Article

Team Management of the Ventricular Tachycardia Patient

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Abstract

Ventricular tachycardia is a common arrhythmia in patients with structural heart disease and heart failure, and is now seen more frequently as these patients survive longer with modern therapies. In addition, these patients often have multiple comorbidities. While anti-arrhythmic drug therapy, implantable cardioverter-defibrillator implantation and ventricular tachycardia ablation are the mainstay of therapy, well managed by the cardiac electrophysiologist, there are many other facets in the care of these patients, such as heart failure management, treatment of comorbidities and anaesthetic interventions, where the expertise of other specialists is essential for optimal patient care. A coordinated team approach is therefore essential to achieve the best possible outcomes for these complex patients.

Disclosure:The authors have no conflict of interest to declare.

Received:

Accepted:

Acknowledgements:The authors acknowledge the efforts of Cynthia Romero in preparing this manuscript.

Correspondence Details:Noel G Boyle, David Geffen School of Medicine at UCLA, 100 UCLA Medical Plaza, Suite 660, Los Angeles, CA 90095-1679, USA. E: NBoyle@mednet.ucla.edu

Copyright Statement:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Ventricular arrhythmias remain a major contributor to cardiac morbidity and mortality worldwide, despite ongoing research and implementation of novel therapeutic interventions. Modern management of patients with ventricular arrhythmias requires a multidisciplinary team approach, especially in complex presentations with a background of multiple medical comorbidities.1,2 Such teams may include cardiac electrophysiologists (EP), heart failure specialists, general cardiologists and cardiac surgeons, as well as nurses, psychologists and primary care physicians. In emergency presentations with sustained or recurrent ventricular tachycardia (VT) or multiple ICD shocks (‘VT storm’), additional involvement of emergency physicians, intensivists, cardiac anaesthetists and coronary care unit (CCU) staff may be required.

Antiarrhythmic medications, ICD implantation and catheter ablation are the cornerstones of current VT management. Recently, catheter ablation has gained a prominent and earlier role in the management of patients with VT. Caring for patients undergoing catheter ablation of VT in dedicated units with integrated multidisciplinary care has been shown to lead to improved outcomes (Figure 1).3

In this article, we review the team approach and process of managing VT patients. The patient’s journey often begins in the clinic or emergency room, proceeding to some or all of the following areas: coronary care unit, cardiac catheterisation and EP labs, cardiac operating room, recovery unit, rehab unit to discharge home.

At each step, multiple teams need to be involved and coordinated to optimise the patient’s care. In our centre, the primary cardiologist coordinates the patient’s care with close involvement of the cardiac EP team throughout the hospital stay. We will first consider the patient presenting with sustained VT, then reviewing the special situation of VT storm or incessant VT.

Sustained Ventricular Tachycardia

Patients with VT may present with palpitations, syncope or ICD shocks where a device is present; in addition, their clinical status and haemodynamic stability will vary. Patients may present to primary or emergency care, or in general cardiology outpatient clinics. Therefore, the recognition of VT through the presence of a wide complex tachycardia on ECG is important for frontline caregivers. Wide complex tachycardias are most often VT and should be treated as such unless proven otherwise. The differential includes supraventricular tachycardia (SVT) with aberrancy, with abnormal baseline QRS, drug effects or electrolyte imbalances, and ventricular pacing. Multiple algorithms for ECG diagnosis of VT have been proposed, which have been well described elsewhere.4 VT algorithms are complex, leading to difficulties in application. With this in mind, simplified algorithms requiring only single-lead measurements such as the Vereckei criteria5 and Pava criteria6 have been developed, although their overall accuracy may be reduced.

Initial Management and Antiarrhythmic Therapy

It is most useful to approach the initial investigation and management of VT by its causes, broadly divided into those occurring in structurally normal hearts and those in the context of structural heart disease (SHD; Figure 2).

In haemodynamically unstable sustained VT, the priority is stabilisation and electrical cardioversion. In haemodynamically stable VT, a history, an examination and a 12-lead ECG should be obtained, and treatment with antiarrhythmic medications initiated. If the VT morphology suggests idiopathic outflow tract VT (left bundle pattern with inferior axis), IV beta-blockers may terminate the arrhythmia. Otherwise, IV amiodarone is considered the most effective first choice for pharmacological management.1,7 IV procainamide can be safely administered at a slow infusion rate, with efficacy for VT termination of 60–80 %, superior to amiodarone.8 Lidocaine has a lower efficacy of around 15–30 %, but is commonly used.7,9 It is important to closely monitor patients while administering antiarrhythmics for haemodynamically stable VT, as hypotension is a side-effect of both amiodarone and procainamide, which can lead to worsening of symptoms and haemodynamically unstable VT: in these cases, prompt sedation and cardioversion is required.

Investigations and Imaging

After acute termination, further investigation into the underlying cause is necessary. A thorough history and examination will help identify any risk factors and potential causes for SHD or primary arrhythmic syndromes. Review of the baseline 12-lead ECG may provide evidence of underlying myocardial disease or arrhythmia syndromes (Wolff-Parkinson-White, long QT, Brugada). A 12-lead ECG of the clinical VT is of great value, as this can indicate aetiology and exit site of VT.10 In rare cases, invasive electrophysiological study may be required to confirm diagnosis.1 Coronary angiography should be undertaken in all patients with recurrent VT to define the coronary anatomy.

In patients with ICDs, device interrogation should be undertaken as soon as the patient is stabilised. The device log can provide a full history of the number of VT episodes, therapies delivered and whether shocks are appropriate, inappropriate or even phantom in nature. Additional ECG investigations, such as signal-averaged ECG, can be useful in detection of late potentials and diagnosis of specific cardiomyopathies, such as arrhythmogenic right ventricular cardiomyopathy (ARVC).

