electrical storm: clinical management
TRANSCRIPT
A.S. Kibos et al. (eds.), Cardiac Arrhythmias, DOI 10.1007/978-1-4471-5316-0_23, © Springer-Verlag London 2014
Definition
The term “electrical storm” (ES) was introduced in the 1990s to describe a life-threatening cardiac syndrome involving incessant or frequently recurrent ventricular fibrillation (VF) or hemody-namically destabilizing ventricular tachycardia (VT) [1, 2]. It is an emergency medical condition associated with increased mor-tality, requiring electrical cardioversion or defibrillation and treatment of underlying causes in the intensive care unit.
Electrical storm is defined as three or more sustained epi-sodes of VT, VF, or appropriate implantable cardioverter- defibrillator (ICD) shocks during a period of 24 h [3–5]. Nowadays, with the availability and proven efficacy of ICDs for primary and secondary prevention of sudden cardiac death (SCD), ES does not necessarily imply hemodynamic instabil-ity since antitachycardia pacing (ATP) or shock delivered by the ICD device may prevent the hemodynamic compromise of these patients. An inappropriate intervention of the ICD does not count for the episodes defining an ES. On the other hand, the episodes of VT/VF should be intermittent (Fig. 23.1), meaning that the persistence of the ventricular arrhythmia after an unsuccessful intervention of the ICD is not regarded as a second episode. Moreover, when sustained VT resumes immediately (≥1 sinus cycle and within 5 min)after a technically successful therapy, it is regarded as a severe form of ES, while repetitive VTs within the first week after ICD implantation should not be considered as an ES [6].
Incidence, Triggers, Risk Factors, and Prognosis
Over the last decades, several studies, which have been car-ried out to determine the incidence, triggers, and risk factors of ES in various populations, reported highly variable results
(Table 23.1). Electrical storm tends to develop in the pres-ence of myocardial ischemia or worsening heart failure, and it is estimated to occur in 10–20 % of ICD recipients, depending mainly on the duration of the observational study period. The reported incidence of ES in the ICD patients var-ies from 4 % (primary prevention) to 10–28 % (secondary prevention) [20–22]. Approximately 50–70 % of ICD patients receive appropriate device-based therapies within 2 years following ICD implantation, and the onset of ES after an ICD implantation varies according to myocardial substrate, pharmacologic treatment, and indications for device implantation.
A number of well-known precipitating factors increase the electrical instability of the heart, e.g., myocardial isch-emia, electrolyte disturbances, decompensation of heart fail-ure, fever, hyperthyroidism, and proarrhythmic side effects of antiarrhythmic drugs. Although frequently undetectable, transient aberrations in the electrophysiological substrate of affected patients may occur. Credner et al. [5] demonstrated that triggers for ES can be identified in 26 % of patients, and Hohnloser et al. [14] (SHIELD trial) found that ES was pre-cipitated by new or worsened congestive heart failure in 9 % and by electrolyte disturbances in 4 % of patients. Nevertheless, certain trials report that triggers are identifi-able in 65 % or even 71 % of patients presenting with an ES [9, 13], underlying the role of adrenergic activation (increased incidence during daytime hours, patients with reduced baro-reflex sensitivity), emotional stress, and seasonal occurrence (winter and summer preponderance).
Apart from conflicting results about triggers, risk fac-tors for ES are also difficult to identify. Brigadeau et al. [8] reported that patients predisposed to ES are those with severely compromised left ventricular ejection fraction (LVEF), chronic renal failure (CRF), older age, VT as presenting arrhythmia, and absence of lipid-lowering drugs. Ventricular fibrillation as presenting arrhythmia and surprisingly enough, diabetes mellitus appear more frequently in the ES-free patients, although such a para-doxical effect of diabetes was argued in the SCD-HeFT
Electrical Storm: Overview
Sofia Metaxa, Spyridon Koulouris, and Antonis S. Manolis
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S. Metaxa, MD • S. Koulouris, MD • A.S. Manolis, MD (*) Department of Cardiology, Evagelismos General Hospital of Athens, Athens, Greecee-mail: [email protected]
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study [23]. The relation of CRF with ES has also been demonstrated in patients admitted in the coronary care unit by Soman et al. [24]; a relative risk 2.07 of sustained VT was found for patients with CRF compared with patients with normal renal function, while patients with CRF and prior myocardial infarction had a higher arrhyth-mic mortality.
