as a therapeutic strategy for patients with severe refractory electrical storm (ES). Data in the literature are scarce and based on case reports. We aimed at determining the characteristics and survival of patients transplanted for refractory ES. Patients registered on HT waiting list during the following days after ES and eventually transplanted, from 2010 to 2021, were retrospectively included in 11 French centers. The primary endpoint was in-hospital mortality. 45 patients were included (82% men; 55.0 (47.8-59.3) years old; 42.2% and 26.7% non-ischemic dilated or ischemic cardiomyopathies, respectively). Among them, 42 (93.3%) received amiodarone, 29 (64.4%) betablockers; 19 (42.2%) required deep sedation, 22 (48.9%) mechanical circulatory support, and 9 (20.0%) had radiofrequency catheter ablation. Twenty-two patients (62%) were in cardiogenic shock. Inscription on wait list and transplantation occurred 3.0 (1.0-5.0) days and 9.0 (4.0-14.0) days after ES onset, respectively. After transplantation, 20 patients (44.4%) needed immediate hemodynamic support by extracorporeal membrane oxygenation (ECMO). In-hospital mortality rate was 28.9%. Predictors of in-hospital mortality were serum creatinine/urea levels, need for immediate post-operative ECMO support, post-operative complications, and surgical re-interventions. One-year survival was 68.9%. ES is a rare indication of HT but may be lifesaving in those patients presenting intractable arrhythmias despite usual care. Most patients can be safely discharged from hospital, although post-operative mortality remains substantial in this context of emergency transplantation. Larger studies are warranted to precisely determine those patients at higher risk of in-hospital mortality.

Early catheter ablation versus conservative- only management in patients with electrical storm. Systematic review and meta- analysis.

Ventricular tachycardia represents life-threatening cardiac rhythm disturbance and catheter ablation using radiofrequency current provides powerful means for definitive cure of almost all monomorphic tachyarrhythmias. Presence and extent of underlying structural heart disease is important for further prognosis of the patients, who undergo catheter ablation of ventricular tachycardia. Long-term results of catheter ablation for ventricular tachycarida in patients with and without structural heart disease are presented. Patients and results: Twenty three patients (9 females) aged 49.1 ± 15.6 (18–72) years underwent catheter ablation for monomorphic (resp. polymorphic in one patient) ventricular tqachycardia in 30 ablation procedures. Patients with structural heart disease: Seven patients (2 females) aged 54.2 ± 19.8 (21–72) years had structural heart disease (5 patients – post myocardial infarction, 1 patient – arrhythmogenic right ventricular dysplasia, 1 patient – surgically corrected transposition of great arteries). All sustained monomorphic ventricular tachycardias were eliminated during the catheter ablation and no ventricular tachycardia recurred during the follow-up period in 4 patients. In two patients sustained monomorphic ventricular tachycardia was not eliminated with radiofrequency current. One of the patients remains free of ventricular tachycardia and one patient experienced one recurrence of slowed ventricular tachycardia. Thus long-term clinical success was achieved in 4 patients and some clinical benefit probably also in the latter two patients. A different ablation strategy targeting large arrhythmogenic area at the border of postmyocardial infarction scar was employed in the last patient with frequent ICD discharges for polymorphic ventricular tachycardia associated with hemodynamic deterioration. This procedure brought immediate and long-term significant reduction of ICD shocks and rehospitalizations and probably was life-saving. Patients without structural heart disease: In sixteen patients (7 females) aged 44.2 ± 12.8 (18–66) years no structural heart disease was found. These patients presented with documented ventricular ectopy in different forms from incessant ventricular premature beats through repetitive nonsustained ventricular tachycardia to paroxysmal sustained ventricular tachycardia. The arrhythmia originated in the right ventricle in 11 patients (right ventricular outflow tract in 10 patients and basolateral wall in 1 patient) and in the left ventricle in 5 patients (inferoapicoseptal region in 4 patients and basoinferoseptal region in 1 patient). Eleven patients (68.7 %) had the arrhythmia eliminated or markedly suppressed during the ablation procedure and remain free of palpitations and antiarrhythmic drugs. Two patients with partial suppression of the ectopic rhythm are less symptomatic and the antiarrhythmic drugs could be reduced. In one patient one ventricular tachycardia morphology from the right ventricular outflow tract was eliminated while the second ventricular tachycardia morphology was not targeted (and was suppressed by antiarrhythmic drug) for close vicinity of the arrhythmogenic focus to the left anterior descending artery. Thus the clinical benefit of the ablation procedure is enhanced to 14 (87.5 %) patients. Ablation completely failed in two patients. Conclusion: Radiofrequency catheter ablation of ventricular tachycardia is highly effective and safe and results in long-term arrhythmia elimination. In patients with underlying structural heart disease it should be currently viewed as a adjunctive therapy to a complex management of the patient, while in otherwise healthy patients it can be considered a method for permanent cure.