Imaging is also indicated to detect the presence of SHD. In patients with known SHD, it may be useful to perform repeat imaging to assess current function and progression of disease. Echocardiography is the first-line investigation and can also provide an acute estimate of the left ventricular ejection fraction (LVEF). Where there is diagnostic uncertainty, contrast-enhanced cardiac MRI (CMR) can give further clarity; in addition, a significant proportion of apparently normal hearts at echocardiography may subsequently display structural disease on CMR imaging.11 Detection of late gadolinium enhancement (LGE) has been shown to correlate with the risk of arrhythmia and sudden cardiac death, and areas of scarring identified on CMR imaging have been demonstrated to correlate with areas of scarring on electroanatomic mapping and histopathology.12,13 CMR imaging aids diagnosis, risk stratification and planning for ablation. It can reveal significant details of complex scars, which can help focus mapping and ablation efforts.14

However, CMR imaging has been an investigation that has previously been contraindicated in many patients with ventricular arrhythmias, SHD and heart failure, where the prevalence of implanted cardiac devices is high. Specific concerns have included device lead heating causing thermal myocardial injury, arrhythmias, lead failure, and device failure or malfunction.15 To overcome this, MRI-conditional devices and imaging protocols for extra-thoracic studies with non-conditional devices have been developed over recent years with demonstration of safety.16 This involves assessment of specific criteria (strong indication for imaging, no abandoned leads, device implant older than 6 weeks), use of a strict protocol with continuous monitoring during imaging, and cooperation between radiologists, radiographers and a supervising appropriately trained (advanced cardiovascular life support [ACLS]) physician or specialist nurse practitioner.17

Schematic Showing the Progression of Patients through Multidisciplinary Management of Ventricular Tachycardia

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The effects of device artefact on image interpretability have also been a significant problem with MRI. In a single-centre observational study of a standardised CMR imaging protocol in 111 consecutive cardiac MRI studies in patients with ICDs, Do et al. found that use of a wideband protocol for LGE imaging led to a high proportion of interpretable studies unaffected by artefact (87 %).18 No adverse events (arrhythmias, generator/lead failures) were detected during imaging or up to 6 months’ follow-up.

Nuclear imaging may be of value in selected cases. A study of patients with unexplained non-ischaemic cardiomyopathy and ventricular arrhythmias showed that nearly half had focal abnormal cardiac fluorine-18 fluoro-2-deoxyglucose (FDG) uptake when investigated with fasting PET/CT. Notably, over half of PET-positive patients who underwent CMR imaging had studies negative for LGE; in the rest, LGE and FDG uptake were well correlated. Areas of PET abnormality matched low-voltage scar regions on electroanatomic mapping, which further corresponded with histological analysis.19

Management of ICDs

In patients with ventricular arrhythmias in the context of SHD (i.e. the secondary prevention population), ICD implantation is indicated in almost all cases. While the ICD is effective in preventing sudden cardiac death due to VT or ventricular fibrillation in patients with heart failure, it does not prevent occurrence of VT, and many patients with an ICD will present with one or multiple shocks.20–22 Recurrent ICD shocks have been shown to lead to increased morbidity and mortality, likely a reflection of the progression of underlying cardiac disease.23–25

In patients with recurrent ICD shocks, reprogramming of ICDs by the EP team can help to minimise shocks. The use of overdrive or anti-tachycardia pacing (ATP) to terminate haemodynamically stable VTs before shocks has been shown to be effective, with similar rates of VT acceleration, VT duration, syncope and sudden death when compared to shock only.26 Reprogramming detection zones and detection intervals is a balancing act that involves allowing for self-termination of ventricular arrhythmias against not delaying therapy for symptomatic or haemodynamically unstable arrhythmias.

The Aetiology of VT in the Structurally Normal Heart and in Structural Heart Disease

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In patients presenting with ventricular arrhythmias and recurrent device therapies, device interrogation should be performed, with adjustment of rate detection zones and intervals based on the cycle length of clinical VTs; this is in contrast with primary prevention devices, where higher rate cut-offs and longer detection intervals are usually feasible to prevent shocks.27 Finally, the role of inappropriate shocks in recurrent therapies should not be ignored. SVTs represent the most common cause of these, and the use of SVT discriminators can help reduce inappropriate shocks. Onset, stability and morphology criteria help discrimination between SVTs and VTs; this is particularly the case in patients with a history of VT in lower rate zones, where clinical VT characteristics can be accounted for in the discriminator algorithm.28

Medical Therapy

In the structurally normal heart with normal heart function, idiopathic VTs such as outflow tract VT, papillary muscle VT and fascicular VT can be managed with an initial trial of beta-blockers or calcium channel blockers. Although efficacy can be limited, their side-effect profile is relatively favourable. These are used both acutely and for long-term suppression of arrhythmias.

In patients with SHD and VT, antiarrhythmic drugs can be used in conjunction with ICD programming to minimise shocks. Beta-blockers have been shown to decrease mortality in patients with VT, heart failure and reduced EF, and are often used in the absence of contra-indications. However, they are ineffective when used as monotherapy for prevention of VT recurrence.

In a recent meta-analysis, the use of antiarrhythmic drugs led to a 34 % reduction in appropriate ICD therapies;29 the majority of these effects were observed in studies of amiodarone against control medical therapy. Beta-blockers and amiodarone are often used as combination therapy, with improved outcomes and suppression of VT recurrence. This has been shown to be superior to both beta-blockers alone, and sotalol alone.30 Mexiletine, a class IB antiarrhythmic, has been shown in small non-randomised studies to reduce VT recurrence when used as an adjunct to amiodarone in amiodarone-refractory VT,31 and is most commonly used in this setting.

Sotalol has been shown to be safe and effective in reducing mortality and ICD shocks.32 However, given its inferiority in subsequent studies when compared against beta-blockers and amiodarone,30 it is primarily used as a second-line therapy. Finally, ranolazine is an inhibitor of the late inward sodium current initially used in the anti-anginal and anti-ischaemic setting, and subsequently found to be effective in VT suppression in the setting of recurrent ICD shocks refractory to other antiarrhythmic drugs.33 This is currently being investigated in a larger scale population in the Ranolazine Implantable Cardioverter-Defibrillator trial (RAID, NCT01215253).34

However, antiarrhythmic drug use has not been shown to improve survival. In particular, despite well-characterised benefits in VT suppression, amiodarone appears to be associated with increased all-cause mortality.29 Amiodarone use is associated with a high incidence of side effects, primarily affecting the thyroid, lungs, liver and skin;35 patients on amiodarone need to be regularly monitored with blood tests. Significant discontinuation rates (18–38 %) for amiodarone have been noted in multiple trials.30,36–38

Catheter Ablation of Ventricular Tachycardia

Catheter ablation of VT was first described in the 1980s,39 and has since gained an increasingly prominent role in the management of many types of VT.40 With the development of electroanatomic mapping, advances in ablation technology and the development of epicardial approaches, ablation has become an effective intervention in an increasingly broad range of VT aetiologies, and is now deployed increasingly early in the management of recurrent VT.