Patients experiencing ES have a poor outcome, suggest-ing that ES might be an independent risk factor for cardiac death. In the AVID trial, patients with ES had an increased
risk of sudden noncardiac death, and in the MADIT-II sub- study, patients with ES had a 7.4-fold higher risk of death during the first 3 months after the ES than patients without ES [20]. It is unclear whether ES contributes directly to a poor outcome or it is simply an epiphenomenon of advanced structural heart disease; shocks may provoke myocardial damage, inflammation, and remodeling leading to progres-sion of heart failure. On the other hand, malignant arrhyth-mias may constitute the initial manifestation of irreversible heart failure [21].
Fig. 23.1 Electrical storm in an ICD patient with ischemic cardiomyopathy
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Electrocardiographic Classification of Electrical Storm
Electrical storm has been described during the acute phase of myocardial infarction (MI), in patients with postinfarction coronary artery disease and in various other forms of cardio-myopathy, valvular disease, surgically corrected congenital heart disease, and genetically determined cardiac diseases, e.g., Brugada syndrome [22]. The clinical presentation isoften dramatic, involving cardiac arrest or major symptoms like palpitations, dizziness, and often syncope.
Admission to the hospital is the most important step in the care of ES patients (required in approximately 80 % of patients, 100 % for patients with >3 shocks) [9] to ensure critical care management of a compromised airway, post- shock bradycardia, hypotension, ischemia, and defibrillation of symptomatic or hemodynamically unstable patients. Patients who are hemodynamically stable can be treated with antiarrhythmic medications, while patients with poor LVEF or rapid VT may require multiple electrical cardioversions or defibrillations.
According to the surface electrocardiogram (ECG), ES can present with one of the three following major morpholo-gies: monomorphic VT (86–97 %), polymorphic VT, and VF which are unusual cases (1–7 %) [6, 20].
Monomorphic Ventricular Tachycardia
Monomorphic VT occurs when ventricular activation sequence is the same without any variation in the QRS com-plexes. It presents in ischemic or nonischemic cardiomyopa-thy due to electrical wave front reentry around a fixed anatomic barrier, most commonly scar tissue after MI. It does
not require active ischemia as a trigger. The burden of ven-tricular arrhythmias is higher when inadequate reperfusion or large areas of infarction are present. The surface ECG mor-phology depends upon the location of the scar and the exit site into the ventricle. The clinical presentation of monomor-phic VT depends upon ventricular rate, LV function, presence of heart failure, loss of atrioventricular synchrony, and the pattern of ventricular activation [25]. It is usually managed pharmacologically with β-blockers and amiodarone.
Polymorphic Ventricular Tachycardia
Polymorphic VT is characterized by beat-to-beat variations in the QRS complexes and is associated with a normal or a prolonged QT interval in sinus rhythm. It usually appears in acute ischemic syndromes (during the first 72 h of ischemia, unless the patient had a previous MI which created a sub-strate for reentry), acute myocarditis, or hypertrophic cardio-myopathy. It may also occur in the absence of organic heart disease. During an acute MI various mechanisms (ischemia, altered membrane potential, triggered activity, necrosis, or scar formation) result in polymorphic VT, and the most effective treatment is to abolish ischemia with emergency coronary revascularization, thrombolytic agents, and anti- ischemic/antiplatelet agents. In addition, the use of beta- blockers and certain antiarrhythmic agents (lidocaine, amiodarone) has been proven of great value.
