DOCSLIB.ORG

Nifekalant Hydrochloride, a Novel Class III Antiarrhythmic Agent

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Nifekalant Hydrochloride, a Novel Class III Antiarrhythmic Agent CASE REPORTS Circ J 2003; 67: 712–714 Nifekalant Hydrochloride, a Novel Class III Antiarrhythmic Agent, Suppressed Postoperative Recurrent Ventricular Tachycardia in a Patient Undergoing Coronary Artery Bypass Grafting and the Dor Approach Makoto Sahara, MD; Kouichi Sagara, MD; Takeshi Yamashita, MD; Hiroyuki Iinuma, MD; Long-Tai Fu, MD; Hiroshi Watanabe, MD A patient with 3-vessel coronary artery disease and left ventricular aneurysm underwent coronary artery bypass grafting combined with the Dor approach. Five days later, ventricular tachycardia following short-coupled ven- tricular premature contractions suddenly occurred and was not responsive to class IB drugs (lidocaine and mexi- letine), requiring frequent electrical cardioversion. After the administration of a novel class III drug, nifekalant hydrochloride, this electrical storm of ventricular tachycardia was completely suppressed together with the dis- appearance of ventricular premature contractions. Nifekalant hydrochloride (MS-551), a pure K+ channel blocker, might be effective for postoperative recurrent ventricular tachyarrhythmias that are refractory to other antiarrhythmic agents. (Circ J 2003; 67: 712–714) Key Words: Dor approach; Electrical storm; Myocardial infarction; Nifekalant hydrochloride; Postoperative ventricular tachyarrhythmias ifekalant hydrochloride is a novel class III antiar- saphenous vein grafts and endoventricular circular patch rhythmic agent that has been developed in Japan plasty (the Dor approach) for the left ventricular aneurysm N and has attracted much attention in recent years were performed. because it has a unique function of selectively blocking the In the early morning on the fifth day after the operation, rapid component of the delayed rectifier K+ current (IKr) at ventricular tachycardia (VT) suddenly occurred, despite the a therapeutic concentration.1–3 In experimental models of absence of preoperative sustained VT or syncope. Mono- myocardial infarction, nifekalant has proved to be effective morphic non-sustained VT triggered by ventricular prema- in suppressing ventricular tachyarrhythmias without aggra- ture contractions (VPCs) with short coupling intervals vating the hemodynamics.4,5 We present a patient with (240–270ms) appeared incessantly (Fig2A) and was trans- unstable angina pectoris, old myocardial infarction and left formed into monomorphic sustained VT successively ventricular aneurysm who underwent coronary artery (Fig2B). Because the VT could not be suppressed by intra- bypass grafting (CABG) combined with the Dor approach venous administration of boluses of class IB antiarrhythmic and who had a postoperative electrical storm of ventricular agents (lidocaine 2.0 mg/kg and mexiletine 2.0mg/kg), tachycardia that was refractory to class IB drugs. We discuss the effect of nifekalant in this case report. Case Report A 77-year-old man with an old myocardial infarction, left ventricular aneurysm and severe ventricular dysfunc- tion (ejection fraction (EF): 24%) was admitted because of unstable angina pectoris in October 2000. On admission, his ECG showed no remarkable changes compared with his previous records (Fig1), but coronary angiography (CAG) revealed progression of 3-vessel coronary artery disease in addition to 75% stenosis of the left main trunk. Therefore, emergency CABG to all three coronary arteries with (Received November 19, 2001; revised manuscript received February 4, 2002; accepted February 27, 2002) The Cardiovascular Institute Hospital, Tokyo, Japan Fig1. Twelve-lead ECG on admission shows right axis deviation, Mailing address: Makoto