The impact of catheter ablation has been studied in a variety of causes of VT. In idiopathic VT (outflow tract, fascicular, papillary), ablation can be undertaken in patients intolerant of or refusing medical therapy, in cases where VT has led to reduction in LVEF, or where outflow tract PVCs are found to trigger malignant arrhythmias; procedural success rate is high, with low risk.41

In ischaemic cardiomyopathy, multiple small-scale trials (‘Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia’, SMASH-VT; ‘Ventricular Tachycardia Ablation in Coronary Heart Disease’, VTACH) have demonstrated reductions in ICD therapies and greater freedom from VT for patients undergoing ablation and ICD implantation compared to ICD implantation alone.42,43 In the recent ‘Ventricular Tachycardia Ablation Versus Escalated Antiarrhythmic Drug Therapy in Ischemic Heart Disease’ (VANISH) trial, catheter ablation was also found to be superior to escalation of antiarrhythmic therapy in reducing the incidence of a composite primary endpoint of death, VT storm and appropriate ICD shocks.35

In non-ischaemic cardiomyopathies, outcomes are mixed. Studies in idiopathic dilated cardiomyopathy (IDCM) appear to show higher rates of VT recurrence when compared to ablation in ischaemic cardiomyopathy,44 for multiple underlying reasons. Mapping and ablation of IDCM is more challenging: the substrate is often less well defined and patchy, and in locations where ablation is less effective such as intramurally, septally or in the basal anterior LV wall.45 A study of patients with unexplained cardiomyopathy and ventricular arrhythmias who underwent PET/CT showed that a significant proportion had arrhythmogenic inflammatory cardiomyopathy, with diagnoses of cardiac sarcoidosis in 36 %.19 Immunosuppressive therapy was effective in controlling VT and preventing recurrence either as monotherapy or in conjunction with ablation, demonstrating a role for inflammation in the generation and maintenance of ventricular arrhythmias. In these cases, patients may benefit from joint management with other specialties, such as pulmonologists in sarcoidosis, as cardiomyopathy is rarely the sole manifestation of this disease.

The use of combined endo-epicardial mapping and ablation in ARVC has achieved good outcomes,46,47 with significantly less VT recurrence than with endocardial mapping only.48–50 The application of epicardial ablation has recently been extended to Brugada syndrome, where targeting of the right ventricular outflow tract can eliminate the Brugada pattern and prevent recurrence of VT in a subset of cases.51,52

The trend towards earlier ablation appears to be supported by improved outcomes in the literature: in one retrospective study of ischaemic and non-ischaemic cardiomyopathy, ablation within 30 days of first documented VT was associated with significantly higher rates of acute procedural success (defined as noninducibility of VT at end of ablation), and freedom from VT recurrence, although cardiac mortality was not significantly different;53 this is a finding replicated by other studies in the field.42,43,54 Although none of the aforementioned studies have demonstrated a reduction in all-cause mortality with catheter ablation, analysis of patient outcomes from large multicentre registries has demonstrated that freedom from VT recurrence post-procedure is associated with lower all-cause mortality and progression to transplantation.55

Catheter ablation of VT is a complex procedure: management is best undertaken in dedicated units, with integrated multidisciplinary care.3 Some evidence suggests that increased procedural time may result in higher rates of in-hospital mortality.56 As a result, a structured approach to ablation is necessary.

Pre-procedurally, this includes optimisation of patient comorbidities, particularly heart failure with specialist input, withholding anticoagulants and antiarrhythmic medications, and planning for approach of the arrhythmogenic substrate with imaging and preparation of equipment and personnel. Although pre-procedural protocols vary between centres, specific examples of the general approach are available in the literature.57

Intra-procedurally, familiarity with mapping techniques and manoeuvres, ability to appropriately assimilate information, and awareness of limitations and alternatives is essential to prevent the futility of inefficient or ineffectual procedure time.57 The development of modern electroanatomic mapping systems, in combination with pre-procedural imaging, has enabled real-time visualisation of substrates during mapping.58

Post-procedurally, admission to CCU, with multidisciplinary input from CCU staff, EP teams, heart failure specialists, nursing staff and physiotherapists, helps detection of complications and optimisation of post-procedural recovery. Post-procedural testing can help identify patients who may need further interventions.57

Management of VT Storm and Incessant VT

VT storm is defined as three or more separate episodes of sustained VT requiring intervention (such as ICD shock or ATP) within 24 hours. This is a medical emergency requiring prompt intervention with a multidisciplinary team approach to stabilise the patient, initiate therapies and optimise the patient for further interventions (Table 1 and Figure 3). On admission, patients with significant medical comorbidities, or with VT that is not haemodynamically tolerated, should be admitted to a coronary care or intensive care unit.

Initial stabilisation and resuscitation is often carried out by the CCU team following ACLS protocols to stabilise the patient, with cardioversion if necessary. Reversible causes of electrical storm should be sought and corrected where applicable, such as acute ischaemia, electrolyte imbalances, drug-induced proarrhythmia and decompensated heart failure.

ICD Programming and Initiation of Antiarrhythmic Medications

If the patient has an ICD in situ, device interrogation is required to determine the nature of shocks, and to reprogram the device to minimise shocks, through the use of ATP, extending VT detection duration and increasing rate detection thresholds where appropriate. Anti-arrhythmic medications are the first-line therapy in emergency departments and CCUs, as discussed earlier. Amiodarone is most commonly used, along with lidocaine, and in some cases procainamide. Maximising beta-blockade in this situation is important in breaking the cycle of sympathetic stimulation, which initiates VT, and, fuelled by ongoing stress responses from repeated shocks, often provokes further episodes of VT.

Phases and Teams in the Management of VT Storm

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Sedation

Sedation in VT storm can be beneficial in reducing sympathetic tone, along with the pain associated with repeated shocks, and is used often. In particular, patients who are haemodynamically unstable with VT may require general anaesthesia with intubation, potentially with mechanical haemodynamic support. However, sedation can lead to further decompensation in the form of severe hypotension in patients who have limited haemodynamic reserve, and must be managed carefully; in addition, prolonged intubation is not ideal.

Thoracic Epidural Anaesthesia and Percutaneous Stellate Ganglion Blockade

As the role of the sympathetic nervous system in the generation and maintenance of ventricular arrhythmias is increasingly recognised, therapies that modulate the sympathetic nervous system, such as cardiac sympathetic denervation and renal denervation have gained prominence in the management of refractory VT.59 However, these procedures cannot be feasibly performed in the acute phase, and are usually reserved for those patients with VT refractory to catheter ablation. Thoracic epidural anaesthesia (TEA), on the other hand, is an intervention that can be more easily instigated acutely: originally used for perioperative pain relief, it also provides sympathetic blockade at the level of T1–T4, and has been shown to be effective in controlling VT storm.60,61 The largest study to date of patients presenting with VT storm or incessant VT found that TEA could be safely performed, with a response seen in over half of patients.62 In some patients where response was observed, it was possible to wean off antiarrhythmic medications, or extubate patients. Thus, TEA can be employed as a substitute for deep sedation, and can be an effective bridging therapy allowing for stabilisation before further definitive therapy, such as catheter ablation (Figure 3). The authors suggest that TEA should be considered in patients without other reversible factors for VT storm, no contraindications to thoracic epidural catheter placement (e.g. infection or continuous therapeutic anticoagulation required), and where VT is not controlled despite the use of two or more antiarrhythmic medications.