Patients with polymorphic VT should have their baseline ECG carefully evaluated for a prolonged QT interval. Torsades de pointes is pause-dependent polymorphic VT with a long QT interval associated with certain risk factors like female gender, bradycardia, heart block, QT-prolonging drugs (sotalol, ibutilide, quinidine, haloperidol, methadone,
Table 23.1 Incidence of electrical storm
Author (ref) Patients Definition (VT/VF) Follow-up (months) Incidence (%)
Arya et al. [7] 126 >3 14.3 ± 10 14Brigadeau et al. [8] 307 >2 28 ± 10 40Bansch et al. [9] 106 >3 33 ± 23 28Credner et al. [5] 136 >3 13 ± 7 10Exner et al. [4] 457 >3 31 ± 13 20Fries et al. [10] 119 >2 36 ± 18 60Gasparini et al. [11] 631 >3 19 ± 11 7Gatzoulis et al. [12] 169 >3 33 ± 26 19Greene et al. [13] 222 >3 34 ± 31 18Hohnloser et al. [14] 633 >3 2–12.3 23Sesselberg et al. [15] 719 >3 48 4Stuber et al. [16] 214 >3 39.6 ± 26.4 24Verma et al. [17] 2,028 >2 22 ± 5 10Villacastin et al. [18] 80 >2 21 ± 19 20Wood et al. [19] 31 >3 7.5 ± 6.1 10
23 Electrical Storm: Overview
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erythromycin, etc.), hypokalemia, hypomagnesaemia, and inherited long QT syndrome. In the case of bradycardia or heart block, torsades de pointes should be managed with temporary overdrive pacing and implantation of a permanent pacemaker in refractory cases. Intravenous magnesium administration is a reasonable therapy for polymorphic VT with a long QT interval along with potassium repletion (serum level above 4.5 mmol/L).
Ventricular Fibrillation
VF is characterized by chaotic activation on ECG which may recur repeatedly despite defibrillation. When VF presents as ES, mortality rates are high (85–97 %) and ischemia is the primary related mechanism. ES associated with Brugada syndrome is a seldom reported, potentially lethal, event.
Brugada syndrome accounts for 4 % of all sudden deaths and for 20 % of sudden deaths in those without structural heart disease and is one of the leading causes of sudden death in subjects under the age of 40 years. It is an inherited electrical disorder caused by a defective cardiac sodium-channel gene, diagnosed clinically by its characteristic ECG patterns. It requires aggressive treatment when presented as an ES [26]. In most of the cases, continuous infusion of isoproterenol termi-nates ES and completely normalizes ST-segment elevation [27]. Oral antiarrhythmic therapy may be required because attempts to wean patients from isoproterenol may result in recurrent VF. Although class I antiarrhythmic agents are potent sodium-channel blockers and are contraindicated in patients with Brugada syndrome, yet quinidine has prevented ventricu-lar arrhythmias in these patients and is a recommended therapy for refractory cases of ES caused by Brugada syndrome [20].
Pharmacologic Therapy for Electrical Storm
The clinical management of ES can be very challenging. Various pharmacologic therapies have been proposed, yet mortality remains extremely high.
Adrenergic Blockade
The cornerstone of ES treatment is the reduction of elevated sympathetic tone by beta-blockers or non-pharmacologic inter-ventions. It has been known for years that ischemia or infarc-tion and reperfusion can trigger cardiac reflexes (acute inferoposterior MI may result in bradycardia, whereas anterior MI more frequently provokes tachycardia) [28]. Nevertheless, ischemia can also inhibit these reflexes; it has been reported that several minutes after the initiation of transmural myocar-dial ischemia, sympathetic reflexes become interrupted or
attenuated, while non-transmural ischemia attenuates vagal vasodepressor response [29]. Along with ischemia-produced efferent sympathetic denervation, a complex mechanism is responsible for the sympathetic supersensitivity [30]. Sympathetic supersensitivity elicits inhomogeneous autonomic and electrophysiological changes and makes the heart more vulnerable to the induction of ventricular arrhythmias [31].
Experimental studies have shown that beta-blockers increase the fibrillation threshold sixfold under ischemic and nonischemic conditions, and potent nonselective beta- blockers have been proven more effective in decreasing sympathetic outflow, perhaps because β2-receptors prevail in the failinghearts [32]. According to Lombardi et al. [33], sympathetic activity is reflexively increased during myocardial ischemia, resulting in decreased VF threshold in the case of coronary artery occlusion, and Schwartz et al. [34] demonstrated that pharmacologic or surgical antiadrenergic interventions prevent sudden cardiac death in high-risk post-MI patients. Nademanee et al. [35] investigated sympathetic blockade (esmolol, pro-pranolol, left stellate ganglion blockade) versus the antiarrhyth-mic therapy (lidocaine, procainamide, bretylium) recommended by the American Heart Association Advanced Cardiac Life Support (ACLS) guidelines and found that short-term outcome is much better in patients treated with sympathetic blockade (1-week survival 82 % for sympathetic blockade and 22 % for antiarrhythmic therapy), while patients who survived the first week after the onset of ES continued to do well during the 1-year follow-up period (1-year survival 67 % for sympathetic blockade and 5 % for antiarrhythmic therapy).
