El-Sherif, Nabil

English

Via Medica Journals

EDITORIALCardiology Journal2007, Vol. 14, No. 4, pp. 326–328Copyright © 2007 Via MedicaISSN 1897–5593326 www.cardiologyjournal.orgAddress for correspondence: Nabil El-Sherif, MDVA NY Harbor Healthcare System800 Poly Place, Cardiology (111A-BK)Brooklyn, NY 11209, USAe-mail: nelsherif@aol.comThe challenge of management of electricalstorm and out-of-hospital cardiac arrestNabil El-SherifState University of New York, Downstate Medical Center andVA New York Harbor Healthcare System, Brooklyn, NY, USAArticle p. 355Electrical storm refers to a situation when rapidclustering of episodes of malignant ventricular tachy-arrhythmias (VT) develops requiring repetitive at-tempts at cardioversion. This situation is seen inpatients with acute coronary syndrome (ACS) aswell as in some patients with the implantable car-dioverter-defibrillator (ICD). A similar situation isencounterd in victims of out-of-hospital cardiac ar-rest in whom VT is the mechanism of out-of-hospi-tal cardiac arrest. In this group of patients, besidesmanagement of hypoxia, electrolyte disturbances,acidosis, volume depletion, etc., drugs are admin-istered to either assist direct current (DC) cardio-version and/or maintain a stable rhythm. The firstline recommended anti-arrhythmic therapy thesedays is intravenous (IV) amiodarone and not lido-caine [1]. This change came around gradually in thelast several years when head-to-head comparisonof IV amiodarone and lidocaine showed the firstdrug to be unequivocally superior [2]. In fact lido-caine prophylaxis in ACS appears to be associatedwith increased mortality and this practice has large-ly been abandoned [3]. However, lidocaine is stillbeing used by some for out-of-hospital cardiac ar-rest as a second tier drug. Other second-tier drugtherapy in this situation also includes intravenousmagnesium and procainamide.Although IV amiodarone is available worldwide,its use is disallowed in Japan. However, luckily forthe Japanese, one of their drug companies hasintroduced a new selective Ikr blocker [4] that hasbeen in use since June 2000 in situations whenIV amiodarone would be indicated, i.e., primarily inpatients with electrical storm and out-of-hospitalcardiac arrest [5–7]. Although the drug, Nifekalant,is a pure Ikr blocker and as such is reverse-usedependent specially in the presence of fast VT, yetit has proven effective. An efficacy rate approach-ing 75% has been reported both in patients withelectrical storm and in out-of-hospital cardiac arrest.However, the drug as in the case of other pure Ikrblockers can result in significant QT prolongationand induce torsade de pointe VT. In other words,the drug can successfully terminate, for instance,VT in the setting of ACS and then induce a torsadede pointe type VT [7]. In this issue of CardiologyJournal, Dr. Amino and associates from Japan re-ported on the efficacy of the combination of Nifeka-lant with acute left stellate ganglion blockade (LSGB)in patients with intractable VT in out-of-hospital car-diac arrest [8]. As expected DC cardioversion andNifekalant were effective in 40 of 55 patients (73%).In the remaining 15 patients, VT continued in spite ofrepeated doses of Nifekalant. In this group, acuteLSGB was performed in 11 patients and resulted ina stable sinus rhythm in 7 (64%). The short-term mor-tality was 45% in the LSGB group and 100% in the4 patients who comprised the non-LSGB group. Thenumbers are relatively small and the results are hardlyimpressive if we remember that only 2 patients outof the LSGB group seem to have survived long term.Never the less, the study is of interest because itre-focuses attention on a rarely utilized managementmodality in a very serious clinical situation.The rationale for the use of acute LSGB asmeans of sympathetic blockade in the setup of elec-trical storm or out-of-hospital cardiac arrest isstraight forward. A majority, if not all, of these pa-tients will have an increased sympathetic drive. Thelatter, is universally accepted as arrhythmogenic327Nabil El-Sherif, Management of electrical storm and out-of hospital cardiac arrestwww.cardiologyjournal.orgespecially in patients with ACS, patients withischemic and non-ischemic cardiomyopathy, andpatients with certain channelopathies. The exactelectrophysiological mechanism(s) by which in-creased sympathetic drive to the heart can be ar-rhythmogenic in most of the above situations is notfully understood. However, innumerable experi-mental [9, 10] and clinical [11, 12] data have shownthat blocking the increased sympathetic drive to theheart in both its acute and chronic versions can besignificantly antiarrhythmic. Sympathetic blockadecould be achieved by intravenous beta-blockingdrugs like propanolol or esmolol or by acute LSGB.The authors argue in favor of LSGB by citing itsspecific blockade of sympathetic innervations to theleft ventricle and the potentially