Sahara, MD, The Cardiovascular Institute complete right bundle branch block, abnormal Q wave and ST Hospital, 7-3-10 Roppongi, Minato-Ku, Tokyo 106-0032, Japan. segment elevation in leads I, aVL and V1–6, which were similar find- E-mail: [email protected] ings to previous ECG recordings. Circulation Journal Vol.67, August 2003 Nifekalant and Postoperative VT 713 Fig 3. Clinical course. EC, electrical cardioversion; Mono-VT, Fig2. (A) Incessant monomorphic non-sustained VT triggered by monomorphic ventricular tachycardia; NSVT, non-sustained ventric- ventricular premature contractions with short coupling times (240– ular tachycardia; Poly-VT, polymorphic ventricular tachycardia. 270ms) (arrow). (B) Non-sustained VT was successively transformed into monomorphic sustained VT. (C) Early next morning, monomor- phic sustained VT triggered by the short-coupled VPC re-appeared and was transformed into polymorphic VT successively. electrical cardioversion was frequently required. Beta blockers and class IA antiarrhythmic agents could not be administered because of his low cardiac function. Although the continuous intravenous administration of lidocaine (1.0 mg·kg–1·h–1) and AAI pacing (rate = 100 /min) sup- pressed the occurrence of sustained VT for approx 22h, early the next morning, monomorphic sustained VT trig- gered by the short-coupled VPC re-appeared and was trans- formed into polymorphic VT successively (Fig2C), again requiring electrical cardioversion. There were no signifi- cant changes in cardiac enzymes, serum electrolytes, ECG and echocardiogram. Moreover, emergency CAG revealed good patency of all the bypass grafts, so it was unlikely that Fig4. Preoperative (A, B) and postoperative (C, D) left ventriculog- myocardial ischemia and/or infarction were associated raphy showing a decrease in the left ventricular end-diastolic volume index (215.4 to 113.8ml/m2) and an increase in the left ventricular EF with the VT. After beginning intravenous administration of (19.5 to 50.5%). (A) and (C) End diastole, (B) and (D) end systole. nifekalant, at a maintenance dose of 0.40mg·kg–1·h–1 in the afternoon of that day, the VPC completely disappeared and the electrical storm of VT was suppressed. Although the substrate. During an electrophysiologic study, sustained QTc intervals were prolonged from 0.43s to 0.49s, there VT could not be induced by triple extrastimuli from the was no sign of proarrhythmia related to nifekalant and no right ventricular apex. He was discharged on amiodarone aggravation of his hemodynamics [pulmonary artery pres- (200mg/day) and was without recurrence of VT for the sure (systole/diastole; mmHg):(pre) 22/12, (24h after the next 5 months. loading of nifekalant) 23/10; cardiac output (L/min):(pre) 4.87, (24h after the loading of nifekalant) 4.91]. On the third day after the administration of nifekalant, we began Discussion oral amiodarone at a loading dose of 600mg/day (Fig3) It has been reported that 0.68–3.1% of patients under- and when nifekalant was discontinued after 1 week, VT did going open heart surgery, including CABG, experience not recur. unexpected postoperative de novo sustained ventricular Postoperative cardiac catheterization 1 month later tachyarrhythmias (sustained VT and/or fibrillation),6–9 demonstrated good patency in all bypass grafts, decreased particularly in the first 7 postoperative days.8 The Dor left ventricular end-diastolic volume index (215.4 to approach (ie, endoventricular circular patch plasty) had 113.8ml/m2), increased left ventricular EF (19.5 to 50.5%) been reported to improve hemodynamics and significantly (Fig4) and improved hemodynamics (pulmonary capillary suppress the occurrence of postoperative ventricular tachy- wedge pressure: 23 to 18 mmHg; cardiac index: 1.6 to cardia when combined with cryotherapy.10,11 