The finding that sympathetic blockade dramatically reduces mortality rates is in accordance with the evidence that beta-blockers prevent ventricular tachyarrhythmias in post-MI patients, while the Beta-Blocker Heart Attack Trial confirmed that the more severe the left ventricular dysfunc-tion, the more beneficial β-blockade is [36, 37]. Variousbeta-blockers have been studied in the treatment of ES. Metoprolol (oral β1-blocker) inhibits ventricular arrhythmiasin patients with acute MI [38, 39] and should be given in high doses (>200 mg/day) [40]. Propranolol, an oral nonse-lective beta-blocker, has been proved more effective than metoprolol in establishing electrical stability (doses ~400 mg/day) [41] but requires careful monitoring because it can exacerbate heart failure in patients with poor systolic function. Esmolol and landiolol are selective β1-blockerswith short plasma half-lives (esmolol 9 min, landiolol 4 min) given intravenously, suitable for emergency medical care of ES [35, 42]. Carvedilol (multi-acting β-blocker that blocksα-receptors) and bisoprolol (pure β1-blocker) are also appro-priate oral beta-blockers for patients in ES [42]. It has been suggested that the combination of a beta-blocker with amio-darone is the mainstay of therapy for patients with ES. Indeed in the OPTIC trial which included high-risk ICD patients, electrical discharges were delivered in 38.5 % of patients on
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beta-blockers, in 24.3 % of patients on sotalol, and in only 10.3 % of patients who were taking beta-blocker combined with amiodarone [20, 35, 42–44].
Antiarrhythmic Agents
Amiodarone is widely used in the treatment of ES, both for the termination and the prevention of ES recurrences. The electro-physiological effects of amiodarone are complex. In the acute phase of ES, rapid intravenous administration of amiodarone blocks inward sodium (class I effect) and calcium (class IV effect) currents and has a noncompetitive alpha- and beta-blockade effect (class II effect), while during chronic adminis-tration, it inhibits outward potassium currents (class III effect), resulting in prolongation of action potential duration and pro-longation of the effective refractory period [45]. The ARREST and the ALIVE studies were two randomized clinical trials which demonstrated the efficacy of amiodarone in the termi-nation of ventricular arrhythmias. Amiodarone improved sur-vival-to-hospital admission rates in patients who had an ES (VF or pulseless VT) and resolved ES at approximately 60 % [20, 46, 47]. Levine et al. [48] examined 273 hospitalized patients with ES refractory to lidocaine, procainamide, or bre-tylium therapy and suggested that when amiodarone was given, 46 % of the patients survived for 24 h without other episodes of VT and 12 % of patients responded to the admin-istration of amiodarone plus another agent. Although certain concern has been expressed regarding the increase in defibril-lation threshold due to amiodarone, the combination of amio-darone with beta-blocker and mexiletine (class Ib agent, decreases action potential duration by shortening the repolar-ization phase) particularly in resistant cases seems to be an alternative and effective therapeutic choice [12, 49, 50].
Apart from amiodarone, sotalol is another class III antiar-rhythmic agent (a relatively weak β-blocker as well) used totreat patients with ES as monotherapy or in combination with other antiarrhythmic agents [51, 52]. Sotalol was found to be an effective antiarrhythmic agent in the ESVEM trial [53], but in the SWORD trial [54], d-sotalol was associated with excess mortality for patients surviving MI with left ven-tricular dysfunction, and thus, its clinical use since then has been rather limited. Nifekalant hydrochloride is a novel class III agent developed in Japan, which has attracted much atten-tion in recent years due to its efficacy in suppressing ven-tricular tachyarrhythmias without aggravating the patient’s hemodynamic stability. It selectively blocks IKr, can only be used intravenously, has a relatively short half-life, has no negative inotropic effects, and does not affect cardiac con-duction. The true functional mechanism of nifekalant is still unclear; in electrophysiological studies nifekalant has been shown to inhibit or prevent reentrant VT in humans and aggravate adrenaline-induced arrhythmias (due to abnormal
automaticity and/or triggered activity) [55]. In clinical prac-tice, nifekalant has been proven effective and safe for severe ES cases refractory to amiodarone [56–58].