negative inotropicand chronotropic effects of IV beta-blockade in thesesettings. Even though LSGB has an alpha-blockingeffect in addition to beta-blocking effect, severalstudies have demonstrated that LSGB and beta-blockade are equally effective in treating post-myo-cardial infarction malignant VT [11, 13]. Few patientsreceiving beta-blocking agents for electrical stormcan develop electromechanical dissociation [13].However, a strong counter argument in favor of IVbeta-blockade is its ease of use and ready availabil-ity compared to acute LSGB. The latter requiressome degree of expertise, is not always success-ful, and is more difficult to implement when time isof the essence. Further, the effects of acute LSGBcan dissipate resulting in recurrence of malignantVT [13]. The present report did not comment onthis event and the strategy put in place to rectifythe situation. In fact it may turn out that the best useof acute LSGB would be in hospitalized patients withelectrical storm who are relatively more stable com-pared to out-of-hospital cardiac arrest patients.Acute LSGB is just one attempt to address thechallenge of current management of electrical stormand out-of-hospital cardiac arrest. Another manage-ment modality has been rescue VT ablation of drugrefractory electrical storm in patients with acutecoronary syndrome [14], with ischemic cardiomy-opathy [15], or ICD [16].The dramatic change in the last decade in themanagement of malignant VT is explained both bythe development of effective nonpharmacologictherapies such as targeted ablation of the arrhyth-mogenic tissue and the ICD as well as the limitedefficacy and proarrhythmic potential of current an-tiarrhythmic agents. The failure of development ofa new antiarrhythmic drug particularly for electri-cal storm in the setting of acute coronary syndromeis not because of lack of trying on the part of thepharmaceutical industry. In fact different innovativeapproaches to antiarrhythmic drug therapy havebeen exploited [17]. To mention a few: 1) The ade-nosine-triphosphate sensitive (KATP) K+ channel isa metabolic sensor that opens during myocardialischemia [18] and has a key role in ischemic actionpotential duration shortening. KATP has a complexrole, mediating cardiac protective as well as ar-rhythmogenic functions. These actions can be dis-sociated with cardioprotective function mediatedlargely by a mitochondrial KATP channel and elec-trical changes due to a sarcolemmal channel [19].Certain compounds can selectively block the sar-colemmal KATP channels and prevent associatedmalignant VT [20]; 2) Cell-to-cell communicationsand their pharmacological manipulation has yieldednew approaches to ischemia-associated uncouplingof gap junctions and its role in promoting malignantVT [21]. Several recent experimental studies haveshown that drugs that enhance gap junction conduct-ance like rotigaptide can be antiarrhythmic in thesetting of acute ischemia [22]; 3) The identificationof calstabin2 depleted ryanodine receptor (RyR2) asa source of diastolic sarcoplasmic reticulum (SR) Ca2+leak in catcholaminergic polymorphic ventriculartachycardia and in patients with heart failure sus-ceptible to malignant VT has led to the hypothesisthat increasing calstabin2 binding to RyR2 could bea potential new target to treat triggered malignantVT [23]. Whether this approach is helpful in arrhyth-mias secondary to acute ischemia is not known.There are at least 3 reasons why no new effec-tive antiarrhythmic drug against ischemia-relatedmalignant VT has made it to the clinical setting inthe past several years: 1) The heterogeneity of thearrhythmogenic substrate during ischemia and inthe post-infarction period is a daunting obstacle;2) There is a plethora of experimental studies show-ing significant antiarrhythmic effect of one or an-other new drug but preciously little clinical data. Itis indeed reasonable to question the validity of someof the experimental models currently in use for newantiarrhythmic drug development; 3) In view of thisauthor, a main limitation for the development ofa new clinically effective antiarrhythmic drug ther-apy for ischemia-related VT is simply our currentincomplete understanding of the underlying elec-trophysiological mechanisms. One prominent ex-ample is the recent report showing that ischemia//reperfusion associated ventricular arrhythmiasmay be secondary to fast oscillatory intracellularCa2+ responses that can trigger local ventricular de-polarizations [24]. The latter, based on how theseconduct to the surrounding myocardium can explain328Cardiology Journal 2007, Vol. 14, No. 4www.cardiologyjournal.orgboth the sporadic ventricular premature beat as wellas ventricular fibrillation.In summary, the report of Amino and associ-ates is important for focusing the attention on thechallenge in management of electrical storm andout-of-hospital cardiac arrest and the need for con-tinued