Percutaneous stellate ganglion blockade is another autonomic modulatory intervention that can be performed at the bedside. Although descriptions of its efficacy have primarily taken the form of case reports, a recent meta-analysis showed beneficial effects in reduction of ventricular arrhythmia episodes and defibrillation, allowing patients in some cases to proceed to further definitive treatment such as ablation or transplantation.63

Mechanical Haemodynamic Support Devices

The use of mechanical haemodynamic support may be necessary to maintain end-organ perfusion in presentations with VT storm. It is essential to seek input from heart failure specialists and cardiac surgeons in assessing and planning to use haemodynamic support options. Available devices include intra-aortic balloon pumps (IABP), percutaneous left ventricular assist devices (pLVAD) such as the Impella and TandemHeart systems, and extracorporeal membrane oxygenation (ECMO). The IABP has historically been the most commonly used of these, although pLVAD and ECMO, which give additional support, are being increasingly employed in specialised centres in recent years.

Haemodynamically unstable VT storm is not the only setting in which mechanical haemodynamic support is used in VT. It is also used in preparation for ablation in patients with poor LVEF at baseline, when VT induction will likely result in acute haemodynamic decompensation (AHD).64 The need for a large arterial cannula for maximal output in the TandemHeart system necessitates arterial cutdown and insertion by an interventionalist with experience in use of the device. ECMO presents an even greater challenge, requiring coordination from intensivists, perfusionists and cardiac/vascular surgeons to initiate and monitor its use.

Risk Stratification and Patient Management for Catheter Ablation of VT

Catheter ablation in the setting of VT storm has been shown to suppress acute recurrence and stabilise the patient in the short term, even if the procedure is not completely successful;65 in longer term follow-up, procedural success is associated with reduced VT storm and improved survival, although risk of recurrence remains high.65,66 In the VANISH trial, catheter ablation led to reduced occurrence of VT storm compared with escalation in antiarrhythmic therapy.35 Combined endocardial and epicardial mapping and ablation can be used in this setting, in patients who satisfy criteria suggestive of epicardial substrate or circuit.67

As VT ablation carries high risk of post-procedural morbidity and mortality, pre-procedural risk assessment is important. This should aim to guide selection of patients not appropriate for ablation, and to identify high-risk cases that may require more aggressive optimisation with involvement of intensivists and perfusionists for prophylactic haemodynamic support.

The use of existing models can be useful to predict medium- to long-term survival in patients being considered for catheter ablation, which can then be weighed against the risk/benefit of proceeding. The Seattle Heart Failure Model, a commonly used and widely available tool for estimating mortality in patients with heart failure, has been shown to accurately identify those at high risk of mortality within 6 months of VT ablation when modified with the inclusion of risk modifiers for VT storm and ICD shocks. This not only acts as a useful tool to justify not undertaking ablation in some patients, but also aids discussions with patients and families regarding expectations for prognosis.68

A major risk of performing VT ablation is periprocedural acute haemodynamic decompensation (AHD), defined as persistent hypotension that requires mechanical support or procedure discontinuation. This is often secondary to the severity of the underlying cardiac disease, and aspects of ablation, such as induction of anaesthesia, repeated induction and termination of VT, and fluid overload from catheter irrigation. AHD is a particular concern for patients with heart failure and multiple comorbidities – common findings in patients undergoing ablation – although identification of those most at risk has not always been simple.

A single-centre study characterised the incidence of and risk factors for AHD in 193 patients undergoing catheter ablation.69 This occurred in 11 % of cases, and eight clinical variables were significantly associated with increased risk: age over 60 years; use of general anaesthesia; ischaemic cardiomyopathy; more severe heart failure (New York Heart Association [NYHA] class III/IV); reduced LVEF; presentation with VT storm; diabetes; and chronic obstructive pulmonary disease. Based on the associated odds ratios, the authors developed the PAAINESD score, a 35-point scale divided into three risk categories (Figure 4 and Table 1). In the study, AHD occurred in 2 %, 6 % and 24 % of patients in each category, respectively. Additionally, patients with AHD in the study had significantly higher mortality at 6 months and 1 year, with a tendency towards higher 30-day mortality. This was supported by a subsequent large-scale multicentre retrospective application of the PAAINESD score to 2,061 patients undergoing VT ablation, using data from the International VT Ablation Center Collaboration Group (IVTCC). PAAINESD scores were significantly higher in cases of early mortality (within 31 days post-ablation), compared with survivors and deaths beyond 31 days.70 The developers of the PAAINESD score thus suggest that it could be used to predict AHD and early mortality in patients undergoing catheter ablation, which could be minimised not only with appropriate patient selection, but also through more aggressive pre-procedural optimisation and use of prophylactic haemodynamic support.

In support of this, one nonrandomised study investigating the role of pre-emptive implantation of pLVAD (Impella, TandemHeart) before ablation compared with rescue pLVAD reported similar PAAINESD scores in the pre-emptive and rescue pLVAD groups, but a significantly higher 30-day mortality rate in the rescue pLVAD group (58 %), compared against both the pre-emptive pLVAD (4 %) and no-pLVAD (2 %) groups.71 Similarly, in a separate retrospective uncontrolled observational study, the use of ECMO as rescue haemodynamic support was associated with a high mortality rate (overall 76 %).72

An Overview of Management for Patients Presenting with VT Storm

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The PAAINESD score may also help to improve quantification of risk in patients who have risk factors for early mortality, but may actually represent lower risk candidates for ablation. Surveys of centres offering VT ablation and analyses of registries indicate that the rate of ablation is lower in groups such as the elderly and those with severe heart failure.73 Data suggest that ablation often occurs later in the management pathway, and thus likely later in the disease course for elderly patients, with a preference for escalation of antiarrhythmic medications.74 Rates of elective VT ablation in the elderly tend to be lower than in younger populations.75 Following on from this, ablation later in disease, in the emergency setting of VT storm or delaying ablation in presentations with VT storm may increase procedural risk and adversely affect outcomes.54

Such issues are highlighted by IVTCC group registry analyses that have investigated safety and efficacy outcomes, firstly in elderly patients (over 70 years) compared with younger patients,76 and secondly in severe heart failure patients (NYHA class IV compared with NYHA class II/III).77 In general, in-hospital and 1-year mortality were higher in elderly and NYHA IV patients, who overall represented a higher risk group, although acute procedural success and complication rates were not significantly different. Notably, in both studies, rates of successful ablation with long-term VT-free survival were not significantly different between groups. In addition, long-term VT-free survival translated to improved overall survival in elderly/severe heart failure patients compared with patients in the same group with VT recurrence. These results are consistent with smaller scale studies of elderly patients undergoing VT ablation, and subgroup analyses of SMASH-VT and VANISH.35,42,74

The PAAINESD Score for Predicting Risk of Acute Haemodynamic Decompensation

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These studies demonstrate that VT ablation can be performed safely in appropriately selected patients with high-risk features. It is important to note that freedom from VT recurrence resulted in significantly better overall survival than in patients where VT recurred. This highlights an area of risk stratification that might benefit from further study: the identification of patients who are most likely to respond to VT ablation, with low rates of VT recurrence, and who therefore have the most potential for survival benefit.