HomeCirculationVol. 106, No. 2Ventricular Tachycardia Associated With Myocardial Infarct Scar Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBVentricular Tachycardia Associated With Myocardial Infarct ScarA Spectrum of Therapies for a Single Patient Kyoko Soejima, MD and William G. Stevenson, MD Kyoko SoejimaKyoko Soejima From the Cardiovascular Division, Department of Internal Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Mass. and William G. StevensonWilliam G. Stevenson From the Cardiovascular Division, Department of Internal Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Mass. Originally published9 Jul 2002https://doi.org/10.1161/01.CIR.0000019361.34897.75Circulation. 2002;106:176–179Case: A 73-year-old woman is referred for management of recurrent ventricular tachycardia (VT). She had suffered an inferior wall myocardial infarction in 1970. Fifteen years later, she presented with a wide QRS tachycardia, palpitations, and dizziness. Therapy with amiodarone was initiated but discontinued in 1997 because of toxicity, and she received an implantable cardioverter-defibrillator (ICD). She did well until July 2000, when she had several shocks from the ICD, all of which were preceded by syncope. Interrogation of the ICD confirmed 23 episodes of VT, 20 asymptomatic runs terminated by antitachycardia pacing (ATP), and 3 episodes requiring cardioversion from the ICD. Her left ventricular ejection fraction was 25%. Sotalol failed to prevent VT recurrences and mexiletine produced nausea and tremor.She was referred for catheter ablation. An echocardiogram revealed akinesis of the inferior wall and no left ventricular thrombus. In the electrophysiology laboratory, programmed stimulation induced 5 different morphologies of VT (Figure 1) with rates ranging from 180 to 220 bpm. Because the induced VTs were unstable, producing hypotension and often changing from one VT to another, catheter mapping and ablation were performed largely during sinus rhythm, guided by electrogram characteristics and pacing during sinus rhythm (pace-mapping) that marked the location of the infarct scar and likely reentry paths in the subendocardium. After placement of lines of radiofrequency (RF) lesions through these abnormal regions, only ventricular flutter (280 bpm) was inducible; the slower VTs were no longer inducible. There have been no VT recurrences in the 18 months of follow-up after ablation. Download figureDownload PowerPointFigure 1. Twelve-lead ECGs of the inducible VTs were obtained in the electrophysiology laboratory.DiscussionVentricular arrhythmias associated with myocardial infarction (MI) occur in 2 distinct phases. During the acute phase of infarction, polymorphic VT that degenerates to ventricular fibrillation is most common. In the weeks that follow, the healing infarct undergoes structural changes. Fibrosis creates areas of conduction block and also increases separation of myocyte bundles, slowing conduction through myocyte pathways in the border of the infarct.1,2 These pathways or channels can support stable reentry circuits, leading to monomorphic VT, when an appropriate trigger (such as a change in sinus rate or a premature depolarization) occurs. After surviving the acute phase of the infarct, monomorphic VT may emerge at any time. With present management of myocardial infarction, the incidence of sustained VT is relatively low, and fewer than 5% of infarct survivors have inducible VT when studied early after the infarct.3 Patients with large infarcts, often those who are not successfully reperfused, are at greatest risk for VT. Although the first 6 months after infarction is thought to be the period of greatest risk for VT and sudden death, some patients develop VT much later, as in the case presented above. Whether late development of VT is related to electrical and mechanical remodeling or additional ischemic events contributing to the development of the substrate for the VT is not known. Because the arrhythmia substrate for