Azimilide is another class III antiarrhythmic agent, devel-oped for treating both supraventricular and ventricular tachyarrhythmias, that prolongs repolarization in a dose- dependent manner by increasing the action potential dura-tion, QT interval, and effective refractory period [59]: in the SHIELD trial, azimilide was proven effective in reducing the incidence of ES in patients with implantable cardioverter- defibrillators (reduction of recurrent ES by 37 and 55 % in doses of 75 and 125 mg/day respectively) [14, 60]. Bretylium, a class III antiarrhythmic which blocks K+ channels and the release of noradrenaline from nerve terminals, was found effective in the treatment of ES in certain cases, but its use is not currently recommended due to its frequent adverse effects (especially hypotension) [61, 62].
According to the 2006 American College of Cardiology/American Heart Association guidelines for treating ventricu-lar arrhythmias, intravenous lidocaine (class Ic) has a IIb rec-ommendation for the treatment of polymorphic VT associated with ischemia [63]. On the other hand, procainamide (class Ia), which blocks fast sodium channels and prolongs cardiac action potential, is a reasonable choice for terminating monomorphic VT but may cause hypotension or prolong the width of QRS complex by more than 50 %, resulting in the discontinuation of the drug [20]. Although ES is a rare phe-nomenon in Brugada syndrome, there are data suggesting that isoproterenol and orciprenaline (β-adrenergic stimula-tors) are effective in terminating ES and improving the elec-trocardiographic pattern of Brugada syndrome, while quinidine/hydroquinidine prevent the recurrence of VF dur-ing the electrophysiological study [26, 64–66].
Apart from adrenergic blockade and antiarrhythmic treat-ment, sedation or even general anesthesia/intubation is involved in the treatment of ES due to induction of central inhibition of the cardiac sympathetic drive. The physical and emotional stress experienced during ES often perpetuate arrhythmias; short-acting anesthetics such as propofol, benzodiazepines, and other agents of general anesthesia have been associated with conver-sion and suppression of ES [67, 68]. Further studies are needed to determine which sedative and anesthetic agents should be used and whether they have direct antiarrhythmic effects.
Non-pharmacologic Therapy for Electrical Storm
The suppression of malignant arrhythmias is achieved by various non-pharmacologic measures including the implant-able cardioverter defibrillator, radiofrequency catheter abla-tion, cardiac resynchronization therapy, intra-aortic balloon pumping, and cardiac sympathetic denervation.
23 Electrical Storm: Overview
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Implantable Cardioverter-Defibrillators
Sudden cardiac death (SCD) is a common cause of death throughout the world. The implantation of ICDs for primary prevention of SCD affects two major patient groups: patients whose LVEF is less than or equal to 40 % as a result of prior MI, with spontaneous non-sustained VT and sustained monomorphic VT (SMVT) inducible by EP testing [69], and patients whose LVEF is less than 35 % as a result of MI (which has occurred at least 40 days earlier) with NYHA functional class II or III symptoms [23]. For patients experi-encing cardiac arrest due to VF (not within the first 48 h of acute MI) or sustained VT, the implantation of an ICD refers to secondary prevention [63]. Although ICDs reduce mortal-ity in patients at high risk for arrhythmic death compared with antiarrhythmic drugs, recurrent arrhythmias occur in 40–60 % of ICD recipients over the initial 3 years of follow- up, and ES ranges from 4 % (primary prevention) to 10–28 % (secondary prevention) [70].
Various studies have demonstrated that ES is not rare in the “real world” population with ICDs [5]. Patients with an ICD have increased risk of developing ES due to their typi-cally impaired left ventricular systolic function or history of previous VT. The rate of ES recurrences is high (50.8 %) within the first year after the initial event, and its incidence is 6.6 % during an average follow-up of 4.5 years [70]. Data suggest that VF as the index arrhythmia or a structurally nor-mal heart protect against ES, while dilated cardiomyopathy and old age (patients above the age of 65 years revealed a 2.6-fold higher risk) are independent predictors of ES [70, 71]. Although the development of VT/VF is not associated with increased risk of subsequent death, ES is an important and independent marker of increased mortality, particularly within the first 3 months after its occurrence. Evidence suggests that multiple shocks due to ES lead to elevation of cardiac troponin levels, indicative of minor degrees of myocardial injury, inflammation, and fibrosis which are associated with progressive ventricular dysfunc-tion, cardiac apoptosis, and arrhythmia facilitation contribut-ing to excess mortality [4].