Further Procedures

Although ablation procedures have a relatively high success rate, a significant number of VTs remain refractory to ablation. In such cases, further interventions may be considered. First of all, repeat ablation may be indicated. If the original ablation procedure involved only endocardial mapping and ablation, a repeat procedure with epicardial mapping and ablation may be able to prevent further VT.

In some patients, efforts at ablation may have been hindered by difficulties in accessing the substrate, such as for VT originating from the interventricular septum. In such instances, interventions such as transcoronary ethanol ablation may be effective.78

Traditional epicardial access may be hindered by the presence of pericardial adhesions. Here, surgical epicardial access gained with the assistance of cardiothoracic surgeons may be a safe alternative.79

Autonomic modulation procedures may be indicated in the setting of ongoing refractory VT. Surgical cardiac sympathetic denervation can significantly reduce the incidence of ICD shocks in refractory VT.80 Renal denervation has also been shown to prevent VT recurrence in small case series.59 VT ablation may be used as a bridging procedure to insertion of left ventricular assist devices or cardiac transplant, in which case the procedure and post-operative care should be undertaken with involvement from transplant teams and cardiac surgeons.

In some cases, the role of further interventions may be limited or ablation may have been undertaken as a palliative procedure, to minimise the burden of distressing ventricular arrhythmias. It is important that in cases where these situations are anticipated, that clear discussions with patients and relatives are held in advance to explain the rationale behind clinical decision-making and to determine the wishes of the patient while they are able to communicate them. Discussion regarding measures such as device deactivation should be approached in advance.81 It may be useful to discuss with palliative care teams before procedures, and for them to review and meet the patient and family, to smooth the process of transition to supportive care when this is appropriate.

Relation between the PAAINESD Score and Incidence of Periprocedural Acute Haemodynamic Decompensation

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Outpatient and Home Care

It is difficult to predict the long-term outcomes of VT ablation in individual patients. Estimates of VT recurrence and mortality presented in the literature are based on a wide range of studies that have investigated outcomes of ablation in a variety of VT aetiologies with differences in prior therapy, number of procedures and ablation techniques used.82 In general, 1-year recurrence rates are approximately 30 % to 43 %; 2-year recurrence rates are around 50 %.35,43,44,55,83 Future studies may give more accurate estimates of outcomes in specific populations of patients with VT.82

Recurrent admissions with heart failure are common in patients with SHD, although possibly reduced after ablation, and likely represent progression of disease status.83 The 1-year mortality rate post-ablation is reported at about 15–20 %; again, this varies depending on aetiology and VT-free survival status, and is often reported as a composite with transplant-free survival.55,84 Much of this is driven by progressive heart failure and is not necessarily surprising given the knowledge that ICD shocks are associated with increased risk of mortality from heart failure.25

Patients require ongoing care and regular review after discharge. Care in the community is primarily conducted by the patient’s primary care physician and general cardiologist, heart failure specialist nurses and cardiac device technicians, but further specialist input from heart failure and electrophysiology teams may be required. The use of home monitoring systems in patients with implanted devices may be useful to monitor for VT recurrence. Patients may require re-do ablations, further interventions, or cardiac transplantation, as discussed above.

Finally, psychological support for the patient is important: although life-saving, repetitive shocks can exacerbate anxiety and reduce quality of life, at least in the short term, as well as increasing subsequent risk of death.85,86 It is important to support the patient to build confidence, and to allow patients to maintain a good quality of life despite this.

Conclusion

Management of patients with ventricular arrhythmias is complex. In outpatient or non-specialist settings prompt referral is important, and this is achieved by ensuring good links between community care givers and hospital teams. In-hospital management requires multispecialty input in a dedicated specialist setting. Co-ordination of care, in our hospital by the coronary care unit attending cardiologist and team, ensures that appropriate additional specialist input is sought, and investigations and interventions can be coordinated.

Catheter ablation has assumed an increasingly prominent role in the treatment of VT. Although early referral of patients for catheter ablation is desirable, appropriate patient selection is required using existing risk-stratification schemes. Further studies will better quantify the timing and benefits of catheter ablation in specific subpopulations of patients with VT.

Finally, at the centre of care remains the patient, for whom recurrent arrhythmias and worsening heart failure often bring significant morbidity and mortality. It is important to discuss options, risks and prognosis to allow patients to make informed choices about their care. The combination of a patient-centred approach with modern treatment modalities and appropriate specialist care is vital to ensuring optimal outcomes in patients presenting with VT.

Finally, at the centre of care remains the patient, for whom recurrent arrhythmias and worsening heart failure often bring significant morbidity and mortality. It is important to discuss options, risks and prognosis to allow patients to make informed choices about their care. The combination of a patient-centred approach with modern treatment modalities and appropriate specialist care is vital to ensuring optimal outcomes in patients presenting with VT.

Clinical Perspective

  • Modern management of patients with ventricular arrhythmias is complex, and requires a multidisciplinary team approach in experienced units to ensure optimal outcomes.
  • Appropriate initial investigations and prompt referral to specialist care are key to optimal management of ventricular tachycardia, as well as establishing underlying aetiology, which has significant implications for management.
  • Medical therapy may be effective in some cases, but may have significant side effects. ICD therapy prevents sudden cardiac death, but can lead to recurrent shocks, which results in increased morbidity and mortality, likely an indication progression of underlying disease.
  • Radiofrequency catheter ablation has gained an increasingly prominent role in the management of ventricular arrhythmias, although further studies are required to define the risk and outcomes of procedures in individual patients.
  • We discuss and give an overview of the management of patients presenting with ventricular tachycardia storm, including the evolving role of neuromodulation.

