© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
EDITORIAL
Electrical storm in the ICD era
Department of Clinical Electrophysiology, Thoraxcentre Erasmus MC, Rotterdam, The Netherlands
Manuscript submitted 1 February 2005. *Corresponding author. Department of Cardiology, Erasmus MC, Dr. Molewaterplein 40, NL-3015 GD Rotterdam, The Netherlands. Tel.: +31 10 463 2699; fax: +31 10 463 2701. E-mail address: j.mekel{at}erasmusmc.nl
Key Words: electrical storm, implantable defibrillators, antiarrhythmic therapy
Electrical storm (ES), arbitrarily defined as the occurrence of three or more separate episodes of ventricular tachycardia or fibrillation within a 24 h period, remains a difficult clinical entity to manage. The occurrence of multiple episodes in a short time frame has been described in a wide variety of clinical situations, ranging from the early post-myocardial infarction setting to the critically ill post-operative patient (e.g. electrolyte disturbance) to the patient who has an overdose of tricyclic antidepressants.
There is little doubt that most of these patients died suddenly in the pre-implantable cardioverter defibrillator (ICD) era, when not monitored in an intensive or coronary care unit, as many did not survive the first episode of tachycardia. Fortunately, many ventricular arrhythmias (torsades de pointes, polymorphic ventricular tachycardia, even, exceptionally, ventricular fibrillation) can be self-terminating, so that intervention with defibrillation is not always required to survive the initial event.
A patient with an ICD, however, will present with repetitive shocks (or antitachycardia pacing) from the device, a particularly psychologically and emotionally taxing experience, as it is very likely that he survives until he can get to the hospital. In this issue of Europace, Gatzoulis et al., describe a cohort of patients with ICDs in whom ES supervened [1]
. ES occurred in 18.9% of the study population during the 33 month follow-up period. The demographics of patients with ES differed from those without ES, they were on an average 5 years older, with a more advanced New York Health Association (NYHA) classification (2.4 ± 0.7 vs. 2.1 ± 0.7). Patients with ES also tended to have a lower left ventricular ejection fraction (LVEF). In logistic regression analysis only an advanced NYHA classification and the occurrence of ES were independently associated with an increased mortality. This message is not completely new, but its importance remains underestimated [2].
This report brings to 6 the number of publications focusing on the influence of ES on mortality in ICD recipients [3–7]. Four of these studies [1,3,6,7] report an increase in mortality associated with ES while the other two report no such association [4,5]. However, the larger two of these studies [6,7] with a combined patient total of 2485 both report a significantly increased mortality in patients with ES. The electrical storm could almost always be controlled. In all these studies the mode of death, responsible for the excess mortality is invariably pump failure, reflecting the more severe heart failure and lower ejection fraction (EF) associated with the development of ES. Also, in the recent DINAMIT study, patients receiving an ICD have reduced arrhythmic death, but die in another way, namely heart failure [8]. This points to a relation between multiple shocks and heart failure, so that the chicken and egg story returns...
The management challenge presented by ES in patients with ICDs is substantial and clinicians are likely to encounter it ever more frequently as the number of ICD implantations continues to increase due to a combination of the ever-broadening indications for implantation and the ageing of the population with the commensurate increase in the prevalence of coronary artery disease and heart failure.
As with most arrhythmias there is substantial variation in the relative contribution of the components of the triad of substrate, trigger and modulating factors and every patient presenting with ES should be evaluated thoroughly with a careful search for trigger factors such as electrolyte imbalance or recurrent ischaemia. If these are present and treated appropriately the ES may subside without a need for specific antiarrhythmic therapy [9]. Unfortunately, reversible triggers are found only in a minority of patients who present with ES, as was once again confirmed in the study by Gatzoulis et al., in which 28 of the 32 patients presenting with ES had no evident precipitating factor.
Which antiarrhythmic drug to choose is based on the underlying heart disease, presence and severity of associated heart failure, associated medical disease and the side effects one may expect to develop in an individual patient.
Amiodarone remains the mainstay of therapy despite its poor side effect profile with the evidence, in this condition, from one trial which showed that the outcome during resuscitation is better when the drug is given intravenously [10].
Class 1 agents have repeatedly been used, with variable rates of success, and can play a role in polymorphic arrhythmias [11]. Beta-blockers have proven their usefulness, and careful titration in patients with heart failure is necessary, as the influence of the sympathetic nervous system is often underestimated [12–14] Adequate sedation and in extremely refractory cases even general anaesthesia may prove to be life-saving [14–16]. Catheter ablation is now established for monomorphic arrhythmias, and is promising for ventricular fibrillation [17,18]. If all else fails, haemodynamic support or even heart transplantation may be an option. Most patients are not suitable candidates for the latter because of their age or comorbidity. Furthermore, the limited supply of donor organs severely limits the applicability of this treatment.
The recently published SHIELD trial shows that azimilide is effective in reducing shocks, without affecting mortality [19]. This implies that we suddenly may have an additional option, if the product is released on the market. We believe, that the existing data on ES strongly support the addition of new agents to our poor antiarrhythmic drug arsenal. Preventing further episodes by adjusting general therapy (statins, ACE inhibitors) or with measures to prevent atrial fibrillation is a wise next step [20,21]. Atrial fibrillation can trigger shocks, and subsequently initiate ES [22]. SHIELD dealt with all ICD interventions, so part of the efficacy of azimilide might be due to its effect on atrial fibrillation.
The report by Gatzoulis et al. is important in that it highlights the influence of ES occurrence on the prognosis of the patient and has analysed trigger factors for ES. It does not bring us a strategy for coping with the problem. Prospective studies in this area are warranted, but might be difficult to undertake.
Preventing a difficult and protracted death in patients with advanced cardiac disease can sometimes be achieved. This requires an understanding of heart failure, knowledge of antiarrhythmic and other drug therapy, sometimes employing catheter intervention, usually catheter ablation. Ischaemia and other triggers, although not common, should be corrected if present.
References
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