Soon after the occurrence ES in a patient who carries an ICD, interpretation of stored electrograms should be performed depending on device filters, amplifiers, and com-pression algorithms in order to determine inappropriate ther-apies (e.g., supraventricular tachycardia, noise). In some cases, it is difficult to distinguish VT from VF in the absence of a surface ECG because the type of arrhythmia is mainly classified according to its morphology (monomorphic sig-nals or not) and cycle length. ICD reprogramming is an issue of major importance; data suggest that antitachycardia pac-ing (ATP) can successfully terminate a significant percent-age of fast VTs in a harmless and pain-free way, providing a good quality of life [72]. Nevertheless, subclinical
termination of VT by ATP may lead to an underestimate of the true incidence of ES since the patients do not seek medi-cal assistance or hospitalization after such an event. Other safety features of the device should also be reprogrammed; prolongation of the time window (30 s altered to 2–5 min) to allow spontaneous termination of VT has been proposed, according to the DEFINITE trial which supported the con-cept that many VT episodes do not need to be treated [73]. Moreover, unnecessary right ventricular pacing in ICD patients may have a detrimental impact upon myocardial contractility functioning, acting as a trigger for ES. This could be prevented by using alternative right ventricular pac-ing sites and appropriate programming [74]. Apart from ICD interrogation, a thorough evaluation of the ICD patient should be performed to decide about other therapeutic strate-gies including catheter ablation.
Catheter Ablation Therapy
Episodes of ES are a marker of increased mortality and worsen the quality of life in patients with structural heart dis-ease and ICDs. Advances in technology and in our under-standing of VT substrates allow radiofrequency ablation of VTs of various origins and even of hemodynamically unsta-ble ones, with acceptable efficacy and safety. According to the recent EHRA/HRS guidelines on catheter ablation (CA) of ventricular arrhythmias, ablation of VT (associated with ES) is recommended for symptomatic sustained monomor-phic VT or VT terminated by an ICD, despite antiarrhythmic drug therapy or when antiarrhythmic drugs are not tolerated or desired, and sustained monomorphic VT or VT storm not provoked by a transient reversible cause [75]. Prophylactic VT ablation in patients with ICDs (implanted for primary or secondary prevention) is investigational and only rarely performed.
Some type of preprocedural imaging is necessary for patients who undergo ablation therapy; echocardiography, CT/MRI, coronary angiogram, or recent exercise/pharmaco-logic stress evaluation will be required to exclude reversible causes and define hemodynamic tolerance during VT. When scar-related VT is suspected, imaging can be used to charac-terize the location/extent of the myocardial scar that is likely to contain the VT substrate. Transesophageal or intracardiac echocardiography, for operators experienced with their use, are helpful to detect an LV thrombus. Antiarrhythmic drug therapy should be discontinued for four to five half-lives before the procedure for idiopathic VTs, while patients with significant structural heart disease usually undergo catheter ablation under pharmaceutical therapy; in fact, intravenous amiodarone or procainamide may slow the rate of VT and convert pleomorphic to a more stable monomorphic VT. Careful consideration should be taken to lower the significant
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risks of ablation, which may include cardiac tamponade (1 %), vascular injury (2 %), thromboembolism, air embo-lism, damage to the conduction system or to coronary arter-ies, or decompensation of heart failure. In patients with scar-related VT, particularly after MI, heart failure accounts for more than one-third of mortality during follow-up after ablation and exceeds 10 % per year in some studies [75].