We consider 1.8L·min–1·m–2). Although his preoperative signal-aver- that the postoperative aggravated late potentials, which aged ECG had showed late potentials (filtered QRS were possibly associated with the surgical procedures, but complex duration (fQRS) 154 ms; low amplitude signal this is not exactly clear, were one of the factors inducing <40μV (LAS 40) 50ms; root mean square in the last 40ms the electrical storm of VT, and particularly because preop- of the filtered QRS complex (RMS 40) 10.5μV), his post- erative late potentials were recorded, cryotherapy should operative signal-averaged ECG showed an increase in all have been performed in this case. these parameters (fQRS: 179ms; LAS 40: 62ms; RMS 40: The electrical storm following VPCs with short coupling 12μV), indicating deterioration of the arrhythmogenic intervals suddenly occurred on the fifth postoperative day Circulation Journal Vol.67, August 2003 714 SAHARA M et al. after successful surgery and could not be controlled by drug, on programmed stimulation-induced ventricular arrhythmias, class IB antiarrhythmic agents, but was successfully sup- electrophysiology, and hemodynamics in a canine myocardial infarc- tion model. J Cardiovasc Pharmacol 1994; 23: 674–680. pressed by nifekalant. Nifekalant (MS-551; 1,3-dimethyl- 5. Friedrichs GS, Chi L, Gralinski MR, Black SC, Basler GC, Mu DX, 6-{2-[N-(2-hydroxyethyl)-3-(4-nitrophenyl)-propylamino] et al. MS-551 protects against ventricular fibrillation in a chronic ethylamino}-2,4 (1H,3H)-pyrimidinedione hydrochloride) canine model of sudden cardiac death. J Cardiovasc Pharmacol is a novel class III drug that selectively blocks IKr at a ther- 1995; 25: 314–323. 1–3 6. Kron IL, DiMarco JP, Harman PK, Crosby IK, Mentzer RM, Nolan apeutic concentration. It also increases defibrillation effi- SP, et al. Unanticipated postoperative ventricular tachyarrhythmias. 12–14 cacy similar to other class III drugs and effectively sup- Ann Thorac Surg 1984; 38: 317–322. presses ventricular tachyarrhythmias in canine models of 7. Topol EJ, Lerman BB, Baughman KL, Platia EV, Griffith LS. De myocardial infarction.4,5 Although
Load more

Recommended publications
  • Clinical Study of the Acute Effects of Intravenous Nifekalant on the Defibrillation Threshold in Patients with Persistent and Paroxysmal Atrial Fibrillation
    Circ J 2008; 72: 76–80 Clinical Study of the Acute Effects of Intravenous Nifekalant on the Defibrillation Threshold in Patients With Persistent and Paroxysmal Atrial Fibrillation Kaoru Okishige, MD; Hiroki Uehara, MD; Naoto Miyagi, MD; Kentarou Nakamura, MD; Kouji Azegami, MD; Hirofumi Wakimoto, MD; Kageyuki Ohba, MD; Kenzo Hirao, MD*; Mitsuo Shimabukuro, MD**; Mistuaki Isobe, MD* Background Antiarrhythmic agents are considered to have significant effects on the defibrillation energy re- quirement, so this study investigated the effects of nifekalant on defibrillation. Methods and Results Forty-two patients with persistent atrial fibrillation (AF) underwent electrical cardiover- sion via intracardiac electrode catheters prior to and after the intravenous administration of nifekalant. The suc- cess rate of the defibrillation and change in the defibrillation threshold using sequential incremental defibrillation energy deliveries was investigated. In addition, the parameters that could predict the beneficial effects of nifekalant were also assessed. Nifekalant significantly decreased the defibrillation energy requirement in 13 of the 42 cases, and nifekalant also converted AF to sinus rhythm with an identical energy to that of the last unsuccessful defib- rillation in 21 of 42 cases. The success of defibrillation seemed to be dependent on significant prolongation of the intracardiac atrial electrogram intervals during AF by the nifekalant. Conclusions Intravenous nifekalant significantly improved the electrical defibrillation efficacy in patients with persistent