late VT is relatively fixed, this type of VT tends to be recurrent and difficult to suppress with medications.Antiarrhythmic Drugs and ICDsAntiarrhythmic drugs are frequently prescribed because they alter the electrophysiological properties of the reentrant circuit and suppress potential triggers for the development of VT. However, within 2 years, >40% of patients being treated for sustained VT will experience recurrences.4 There is a risk that a VT recurrence will cause sudden death, particularly in patients with depressed ventricular function and those who have presented with a hemodynamically poorly tolerated VT.5Three recent trials support the superiority of ICDs over antiarrhythmic drug therapy for prolonging survival and preventing sudden death in survivors of sustained ventricular arrhythmias.6,7,8 Thus, an ICD is first-line therapy for these patients. For many patients, placement of an ICD prevents the side effects of antiarrhythmic drugs. The most effective drug, amiodarone, produces side effects in almost 75% patients within 5 years. These side effects include hypothyroidism (5% to 25%), blue skin (1% to 6%), corneal pigmentation (1%), pulmonary toxicity (1% per year), tremor, or other neurological toxicity. ICD risks include device failure, lead fractures, and infection, but these are infrequent. ICDs also provide back-up pacing that protects against bradyarrhythmia.Although ICDs extend survival, they only treat the arrhythmia when it occurs, and do not prevent arrhythmia recurrences. Follow-up is required for the infrequent possibility of device malfunction. Within a year of ICD implantation, 68% of patients have recurrent episodes of VT.6 Most monomorphic VTs can be terminated by antitachycardia pacing, which is painless and often asymptomatic, but some patients require electrical cardioversion via the ICD. When VT initially recurs, and particularly when it becomes frequent, an evaluation is required to address potential aggravating factors, such as myocardial ischemia, electrolyte abnormalities, or decompensated heart failure. Most patients with frequent monomorphic VT require additional therapy to reduce VT episodes.Interactions Between ICDs and Antiarrhythmic AgentsAntiarrhythmic drug therapy decreases the frequency of VT episodes in patients with ICDs and may make the VT more amenable to antitachycardia pacing therapy. For some patients, drug therapy is problematic. The antiarrhythmic agent may slow the sinus rate, causing the patient to be paced, potentially with loss of AV synchrony, or producing adverse hemodynamic effects from right ventricular pacing. Antiarrhythmic agents may slow the rate of VT when it occurs such that it falls below the detect rate of the ICD, or falls into the range where sinus tachycardia can also occur, making distinction of sinus tachycardia from VT difficult. Some drugs, notably amiodarone, can increase the energy required for defibrillation, theoretically reducing the likelihood that ventricular fibrillation would be effectively treated by the ICD.AblationRF catheter ablation is a useful adjuvant therapy for frequent episodes of symptomatic VT. Initial ablation studies used careful mapping during VT to identify a critical part of the VT reentry circuit where the relatively small RF ablation lesions could interrupt reentry. The presence of hemodynamically stable VT facilitated mapping and ablation attempts. Patients with unstable VTs that did not allow detailed mapping were largely excluded from initial ablation attempts. Developments in the understanding of the nature of reentrant circuits and in methods to identify the region of the infarct scar and potential reentrant circuit paths through the scar now allow catheter ablation to be effective for many patients who have multiple and unstable VTs.9,10Catheter mapping systems allow electrophysiological data to be integrated in a 3-dimensional anatomic reconstruction of the ventricle (Figure 2A). The map of the left ventricle in Figure 2A, was