Multiple VT morphologies are usually inducible in the same patient due to multiple reentry circuit pathways com-plicating mapping and ablation procedure. Selection of the strategies for ablation is based upon the type and severity of the underlying heart disease, characteristics of the VT, and available technologies. The standard approach is endocar-dial; few experienced centers perform epicardial ablation; only 21 % of the centers apply epicardial approach initially, 62 % use it after failure of the endocardial approach, and 36 % have never performed epicardial approach [76], while surgical ablation of VT and intracoronary ethanol ablation exist as options but are rather rarely used. The most common ablation strategy is substrate mapping and ablation (fre-quently used by the 63 % of arrhythmia centers), performed by creation of connecting lines (from scar to anatomical boundaries, between scars, or within a scar – 75 % of cen-ters) and by targeting late and fractionated potentials around and within scars (70 %). It is reported that 25 % of the cen-ters frequently perform the ablation with conventional cath-eters, while modern electroanatomical tools (CARTO or NavX systems) are altogether used by 90 % of centers, and noncontact mapping or remote navigation is used only by a minority of them [76].
Different centers report varying outcomes of ablation therapy (Table 23.2) depending on disease severity, stability of VTs for mapping, methods for mapping, and ablation or ablation endpoints [77–79]. Kozeluhova et al. [80] found that catheter ablation was effective in suppression of ES in 84 % of cases but repeated procedures were necessary in 13 out of 50 patients. They defined several predictors of adverse out-come within the first 6 months after the procedure including severely depressed LVEF, significantly dilated LV, renal insufficiency, and ES recurrence after previous ablation pro-cedure although they underlined that testing of VT induc-ibility after the procedure is not predictive of ES recurrences during follow-up. The Multicenter Thermocool Ventricular
Tachycardia Ablation Trial enrolled 231 patients with recur-rent VT for ablation with the use of an electroanatomical mapping system using substrate and/or entrainment mapping approaches [81]; ablation abolished at least one VT in 81 % of patients and all VTs in 49 % of patients, while 47 % of patients had recurrent VT during the following 6 months. In 142 patients with an ICD, >75 % reduction of the VT epi-sodes were demonstrated in 67 % of patients. During a 1-year follow-up period, mortality was 15 % (38 % due to ventricu-lar arrhythmias and 35 % due to heart failure). The Euro-VT Study performed catheter ablation in 63 patients with a median of 17 VT episodes in the 6 months prior to ablation and found that the mean number of ICD therapies was decreased from 60 ± 70 prior to ablation to 14 ± 15 6 months after the procedure [82]. According to the findings of the Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH-VT) multicenter study, 33 % of the control group but only 12 % of the ablation group received appropriate ICD therapy for VT or VF during an average follow-up period of 23 months [83]. Although catheter ablation can be immediately lifesaving for patients with ES, it is not indicated prophylactically; nevertheless, it has been suggested that sustained ST-segment elevation and abnormal Q waves could be a risk factor for ES in patients with structural heart disease leading to empiric ablation, but further studies are needed to confirm such a report [84].
Cardiac Resynchronization Therapy
Cardiac resynchronization therapy (CRT) has been recom-mended as a class IA indication by both heart failure (HF) and pacing guidelines for advanced HF patients (NYHA III/IV) with QRS ≥120 ms, ejection fraction (EF) ≤35 %, andsinus rhythm refractory to optimal pharmaceutical treatment [85]. Cardiac resynchronization therapy improves symp-toms, exercise capacity, functional class, ventricular func-tion, and ventricular geometry in patients with moderate-to-severe congestive heart failure and ventricular conduction system abnormalities, while the combination of CRT with an ICD (CRT-D) reduces all-cause mortality [86].
Decompensation of heart failure has been identified as a trigger for ES in certain studies, but electrophysiological
Table 23.2 Catheter ablation therapy
Patients Follow-up (months) Acute prevention of VT (%) Recurrence of VT/ES (%)
Della Bella et al. [77] 218 17.3 ± 18.2 71.6 31.4/−Carbucicchio et al. [78] 95 22 89 34/8Peichl et al. [79] 9 13 ± 7 89 −/11Stevenson et al. [81] 231 6 81 47/−Tanner et al. [82] 63 12 ± 3 81 49Kozeluhova et al. [80] 50 18 ± 16 84 −/26
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effects of CRT are still poorly understood and need to be fur-ther clarified. Some studies demonstrate a decreased incidence of VTs after CRT, but several case reports underline the occur-rence of VT, VF, or ES after biventricular pacing managed by conventional therapy or temporary discontinuation of left ven-tricular pacing. Nevertheless the incidence is low, between 3.4 and 4 %, mainly in patients with ischemic cardiomyopathy, and occurs more frequently within the first h or days of biven-tricular pacing [87–89]. Combes et al. [90] presented a case of severe ES after CRT-D implantation treated with atrioventric-ular delay optimization that led to suppression of VT without the need to turn off LV pacing; it was suggested that LV pacing reverses the direction of transmural activation of LV wall and modifies input to a reentrant circuit leading to VT. Modification of global LV depolarization by modifying CRT programming possibly changes activation around the scar, modifies the sub-strate, and suppresses the arrhythmia.