References

  1. Pedersen CT, Kay GN, Kalman J, et al. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Europace 2014;16:1257–83.
    Crossref | PubMed
  2. Fumagalli S, Chen J, Dobreanu D, et al. The role of the Arrhythmia Team, an integrated, multidisciplinary approach to treatment of patients with cardiac arrhythmias: results of the European Heart Association survey. Europace 2016;18:623–7.
    Crossref | PubMed
  3. Della Bella P, Baratto F, Tsiachris D, et al. Management of ventricular tachycardia in the setting of a dedicated unit for the treatment of complex ventricular arrhythmias. Circulation 2013;127:1359–68.
    Crossref | PubMed
  4. Garner JB, Miller JM. Wide complex tachycardia – ventricular tachycardia or not ventricular tachycardia, that remains the question. Arrhythm Electrophysiol Rev 2013;2:23–9.
    Crossref | PubMed
  5. Vereckei A, Duray G, Szénási G, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm 2008;5:89–98.
    Crossref | PubMed
  6. Pava LF, Perafán P, Badiel M, et al. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm 2010;7:922–6.
    Crossref | PubMed
  7. deSouza IS, Martindale JL, Sinert R. Antidysrhythmic drug therapy for the termination of stable, monomorphic ventricular tachycardia: a systematic review. Emerg Med J 2015;32:161–7.
    Crossref | PubMed
  8. Ortiz M, Martín A, Arribas F, et al. Randomised comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J 2017;38:1329–35.
    Crossref | PubMed
  9. Komura S, Chinushi M, Furushima H, et al. Efficacy of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Circ J 2010;74:864–9.
    Crossref | PubMed
  10. Josephson ME, Callans DJ. Using the twelve-lead electrocardiogram to localize the site of origin of ventricular tachycardia. Heart Rhythm 2005;2:443-446.
    Crossref | PubMed
  11. White JA, Fine NM, Gula L, et al. Utility of cardiovascular magnetic resonance in identifying substrate for malignant ventricular arrhythmias. Circ Cardiovasc Imaging 2012;5:12–20.
    Crossref | PubMed
  12. Watanabe E, Abbasi SA, Heydari B, et al. Infarct tissue heterogeneity by contrast-enhanced magnetic resonance imaging is a novel predictor of mortality in patients with chronic coronary artery disease and left ventricular dysfunction. Circ Cardiovasc Imaging 2014;7:887–94.
    Crossref | PubMed
  13. Nakahara S, Vaseghi M, Ramorez R, et al. Characterization of myocardial scars: electrophysiological imaging correlates in a porcine infarct model. Heart Rhythm 2011;8:1060–7.
    Crossref | PubMed
  14. Ashikaga H, Sasano T, Dong J, et al. Magnetic resonance-based anatomical analysis of scar-related ventricular tachycardia: implications for catheter ablation. Circ Res 2007;101:939–47.
    Crossref | PubMed
  15. Levine GN, Gomes AS, Arai AE, et al. Safety of magnetic resonance imaging in patients with cardiovascular devices: an American Heart Association scientific statement from the Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical Cardiology, and the Council on Cardiovascular Radiology and Intervention: endorsed by the American College of Cardiology Foundation, the North American Society for Cardiac Imaging, and the Society for Cardiovascular Magnetic Resonance. Circulation 2007;116:2878–91.
    Crossref | PubMed
  16. Russo RJ, Costa HS, Silva PD, et al. Assessing the risks associated with MRI in patients with a pacemaker or defibrillator. N Engl J Med 2017;376:755–64.
    Crossref | PubMed
  17. Roguin A, Schwitter J, Valhaus C, et al. Magnetic resonance imaging in individuals with cardiovascular implantable electronic devices. Europace 2008;10:336–46.
    Crossref | PubMed
  18. Do DH, Eyvazian V, Bayoneta AJ, et al. Cardiac magnetic resonance imaging using wideband sequences in patients with nonconditional cardiac implanted electronic devices. Heart Rhythm 2018;15:218–25.
    Crossref | PubMed
  19. Tung R, Bauer B, Schelbert H, et al. Incidence of abnormal positron emission tomography in patients with unexplained cardiomyopathy and ventricular arrhythmias: the potential role of occult inflammation in arrhythmogenesis. Heart Rhythm 2015;12:2488–98.
    Crossref | PubMed
  20. 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;337:1576–84.
    Crossref | PubMed
  21. Kuck KH, Cappato R, Siebels J, Rüppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: The Cardiac Arrest Study Hamburg (CASH). Circulation 2000;102:748–54.
    Crossref | PubMed
  22. 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;101:1297–302.
    Crossref | PubMed
  23. Schron EB, Exner DV, Yao Q, et al. Quality of life in the antiarrhythmics versus implantable defibrillators trial: impact of therapy and influence of adverse symptoms and defibrillator shocks. Circulation 2002;105:589–94.
    Crossref | PubMed
  24. Moss AJ, Greenberg H, Case RB, et al. Long-term clinical course of patients after termination of ventricular tachyarrhythmia by an implanted defibrillator. Circulation 2004;110:3760–5.
    Crossref | PubMed
  25. Poole JE, Johnson GW, Hellkamp AS, et al. Prognostic importance of defibrillator shocks in patients with heart failure. N Engl J Med 2008;359:1009–17.
    Crossref | PubMed
  26. Sweeney MO, Wathen MS, Volosin K, et al. Appropriate and inappropriate ventricular therapies, quality of life, and mortality among primary and secondary prevention implantable cardioverter defibrillator patients: results from the Pacing Fast VT REduces Shock ThErapies (PainFREE Rx II) Trial. Circulation 2005;111:2898–905.
    Crossref | PubMed
  27. Moss AJ, Schuger C, Beck CA, et al. Reduction in inappropriate therapy and mortality through ICD programming. N Engl J Med 2012;367:2275–83.
    Crossref | PubMed
  28. Dorian P, Philippon F, Thibault B, et al. Randomized controlled study of detection enhancements versus rate-only detection to prevent inappropriate therapy in a dual-chamber implantable cardioverter-defibrillator. Heart Rhythm 2004;1:540–7.
    Crossref | PubMed
  29. Santangeli P, Muser D, Maeda S, et al. Comparitive effectiveness of antiarrhythmic drugs and catheter ablation for the prevention of recurrent ventricular tachycardia in patients with implantable cardioverter-defibrillators: a systematic review and meta-analysis of randomized contolled trials. Heart Rhythm 2016;13:1552–9.
    Crossref | PubMed