created during sinus rhythm. The catheter was moved from point to point around the ventricle. At each point, the electrogram amplitude was plotted and color coded, with normal amplitude areas (>1.5 mV) indicated as purple and progressively lower-amplitude regions indicated by blue, green, yellow, and red regions. This patient has a large infero-posterior low-amplitude region consistent with her prior infarction. The area is much larger than that which can be completely ablated by RF energy; however, additional data can be obtained to focus the ablation to an appropriate region.10Download figureDownload PowerPointFigure 2. A, Voltage map of the left ventricle, constructed with an electroanatomic mapping system by moving the mapping catheter point by point over the endocardial surface, is shown. For each point, the electrogram amplitude is indicated by colors: purple indicates >1.5 mV (normal); blue, green, yellow, and red indicate progressively lower-amplitude abnormal regions. The left ventricle is viewed from the PA projection. The infarct area is identified as the extensive low-voltage area (red, yellow, green colors) in the inferior wall. Sites at which pace mapping and limited entrainment mapping were performed are shown with white tags. The gray regions indicate areas of dense scar that create fixed conduction block. B, The locations of RF lesions placed to interrupt pathways between the mitral annulus and areas of dense scars are shown as red tags. EM indicates entrainment mapping; PM, pace mapping matched.Inducing VT once in the electrophysiology laboratory allows confirmation of the diagnosis. In addition, the QRS morphology of the VT is obtained for use as a rough guide to the location of the reentry circuit in the infarct. In lead V1, a right bundle-branch block–like morphology VT suggests a left ventricular origin, and left bundle-branch block–like morphology predicts an origin in the right ventricle or in the interventricular septum. Dominant S waves in V2, V3, and V4 suggest an exit near the apex. Dominant R waves in these leads suggest an exit closer to the mitral annulus. Then, during sinus rhythm, pacing from the mapping catheter (pace-mapping) at sites around the infarct region and comparing the paced QRS with the VT morphology helped identify the VT reentrant circuit.11 The circuits can be large and multiple circuits are common.In the case presented, 5 different VTs were inducible. Figure 2A shows that pace mapping at a site in the low-voltage infarct region, located between two areas of dense unexcitable scar (gray regions), produced a QRS morphology similar to that of one of the VTs. To gain further confirmation that this region was involved in VT, the mapping catheter was placed at the site and VT was induced. After assessing the pattern of electrical activation, burst pacing was initiated to terminate VT. The effects of pacing (entrainment mapping) confirmed that this site was in the circuit12 (Figure 3). During stable sinus rhythm, a line of RF lesions (line 1) was then created through the target region. After the initial RF line was created, programmed stimulation induced other VT morphologies. On the basis of pace-mapping, additional RF lesions (line 2) were created (Figure 2B), which abolished inducible monomorphic VT. Download figureDownload PowerPointFigure 3. An example of entrainment mapping is shown. VT had been induced by right ventricular pacing. Pacing during VT was then performed from the mapping catheter in the left ventricle. The tachycardia was then promptly terminated by rapid burst pacing (not shown) to restore stable sinus rhythm. At this site, pacing accelerates VT to the pacing rate (cycle length of 280 ms) without changing the QRS morphology of the VT. This often indicates that the pacing site, where the mapping catheter is located, is in the reentry circuit. Additional measurements (the postpacing interval and stimulus to QRS interval) confirm that the site is in the reentry circuit. RF