    [Show full text]
  • ILCOR Guidelines 2015 for Web.Pdf
    Supplement to Circulation 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations Dallas, Texas February 1–3, 2015 Editors Mary Fran Hazinski (AHA) Jerry P. Nolan (ERC) International Liaison Committee on Resuscitation (ILCOR) Editorial Board Vinay M. Nadkarni (ILCOR Co-Chair, AHA) Eddy Lang (Grade Expert, HSFC) Gavin D. Perkins (ILCOR Co-Chair, ERC) Swee Han Lim (RCA) William H. Montgomery (C2015 Consensus Ian K. Maconochie (ERC) Conference Coordinator, AHA) Peter T. Morley (Evidence Monica E. Kleinman (Conference Evaluation Expert, ANZCOR) Co-Chair, AHA) Nikolaos I. Nikolaou (ERC) Maaret Castren (Conference Co-Chair, ERC) Robert W. Neumar (AHA) Richard Aickin (COI Co-Chair, ERC) Jeffrey M. Perlman (AHA) John E. Billi (COI Co-Chair, AHA) Eunice M. Singletary (AHA) Farhan Bhanji (HSFC) Jasmeet Soar (ERC) Clifton W. Callaway (AHA) Andrew H. Travers (HSFC) Allan R. de Caen (HSFC) Michelle Welsford (HSFC) Judith C. Finn (ANZCOR) Jonathan Wyllie (ERC) Lana M. Gent (AHA) David A. Zideman (ERC) Participating ILCOR Resuscitation Councils 2015 ILCOR Honorees Acknowledgments American Heart Association (AHA) Tom P. Aufderheide Alicia G. Pederson Australian and New Zealand Committee on Karl B. Kern Russell E. Griffin Resuscitation (ANZCOR) Vinay M. Nadkarni Jose Maria E. Ferrer European Resuscitation Council (ERC) Jerry P. Nolan Mandy L. Cootes Heart and Stroke Foundation of Canada (HSFC) Roger D. White Kara Robinson InterAmerican Heart Foundation (IAHF) Jody Hundley Resuscitation Council of Asia (RCA) Sandra Iverson Resuscitation Council of Southern Africa (RCSA) Joe Loftin We acknowledge the considerable contributions made by the late Professor Ian Jacobs, PhD, to this 2015 International Consensus on CPR Science.
    [Show full text]
  • Modeling Atrial Fibrillation Using Human Embryonic Stem Cell
    www.nature.com/scientificreports OPEN Modeling Atrial Fibrillation using Human Embryonic Stem Cell- Derived Atrial Tissue Received: 9 January 2017 Zachary Laksman1, Marianne Wauchop2, Eric Lin3, Stephanie Protze4, Jeehoon Lee5, Wallace Accepted: 1 June 2017 Yang6, Farzad Izaddoustdar7, Sanam Shafaattalab8, Lior Gepstein9, Glen F. Tibbits 10, Published: xx xx xxxx Gordon Keller11 & Peter H. Backx12 Since current experimental models of Atrial Fibrillation (AF) have significant limitations, we used human embryonic stem cells (hESCs) to generate an atrial-specific tissue model of AF for pharmacologic testing. We generated atrial-like cardiomyocytes (CMs) from hESCs which preferentially expressed atrial-specific genes, and had shorter action potential (AP) durations compared to ventricular-like CMs. We then generated confluent atrial-like CM sheets and interrogated them using optical mapping techniques. Atrial-like CM sheets (~1 cm in diameter) showed uniform AP propagation, and rapid re- entrant rotor patterns, as seen in AF could be induced. Anti-arrhythmic drugs were tested on single atrial-like CMs and cell sheets. Flecainide profoundly slowed upstroke velocity without affecting AP duration, leading to reduced conduction velocities (CVs), curvatures and cycle lengths of rotors, consistent with increased rotor organization and expansion. By contrast, consistent with block of rapid delayed rectifier +K currents (Ikr) and AP prolongation in isolated atrial-like CMs, dofetilide prolonged APs and reduced cycle lengths of rotors in cell sheets without affecting CV. In conclusion, using our hESC-derived atrial CM preparations, we demonstrate that flecainide and dofetilide modulate reentrant arrhythmogenic rotor activation patterns in a manner that helps explain their efficacy in treating and preventing AF.