  30. Connolly SJ, Dorian P, Roberts RS, et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC study: a randomised trial. JAMA 2006;292:165–71.
    Crossref | PubMed
  31. Gao D, Van Herendael H, Alshengeiti L, et al. Mexiletine as an adjunctive therapy to amiodarone reduces the frequency of ventricular tachyarrhythmia events in patients with an implantable defibrillator. J Cardiovasc Pharmacol 2013;62:199–204.
    Crossref | PubMed
  32. Pacifico A, Hohnloser SH, Williams JH, et al. Prevention of implantable-defibrillator shocks by treatment with sotalol. N Engl J Med 1999;340:1855–62.
    Crossref | PubMed
  33. Bunch TJ, Mahapatra S, Murdock D, et al. Ranolazine reduces ventricular tachycardia burden and ICD shocks in patients with drug-refractory ICD shocks. Pacing Clin Electrophysiol 2011;34:1600–6.
    Crossref | PubMed
  34. Ranolazine Implantable Cardioverter-Defibrillator Trial (RAID). 2018. Available at: https://clinicaltrials.gov/ct2/show/NCT01215253 (accessed 26 October 2018).
  35. Sapp JL, Wells GA, Parkash R, et al. Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. N Engl J Med 2016;375:111–21.
    Crossref | PubMed
  36. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005;352:225–37.
    Crossref | PubMed
  37. Julian DG, Camm AJ, Frangin G, et al. Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet 1997;349:667–74.
    Crossref | PubMed
  38. Cairns JA, Connolly SJ, Roberts R, et al. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Lancet 1997;349:675–82.
    Crossref | PubMed
  39. Hartzler GO. Electrode catheter ablation of refractory focal ventricular tachycardia. J Am Coll Cardiol 1983;2:1107–13.
    Crossref | PubMed
  40. Tung R, Boyle NG, Shivkumar K. Clinician update: catheter ablation of ventricular tachycardia. Circulation 2011;123:2284–8.
    Crossref | PubMed
  41. Latchamsetty R, Yokokawa M, Morady F, et al. Multicenter outcomes for catheter ablation of idiopathic premature ventricular complexes. J Am Coll Cardiol EP 2015;1:116–23.
    Crossref | PubMed
  42. Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med 2007;357:2657–65.
    Crossref | PubMed
  43. Kuck KH, Schaumann A, Eckhardt L, et al. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet 2010;375:31–40.
    Crossref | PubMed
  44. Dinov B, Fiedler L, Schönbauer R, et al. Outcomes in catheter ablation of ventricular tachycardia in dilated non-ischemic cardiomyopathy in comparison to ischemic cardiomyopathy: results from the Prospective HEart Centre of LeiPzig VT (HELP-VT) Study. Circulation 2014;129:728–36.
    Crossref | PubMed
  45. Nakahara S, Tung R, Ramirez RJ, et al. Distribution of late potentials within infarct scars assessed by ultra high-density mapping. Heart Rhythm 2010;7:1817–24.
    Crossref | PubMed
  46. Bai R, Di Biase L, Shivkumar K, et al. Ablation of ventricular arrhythmias in arrhythmogenic right ventricular dysplasia/cardiomyopathy: arrhythmia-free survival after endo-epicardial substrate based mapping and ablation. Circ Arrhythm Electrophysiol 2011;4:478–85.
    Crossref | PubMed
  47. Santangeli P, Zado ES, Supple GE, et al. Long-term outcome with catheter ablation of ventricular tachycardia in patients with arrhythmogenic right ventricular cardiomyopathy. Circ Arrhythm Electrophysiol 2015;8:1413–21.
    Crossref | PubMed
  48. Verma A, Kilicaslan F, Schweikert RA, et al. Short- and long-term success of substrate-based mapping and ablation of ventricular tachycardia in arrhythmogenic right ventricular dysplasia. Circulation 2005;111:3209–16.
    Crossref | PubMed
  49. Dalal D, Jain R, Tandri H, et al. Long-term efficacy of catheter ablation of ventricular tachycardia in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy. J Am Coll Cardiol 2007;50:432–40.
    Crossref | PubMed
  50. Philips B, Madhavan S, James C, et al. Outcomes of catheter ablation of ventricular tachycardia in arrhythmogenic right ventricular dysplasia/cardiomyopathy. Circ Arrhythm Electrophysiol 2012;5:499–505.
    Crossref | PubMed
  51. Haïssaguerre M, Extramiana F, Hocini M, et al. Mapping and ablation of ventricular fibrillation associated with long-QT and Brugada syndromes. Circulation 2003;108:925–8.
    Crossref | PubMed
  52. Nademanee K, Veerakul G, Chandanamattha P, et al. Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. Circulation 2011;123:1270–9.
    Crossref | PubMed
  53. Dinov B, Arya A, Bertagnolli L, et al. Early referral for ablation of scar-related ventricular tachycardia is associated with improved acute and long-term outcomes: results from the Heart Center of Leipzig Ventricular Tachycardia Registry. Circ Arrhythm Electrophysiol 2014;7:1144–51.
    Crossref | PubMed
  54. Frankel DS, Mountantonakis SE, Ronbinson MR, et al. Ventricular tachycardia ablation remains treatment of last resort in structural heart disease: argument for earlier intervention. J Cardiovasc Electrophysiol 2011;22:1123–8.
    Crossref | PubMed
  55. Tung R, Vaseghi M, Frankel DS, et al. Freedom from recurrent ventricular tachycardia after catheter ablation is associated in improved survival in patients with structural heart disease: an International VT Ablation Center Collaborative Group Study. Heart Rhythm 2015;12:1997–2007.
    Crossref | PubMed
  56. Yu R, Ma S, Tung R, et al. Catheter ablation of scar-based ventricular tachycardia: Relationship of procedure duration to outcomes and hospital mortality. Heart Rhythm 2015;12:86–94.
    Crossref | PubMed
  57. Sadek MM, Schaller RD, Supple GE, et al. Ventricular tachycardia ablation – the right approach for the right patient. Arrhythm Electrophysiol Rev 2014;3:161–77.
    Crossref | PubMed
  58. Koutalas E, Rolf S, Dinov B, et al. Contemporary mapping techniques of complex cardiac arrhythmias – identifying and modifying the arrhythmogenic substrate. Arrhythm Electrophysiol Rev 2015;4:19–27.
    Crossref | PubMed
  59. Bradfield JS, Ajijola OA, Vaseghi M, et al. Mechanisms and management of refractory ventricular arrhythmias in the age of autonomic modulation. Heart Rhythm 2018;15:1252–60.
    Crossref | PubMed
  60. Mahajan A, Moore J, Cesario DA, et al. Use of thoracic epidural anaesthesia for management of electrical storm: a case report. Heart Rhythm 2005;12:1359–62.
    Crossref | PubMed