ablation was therefore performed at this and adjacent sites, abolishing VT. Abl indicates ablation catheter; RVA, right ventricular apex; VTCL, ventricular tachycardia cycle length.The Role of VT AblationICDs are first-line therapy for many patients with recurrent VT. When antiarrhythmic drug therapy fails to control symptomatic recurrences of VT, catheter ablation should be considered and can be expected to reduce the frequency of recurrent VT in >75% of patients.9,10,13,14 In experienced centers, ablation is now performed regardless of whether the VT rate is rapid and is associated with hemodynamic collapse. The major procedural risks are related to thromboembolism (1.2%), perforation (0.3%), and vascular access complications.15 The procedures can be long and are facilitated by the use of 3-dimensional reconstructions of the ventricular anatomy.When ablation fails, it is usually because of existence of portions of the reentrant circuits deep to the endocardium where they cannot be interrupted with standard endocardial ablation techniques. Ablation with saline-irrigated cooled ablation catheters and percutaneous epicardial mapping and ablation approaches are being evaluated that may allow some of these VTs to be ablated.16,17 Nonpharmacological therapies, such as RF ablation, have an increasingly important role in the management of VT after myocardial infarction, thus expanding the array of options available to clinicians.FootnotesCorrespondence to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women's Hospital 75 Francis St, Boston, MA 02115. E-mail [email protected] References 1 Wit A, Janse MJ. The Ventricular Arrhythmia of Ischemia and Infarction: Electrophysiological Mechanisms. Mount Kisco, NY: Futura; 1993.Google Scholar2 De Bakker JMT, Van Capelle FJL, Janse MJ, et al. Slow conduction in the infarcted human heart: "zigzag" course of activation. Circulation. 1993; 88: 915–926.CrossrefMedlineGoogle Scholar3 Andresen D, Steinbeck G, Bruggemann T, et al. Risk stratification following myocardial infarction in the thrombolytic era. J Am Coll Cardiol. 1999; 33: 131–138.CrossrefMedlineGoogle Scholar4 The ESVEM investigators. Determinants of predicted efficacy of antiarrhythmic drugs in the electrophysiologic study versus electrocardiographic monitoring trial. Circulation. 1993; 87: 323–329.CrossrefMedlineGoogle Scholar5 Wyse DG, Talajic M, Hafley GE, et al. Antiarrhythmic drug therapy in the multicenter unsustained tachycardia trial (MUSTT): drug testing and as-treated analysis. J Am Coll Cardiol. 2001; 38: 344–351.CrossrefMedlineGoogle Scholar6 The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997; 337: 1576–1583.CrossrefMedlineGoogle Scholar7 Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS); a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000; 101: 1297–1302.CrossrefMedlineGoogle Scholar8 Kuck KH, Cappato R, Siebels J, et al. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest. The cardiac arrest study Hamburg (CASH). Circulation. 2000; 102: 748–754.CrossrefMedlineGoogle Scholar9 Marchlinski FE, Callans DJ, Gottlieb CD, et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000; 101: 1288–1296.CrossrefMedlineGoogle Scholar10 Soejima K, Suzuki M, Maisel WH, et al. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation. 2001; 104: 664–669.CrossrefMedlineGoogle Scholar11 Stevenson WG, Sager PT, Natterson PD, et al. Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars. J Am Coll Cardiol. 1995; 226: 481–488.Google Scholar12 Stevenson WG, Khan H, Sager P, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation. 1993; 88: 1647–1670.CrossrefMedlineGoogle Scholar13 Stevenson WG, Friedman PL, Sweeney MO. Catheter ablation as an adjunct to ICD therapy. Circulation. 1997; 96: 1378–1380.CrossrefMedlineGoogle Scholar14 Strickberger SA, Man KC, Daoud EG, et al. A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and implantable cardioverter- defibrillator. Circulation. 