Nordbeck et al. [91] analyzed the incidence of ES in 561 ICD patients and 168 consecutive patients with a CRT-D device with a mean follow-up period of 41 months and con-cluded that ES was much less common in CRT-D patients than in ICD patients (0.6 % vs. 7 %, P < 0.01). They also found that the risk for clustered shocks was clearly elevated for ICD patients with concomitant severe heart failure, but this risk was not elevated for patients treated with CRT-D. Similarly, the TOVA trial demonstrated that class III HF is an important predictor, along with LVEF, of appropriate device discharges in ICD patients [92]. According to Kowal et al. [93] chronic biventricular pacing (BV) results in reduced incidence of ventricular arrhythmias due to its beneficial electrophysiological properties; 18 patients with coronary artery disease were randomized to right ventricular (RV) vs. biventricular (BV) programmed electrical stimulation (PES), and BV-PES was found to be associated with a significant reduction in the induction of monomorphic VT but with no significant effect on VF induction.
Intra-aortic Balloon Pump (IABP)
The suppression of malignant arrhythmias is an acceptable indication for placing an intra-aortic balloon pump (IABP). Intra-aortic balloon pumping improves coronary flow, reduces myocardial distention, stabilizes hemodynamic sta-tus, and relieves the ischemic substrate, thus potentially influencing ventricular irritability by direct and indirect effects [94]. Mechanical support is of potential benefit in patients with end-stage heart failure who poorly tolerate neg-ative inotropic agents and patients under hemodynamic com-promise due to the arrhythmia itself or the administration of antiarrhythmic agents. The mechanism by which IABP helps control ES is unclear, but several possible effects have been suggested. Augmentation of coronary blood flow and
myocardial oxygen supply reduces the potential for ischemia which contributes to arrhythmogenesis; hemodynamic sup-port reduces adrenergic stimulation and its proarrhythmic effects; and numerous studies in both isolated tissue and intact animal hearts have shown that alterations in preload and afterload result in arrhythmogenesis, leading to the con-cept of mechano-electrical feedback [95]. In concordance with such a concept, implantation of a left ventricular assist device was performed successfully as an alternative salvage technique for ES caused by an open heart surgery in a 38-year-old man [96].
Invasive Adrenergic Blockade
Cardiac sympathetic denervation (CSD) decreases the inci-dence of ventricular arrhythmias. In humans left CSD may be ineffective promoting thus the bilateral CSD which is nev-ertheless very rarely performed and its safety is largely unknown. Ajijola et al. [97] reviewed six cases undergoing bilateral CSD and observed complete response in 66.7 % of patients, partial response in 16.7 %, and no response in 16.7 %, but serious postoperative complications were observed in two patients (heart failure and poor tolerance of single-lung ventilation during surgery). Left stellate gan-glion blockade, a safe and effective procedure used for a variety of chronic pain and vascular syndromes, has been documented as an alternative treatment for drug-resistant ES; apart from decreasing sympathetic activity, it also short-ens QTc interval, thus reduces the risk of cardiac arrhyth-mias [98, 99]. Renal sympathetic denervation, a novel catheter-based technology for treatment of refractory arterial hypertension, has been shown to reduce whole-body norepi-nephrine spillover by 42 % and efferent muscle sympathetic nerve activity by 66 % [100]. Uneka et al. [101] studied two patients who underwent renal denervation leading to reduc-tion of ventricular arrhythmias without any apparent hemo-dynamic complications, but obviously, only randomized and controlled trials would justify such a promising strategy for clinical use.
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23 Electrical Storm: Overview
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