  61. Bourke T, Vaseghi M, Michowitz Y, et al. Neuraxial modulation for refractory ventricular arrhythmias: value of thoracic epidural anaesthesia and surgical left cardiac sympathetic denervation. Circulation 2010;121:2255–62.
    Crossref | PubMed
  62. Do DH, Bradfield J, Ajijola OA, et al. Thoracic epidural anesthesia can be effective for the short-term management of ventricular tachycardia storm. J Am Heart Assoc 2017;6:e007080.
    Crossref | PubMed
  63. Fudim M, Boortz-Marx R, Ganesh A, et al. Stellate ganglion blockade for the treatment of refractory ventricular arrhythmias: a systematic review and meta-analysis. J Cardiovasc Electrophysiol 2017;28:1460–7.
    Crossref | PubMed
  64. Turagam MK, Vuddanda V, Atkins D, et al. Hemodynamic support in ventricular tachycardia ablation: an International VT Ablation Center Collaborative Group Study. JACC Clin Electrophysiol 2017;3:1534–43.
    Crossref | PubMed
  65. Carbucicchio C, Santamaria M, Trevisi N, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter defibrillators: short- and long-term outcomes in a prospective singe-center study. Circulation 2008;117:462–9.
    Crossref | PubMed
  66. Vergara P, Tung R, Vaseghi M, et al. Successful ventrifcular tachycardia ablation in patients with electrical storm reduces recurrences and improves survival. Heart Rhythm 2018;15:48–55.
    Crossref | PubMed
  67. Haegeli LM, Della Bella P, Brunckhorst CB. Management of a patient with electrical storm: role of epicardial catheter ablation. Circulation 2016;133:672–6.
    Crossref | PubMed
  68. Vakil KP, Roukoz H, Tung R, et al. Mortality prediction using a modified Seattle Heart Failure Model may improve patient selection for ventricular tachycardia ablation. Am Heart J 2015;170:1099–104.
    Crossref | PubMed
  69. Santangeli P, Muser D, Zado ES, et al. Acute haemodynamic decompensation during catheter ablation of scar-related ventricular tachycardia: incidence, predictors, and impact on mortality. Circ Arrhythm Electrophysiol 2015;8:68–75.
    Crossref | PubMed
  70. Santangeli P, Frankel D, Tung R, et al. Early mortality after catheter ablation of ventricular tachycardia in patients with structural heart disease. J Am Coll Cardiol 2017;69:2105–15.
    Crossref | PubMed
  71. Mathuria N, Wu G, Rojas-Delgado F, et al. Outcomes of pre-emptive and rescue use of percutaneous left ventricular assist device in patients with structural heart disease undergoing catheter ablation of ventricular tachycardia. J Interv Card Electrophysiol 2017;48:27–34.
    Crossref | PubMed
  72. Enriquez A, Liang J, Gentile J, et al. Outcomes of rescue cardiopulmonary support for periprocedural acute haemodynamic decompensation in patients undergoing catheter ablation of electrical storm. Heart Rhythm 2018;15:75–80.
    Crossref | PubMed
  73. Chen J, Hocini M, Larsen TB, et al. Clinical management of arrhythmias in elderly patients: results of the European Heart Rhythm Association Survey. Europace 2015;17:314–7.
    Crossref | PubMed
  74. Inada K, Roberts-Thomson KC, Seiler J, et al. Mortality and safety of catheter ablation for antiarrhythmic drug-refractory ventricular tachycardia in elderly patients with coronary artery disease. Heart Rhythm 2010;7:740–4.
    Crossref | PubMed
  75. Barra S, Begley D, Heck P, et al. Ablation of ventricular tachycardia in the very elderly patient with cardiomyopathy: how old is too old? Can J Cardiol 2015;31:717–22.
    Crossref | PubMed
  76. Vakil K, Garcia S, Tung R, et al. Ventricular tachycardia ablation in the elderly: an International Ventricular Tachycardia Center Collaborative Group analysis. Circ Arrhythm Electrophysiol 2017;10:e005332
    Crossref | PubMed
  77. Tzou WS, Tung R, Frankel DS, et al. Ventricular tachycardia ablation in severe heart failure: an International Ventricular Tachycardia Ablation Center Collaboration Analysis. Circ Arrhythm Electrophysiol 2017;10:e004494.
    Crossref | PubMed
  78. Tokuda M, Sobieszcyzk P, Eisenhauer AC, et al. Transcoronary ethanol ablation for recurrent ventricular tachycardia after failed catheter ablation: an update. Circ Arrhythm Electrophysiol 2011;4:889–6.
    Crossref | PubMed
  79. Li A, Hayase J, Do D, et al. Hybrid surgical vs percutaneous access epicardial ventricular tachycardia ablation. Heart Rhythm 2018;15:512–9.
    Crossref | PubMed
  80. Vaseghi M, Barwad P, Malavassi Corales FJ, et al. Cardiac sympathetic denervation for refractory ventricular arrhythmias. J Am Coll Cardiol 2017;69:3070–80.
    Crossref | PubMed
  81. Padeletti L, Arnar DO, Boncinelli L, et al. EHRA Expert Consensus Statement on the management of cardiovascular implantable electronic devices in patients nearing end of life or requesting withdrawal of therapy. Europace 2010;12:1480–9.
    Crossref | PubMed
  82. Liang JJ, Santangeli P, Callans DJ. Long-term outcomes of ventricular tachycardia ablation in different types of structural heart disease. Arrhythm Electrophysiol Rev 2015;4:177–83.
    Crossref | PubMed
  83. Marchlinski FE, Haffajee CI, Beshai JF, et al. Long-term success of irrigated radiofrequency catheter ablation of sustained ventricular tachycardia: post-approval THERMOCOOL VT trial. J Am Coll Cardiol 2016;67:674–83.
    Crossref | PubMed
  84. Stevenson WG, Wilber DJ, Natale A, et al. Irrigated radiofrequency catheter ablation guided by electroanatomic mapping for recurrent ventricular tachycardia after myocardial infarction: the Multicenter Thermocool Ventricular Tachycaradia Ablation Trial. Circulation 2008;118:2773–82.
    Crossref | PubMed
  85. Kamphuis HC, de Leeuw JR, Derksen R, et al. Implantable cardioverter defibrillator recipients: quality of life in recipients with and without ICD shock delivery: a prospective study. Europace 2003;5:381–9.
    Crossref | PubMed
  86. Mark DB, Anstrom KJ, Sun JL, et al. Quality of life with defibrillator therapy or amiodarone in heart failure. N Engl J Med 2008;359:999–1008.
    Crossref | PubMed
  87. Tung R, Shivkumar K. Integrated care for management of ventricular arrhythmias: can a specialized unit and catheter ablation improve mortality? Circulation 2013;127:1354–6.
    Crossref | PubMed
  88. Santangeli P, Rame E, Berati E, Marchlinski F. Management of ventricular arrhythmias in patients with advanced heart failure. J Am Coll Cardiol 2017;69:1842–60.
    Crossref | PubMed