    [Show full text]
  • The Use of Stems in the Selection of International Nonproprietary Names (INN) for Pharmaceutical Substances
    WHO/PSM/QSM/2006.3 The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances 2006 Programme on International Nonproprietary Names (INN) Quality Assurance and Safety: Medicines Medicines Policy and Standards The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 © World Health Organization 2006 All rights reserved. Publications of the World Health Organization can be obtained from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; e-mail: [email protected]). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
    [Show full text]
  • The Example of Short QT Syndrome Jules C
    Hancox et al. Journal of Congenital Cardiology (2019) 3:3 Journal of https://doi.org/10.1186/s40949-019-0024-7 Congenital Cardiology REVIEW Open Access Learning from studying very rare cardiac conditions: the example of short QT syndrome Jules C. Hancox1,4* , Dominic G. Whittaker2,3, Henggui Zhang4 and Alan G. Stuart5,6 Abstract Background: Some congenital heart conditions are very rare. In a climate of limited resources, a viewpoint could be advanced that identifying diagnostic criteria for such conditions and, through empiricism, effective treatments should suffice and that extensive mechanistic research is unnecessary. Taking the rare but dangerous short QT syndrome (SQTS) as an example, this article makes the case for the imperative to study such rare conditions, highlighting that this yields substantial and sometimes unanticipated benefits. Genetic forms of SQTS are rare, but the condition may be under-diagnosed and carries a risk of sudden death. Genotyping of SQTS patients has led to identification of clear ion channel/transporter culprits in < 30% of cases, highlighting a role for as yet unidentified modulators of repolarization. For example, recent exome sequencing in SQTS has identified SLC4A3 as a novel modifier of ventricular repolarization. The need to distinguish “healthy” from “unhealthy” short QT intervals has led to a search for additional markers of arrhythmia risk. Some overlap may exist between SQTS, Brugada Syndrome, early repolarization and sinus bradycardia. Genotype-phenotype studies have led to identification of arrhythmia substrates and both realistic and theoretical pharmacological approaches for particular forms of SQTS. In turn this has increased understanding of underlying cardiac ion channels.
    [Show full text]
  • Note to Users
    NOTE TO USERS Page(s) not included in the original manuscript and are unavailable from the author or university. The manuscript was microfilmed as received. This reproduction is the best copy available. EFFECT OF COMBINATION POT.-i\SSIL'bI CHANNEL BLOCKERS ON CARDIAC REFEb$.CTORINESS IN ISOLXÎED RABBIT HEARTS AND NTACT GUI'IE.4 PIG HE.4RTS A thssis submitted in conformit>.with the requiremrnts for the degres of hlastrr of Science Graduate Depanment of Medical Science Universit). of Toronto O Copyright by Nikolaos Marnalias 200 1 National Libraiy Bibliothèque nationale du Canada Acquisitions and Acquisitions et Bibliogrâphic Senrices services bibliographiques The author has granted a non- L'auteur a accordé une licence non exclusive licence allowing the exclusive permettant à la National Library of Canada to Bibliothèque nationale du Canada de reproduce, loan, distntbute or sell reproduire, prêter, distribuer ou copies of this thesis in microform, vendre des copies de cette thèse sous paper or electronic formats. la forme de microfiche/film, de reproduction sur papier ou sur format électronique. The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts from it Ni la thèse ni des extraits substantiels may be printed or otherwise de ceiieîi ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation. EFFECT OF COMBINATION POTASSIUM CHANNEL BLOCKERS ON CARDIAC REFRACTORiNESS IN ISOLATED RABBIT HEARTS AND iNTACT GUiNEA PIG HEARTS NIKOLAOS MAM.4LIAS MASTER OF SCIENCE 200 1 GRADUATE DEPARTMENT OF MEDICAL SCIENCE LJNIVERSITY OF TORONTO ABSTRACT Dofetilide and sotaiol prolong ventricular refractorinrss by blocking the rapidly açtivating delayrd rectitier potassium channel (Ikr).