1997; 96: 1525–1531.CrossrefMedlineGoogle Scholar15 Hindricks G. The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. The Multicentre European Radiofrequency Survey (MERFS) investigators of the Working Group on Arrhythmias of the European Society of Cardiology. Eur Heart. 1993; 14: 1644–1653.CrossrefMedlineGoogle Scholar16 Calkins H, Epstein A, Packer D, et al. Catheter ablation of ventricular tachycardia in patients with structural heart disease using cooled radiofrequency energy: results of a prospective multicenter study. Cooled RF Multi Center Investigators Group. J Am Coll Cardiol. 2000; 35: 1905–1914.CrossrefMedlineGoogle Scholar17 Soejima K, Delacretaz E, Suzuki M, et al. Saline-cooled versus standard radiofrequency catheter ablation for infarct related ventricular tachycardias. Circulation. 2001; 103: 1858–1862.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Darden D and Hoffmayer K (2022) The role of coronary artery disease and revascularization in electrical storm: A multidisciplinary team approach, Coronary Artery Disease, 10.1097/MCA.0000000000001144, Publish Ahead of Print Ciuffo L, Bruña V, Martínez‐Sellés M, Vasconcellos H, Tao S, Zghaib T, Nazarian S, Spragg D, Marine J, Berger R, Lima J, Calkins H, Bayés‐de‐Luna A and Ashikaga H (2020) Association between interatrial block, left atrial fibrosis, and mechanical dyssynchrony: Electrocardiography‐magnetic resonance imaging correlation, Journal of Cardiovascular Electrophysiology, 10.1111/jce.14608, 31:7, (1719-1725), Online publication date: 1-Jul-2020. Rosellini E, Lazzeri L, Maltinti S, Vanni F, Barbani N and Cascone M (2019) Development and characterization of a suturable biomimetic patch for cardiac applications, Journal of Materials Science: Materials in Medicine, 10.1007/s10856-019-6327-6, 30:11, Online publication date: 1-Nov-2019. Akhyari P, Barth M and Lichtenberg A (2017) 7.25 Cardiac Patch with Cells: Biological or Synthetic Comprehensive Biomaterials II, 10.1016/B978-0-08-100691-7.00157-9, (482-505), . Castellano D, Blanes M, Marco B, Cerrada I, Ruiz-Saurí A, Pelacho B, Araña M, Montero J, Cambra V, Prosper F and Sepúlveda P (2014) A Comparison of Electrospun Polymers Reveals Poly(3-Hydroxybutyrate) Fiber as a Superior Scaffold for Cardiac Repair, Stem Cells and Development, 10.1089/scd.2013.0578, 23:13, (1479-1490), Online publication date: 1-Jul-2014. Amraoui S, Denis A, Derval N, Zemmoura A, Sacher F, Jais P, Ploux S, Bordachar P, Ritter P, Haissaguerre M and Hocini M (2014) Le futur de la rythmologie interventionnelle, Archives des Maladies du Coeur et des Vaisseaux - Pratique, 10.1016/S1261-694X(14)70608-X, 2014:226, (17-31), Online publication date: 1-Mar-2014. Serpooshan V, Zhao M, Metzler S, Wei K, Shah P, Wang A, Mahmoudi M, Malkovskiy A, Rajadas J, Butte M, Bernstein D and Ruiz-Lozano P (2014) Use of bio-mimetic three-dimensional technology in therapeutics for heart disease, Bioengineered, 10.4161/bioe.27751, 5:3, (193-197), Online publication date: 1-May-2014. Wang B, Williams L, de Jongh Curry A and Liao J (2014) Preparation of Acellular Myocardial Scaffolds with Well-Preserved Cardiomyocyte Lacunae, and Method for Applying Mechanical and Electrical Simulation to Cardiac . N, T, M, B, R, M, B, K and P (2014) site appropriate following right ventricle Online publication date: Le A, A, L, S and D in for cardiac therapies, Online publication date: M, M, S, N, A, E, and M as a for and Journal of and Online publication date: and M for myocardial on Biological Online publication date: Rosellini E, Barbani N and P of Scaffolds for Myocardial and of Biomaterials Myocardial . M, J, D and S for cardiac Materials and Online publication date: Akhyari P, Barth M and Lichtenberg A Cardiac Patch with Cells: Biological or Synthetic Comprehensive . S, M, R, J, M and S of for myocardial Journal of Materials Science: Materials in Medicine, Online publication date: N and M Acellular Cardiac as a Scaffold for In and Online publication date: D and A of with Disease, . J, S and D of by Journal of Online