search for new management modalities inthese situations.References1. Zipes DP, Camm AJ, Borggrefe M et al. ACC/AHA//ESC 2006 guidelines for management of patients withventricular arrhythmias and the prevention of suddencardiac death. Circulation, 2006; 144: e385–e484.2. Dorian P, Cass D, Schwartz B et al. Amiodarone ascompared with lidocaine for shock-resistant ventricu-lar fibrillation. N Engl J Med, 2002; 346: 884–890.3. McMahon S, Collins R, Peto R et al. Effects of pro-phylactic lidocaine in suspected acute myocardial in-farction. An overview of results from the randomizedcontrolled trials. JAMA, 1988; 260: 1910–1916.4. Ishii M, Kawiya J, Hashimoto K. Cellular electro-physiological effects of MS-551, a new class III an-tiarrhythmic agent. Drug Rev Res, 1995; 35: 61–68.5. Katoh T, Mitamara H, Matsuda N et al. Emergencytreatment with Nifekalant, a novel class III an-tiarrhythmic agent, for life-threatening refractoryventricular tachyarrhythmias: post-marketing specialinvestigation. Circ J, 2005; 69: 1237–1243.6. Washizuka T, Chinushi M, Watanabe H et al. Nifeka-lant hydrochloride suppresses severe electricalstorm in patients with malignant ventricular tachy-arrhythmias. Circ J, 2005; 69: 1508–1513.7. Ohashi J, Yasuda S, Miyazaki S et al. Prevention oflife-threatening ventricular tachyarrhythmia bya novel and pure class III agent, Nifekalant hydro-chloride. J Cardiovasc Pharmacol, 2006; 48: 274–249.8. Amino M, Yoshioka K, Morita S et al. Is the combina-tion therapy of IKr-channel blocker and left stellateganglion block effective for intractable ventriculararrhythmia in a cardiopulmonary arrest patient?Cardiol J, 2007; 14: 355–365.9. Anderson JL, Rodier HE, Green LS. Comparativeeffects of beta-adrenergic blocking drugs on experi-mental ventricular fibrillation threshold. Am J Cardiol,1983; 51: 1196–1202.10. Schwartz PJ, La Rovere MT, Vanoli E. Autonomicnervous system and sudden cardiac death: experi-mental basis and clinical observations for post-myo-cardial infarction risk stratification. Circulation, 1992;85: 177–191.11. Schwartz PJ, Motolese M, Polla Vini G et al; theItalian Sudden Death Prevention Group. Preventionof sudden cardiac death after a first myocardial inf-arction by pharmacologic or surgical antiadrenergicinterventions. J Cardiovasc Electrophysiol, 1998; 3:2–16.12. Gottlieb SS, McCarter RJ, Vogel RA. Effect of beta--blockade on mortality among high-risk and low-riskpatients after myocardial infarction. N Engl J Med,1998; 339: 489–497.13. Nademanee K, Taylor R, Bailey W et al. Treatingelectrical storm. Sympathetic blockade versus ad-vanced cardiac life support-guided therapy. Circula-tion, 2000; 102: 742–747.14. Enjoj Y, Mizobuchi M, Shibata K et al. Catheter abla-tion for incessant antiarrhythmic drug-resistant ven-tricular fibrillation after acute coronary syndrome.Pacing Clin Electrophysiol, 2006; 29: 102–105.15. Schreieck J, Zrenner B, Deisenhofer I et al. Rescueablation of electrical storm in patients with ischemiccardiomyopathy: a potential-guided ablation approachby modifying substrate of intractable unmappable ven-tricular tachycardias. Heart Rhythm, 2005; 2: 10–14.16. Silva RM, Mont L, Nova S, et al. Radiofrequencycatheter ablation for arrhythmic storm in patientswith an implantable cardioverter defibrillator. PacingClin Electrphysiol, 2004; 27: 971–975.17. Nattel S, Carlsson L. Innovative approaches to anti-arrhythmic drug therapy. Drug Discovery, 2005; 5:1034–1049.18. Noma A. ATP-regulated K+ channel in cardiac muscle.Nature, 1983; 305: 147–148.19. Gross GJ. The role of mitochondrial KATP channelsin cardioprotection. Basic Res Cardiol, 2000; 95:280–284.20. Billman GE, Englert HC, Scholkens BA. HMR 1803,a novel cardioselective inhibitor of the ATP-sensi-tive potassium channel. Part II: effects on suscepti-bility to ventricular fibrillation induced by myocar-dial ischemia in the conscious dogs. J Pharmacol ExpTher, 1998; 288: 1465–1473.21. Peters NS, Green CR, Poole-Wilson PA et al. Cardiacarrhythmogenesis and the gap junction. J Mol CellCardiol, 1995; 27: 37–44.22. Hennan JK, Swillo RE, Gwen A. Rotigaptide (ZP 123)prevents spontaneous ventricular arrhythmias andreduces infarct size during myocardial ischemia/reperfusion injury in open-chest dogs. J Pharm ExpTher, 2006; 317: 236–243.23. Wehrens X HT, Lehnart SE, Marks AR. Ryanodinereceptor-targeted antiarrhythmic therapy. Ann NYAcad Sci, 2005; 1047: 366–375.24. Lakireddy V, Bub G, Baweja P et al. The kinetics ofspontaneous calcium oscillations and arrhythmogen-esis in the in vivo heart during ischemia/reperfusion.Heart Rhythm, 2006; 3: 58–66.

The challenge of management of electrical storm and out-of-hospital cardiac arrest

https://journals.viamedica.pl/cardiology_journal/article/download/21678/17282

The challenge of management of electrical storm and out-of-hospital cardiac arrest

Abstract

Similar works

Full text

Available Versions

Via Medica Journals