publication date: D, A, A, P, S, I, E, S, P, and and Mechanical Within a Myocardial Patch A, Online publication date: K and J and and in . M, G, S, R and R for Cardiovascular of and Medicine, S, J, M, R, R, M and the of Cardiovascular Online publication date: S, S, J, J, S and with Journal of Materials Online publication date: N and R and of heart using Journal of Materials A, Online publication date: and The Development of for Online publication date: Wang S, I, A, T, Wang S, R, R and Stem and After and Online publication date: N Cardiac Online publication date: T, T, A, T, V, J, J and A In of in Journal of and Online publication date: and R the heart by of the in cardiac Medicine, Online publication date: M, and H of the in Myocardial Online publication date: P and S Therapies for Ventricular Pacing and Electrophysiology, Online publication date: S, P, I, S, A, T, D, R and (2017) The Use of as an Scaffold for the of Online publication date: J, N and S of the with Myocardial Stem and . J Ventricular Online publication date: A, J, J and de a la de de de Online publication date: J, H, M, E, F, M, and Mechanical and of Cardiac from and Online publication date: H, M, J, and A In - . A, J, J and de Radiofrequency Catheter Ablation of Ventricular Tachycardia in Patients With an Implantable de Online publication date: F, F, J, J, J, E, J, D and J Cells: Cardiac for and Online publication date: Ventricular Tachycardia and Associated with Electrical the of the Journal of Cardiovascular Electrophysiology, D, S, M and K Catheter ablation of ventricular tachycardia guided by cardiac Online publication date: N Ventricular in The Journal of Cardiovascular Online publication date: and of the and of on the of Journal of Biomaterials Online publication date: T, D, R, K, T, P, N, and R (2017) in the Ventricular Online publication date: K, P, D, R, and R Ventricular With Online publication date: M, and H of the in Myocardial T, H, S, N, and A conduction slowing and conduction A and D, R and The of electroanatomic mapping during radiofrequency ablation of ventricular tachycardia in patients after myocardial infarction, July 106, 2 Originally

Refractory electrical storm (ES) is a life-threatening condition in which heart transplantation (HTx) can be proposed. Nevertheless, the shortage of donors and subsequent outcomes question its place as a rescue strategy. We aim to describe the prognosis of ES patients listed for HTx but not transplanted. Patients registered on urgent HTx waiting list for refractory ES without being transplanted during initial hospitalization were retrospectively included in five French centres from 2010 to 2022. The primary endpoint was 1-year all-cause mortality. Forty patients were included [90% men; 56.5 (50.0-61.3) years old; 63.6% and 24.2% dilated and ischaemic cardiomyopathies]. Among them, 84.6% received amiodarone, 64.1% received beta-blockers; 50.0% required deep sedation, 35.0% mechanical circulatory support, 10.0% stellate ganglion block; and 57.5% underwent catheter ablation. At 1year, 20 patients (50.0%) died, including 14 in-hospital deaths (35.0%). Within six patients who died post-discharge, four previously underwent HTx, and one received VAD implantation. Twenty patients (50.0%) were still alive at 1year: 10 underwent HTx, 1 received VAD implantation followed by subsequent HTx, while another underwent VAD implantation as destination therapy. Finally, five (12.5%) were removed from the HTx waiting list due to functional improvement, distinguished by a median LVEF of 45.0% (20.0%-45.0%). The remaining three patients (7.5%) were still registered on HTx waiting list. Refractory ES is a critical condition with high short- and long-term mortality. While HTx serves as a rescue strategy, rhythm management can sometimes overcome the critical phase, facilitating subsequent HTx under more favourable conditions or even allowing removal from the HTx waiting list.

VENTRICULAR ARRHYTHMIAS IN A UNEXPECTED CARDIAC MAGNETIC RESONANCE