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2015/0202317 A1 Rau Et Al
    US 20150202317A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2015/0202317 A1 Rau et al. (43) Pub. Date: Jul. 23, 2015 (54) DIPEPTDE-BASED PRODRUG LINKERS Publication Classification FOR ALPHATIC AMNE-CONTAINING DRUGS (51) Int. Cl. A647/48 (2006.01) (71) Applicant: Ascendis Pharma A/S, Hellerup (DK) A638/26 (2006.01) A6M5/9 (2006.01) (72) Inventors: Harald Rau, Heidelberg (DE); Torben A 6LX3/553 (2006.01) Le?mann, Neustadt an der Weinstrasse (52) U.S. Cl. (DE) CPC ......... A61K 47/48338 (2013.01); A61 K3I/553 (2013.01); A61 K38/26 (2013.01); A61 K (21) Appl. No.: 14/674,928 47/48215 (2013.01); A61M 5/19 (2013.01) (22) Filed: Mar. 31, 2015 (57) ABSTRACT The present invention relates to a prodrug or a pharmaceuti Related U.S. Application Data cally acceptable salt thereof, comprising a drug linker conju (63) Continuation of application No. 13/574,092, filed on gate D-L, wherein D being a biologically active moiety con Oct. 15, 2012, filed as application No. PCT/EP2011/ taining an aliphatic amine group is conjugated to one or more 050821 on Jan. 21, 2011. polymeric carriers via dipeptide-containing linkers L. Such carrier-linked prodrugs achieve drug releases with therapeu (30) Foreign Application Priority Data tically useful half-lives. The invention also relates to pharma ceutical compositions comprising said prodrugs and their use Jan. 22, 2010 (EP) ................................ 10 151564.1 as medicaments. US 2015/0202317 A1 Jul. 23, 2015 DIPEPTDE-BASED PRODRUG LINKERS 0007 Alternatively, the drugs may be conjugated to a car FOR ALPHATIC AMNE-CONTAINING rier through permanent covalent bonds.
    [Show full text]
  • Frequency-Dependent Electrophysiological Effects of Flecainide, Nifekalant and D,L-Sotalol on the Human Atrium
    CLINICAL INVESTIGATIONS Jpn Circ J 2001; 65: 1–6 Frequency-Dependent Electrophysiological Effects of Flecainide, Nifekalant and d,l-Sotalol on the Human Atrium Hiromi Watanabe, MD; Ichiro Watanabe, MD; Toshiko Nakai, MD; Naohiro Oshikawa, MD; Satoshi Kunimoto, MD; Riko Masaki, MD; Toshiaki Kojima, MD; Satoshi Saito, MD; Yukio Ozawa, MD; Katsuo Kanmatuse, MD To compare the effects of class Ic and III antiarrhythmic agents on the termination and prevention of atrial fibril- lation, the present study investigated the use-dependent electrophysiological effects of flecainide, nifekalant and d,l-sotalol on the human atrium. Flecainide significantly prolonged effective refractory period (ERP), intra-atrial conduction time (IACT) and monophasic action potential duration (MAPD), and its effects on ERP and IACT were use-dependent. Nifekalalant significantly prolonged ERP and MAPD, and these effects were reverse use- dependent; however, there was no significant change in IACT. d,l-Sotalol significantly prolonged MAPD and the effect was reverse use-dependent. It significantly prolonged ERP, but the effect was not reverse use-dependent. d,l-Sotalol increased IACT in a use-dependent manner. Thus, for atrial fibrillation, class Ic antiarrhythmic agents might be more effective in termination and class III antiarrhythmic agents might be more effective in prevention. (Jpn Circ J 2001; 65: 1–6) Key Words: Antiarrhythmic drugs; Atrial muscle; Monophasic action potential; Reverse use-dependency; Use-dependency lass I antiarrhythmic drugs have use-dependent diac dysfunction
    [Show full text]
  • Antiarrhythmic Drugs for Out-Of-Hospital Cardiac Arrest with Refractory Ventricular Fibrillation Takashi Tagami1,2*, Hideo Yasunaga2 and Hiroyuki Yokota3
    Tagami et al. Critical Care (2017) 21:59 DOI 10.1186/s13054-017-1639-8 REVIEW Open Access Antiarrhythmic drugs for out-of-hospital cardiac arrest with refractory ventricular fibrillation Takashi Tagami1,2*, Hideo Yasunaga2 and Hiroyuki Yokota3 in OHCA patients and that antiarrhythmic drugs can be Abstract used as advanced life support during cardiac arrest in This article is one of ten reviews selected from the patients with refractory ventricular dysrhythmias [5, 6]. Annual Update in Intensive Care and Emergency Refractory VF/pVT is generally defined as failure to ter- medicine 2017. Other selected articles can be found minate VF/pVT with one to three stacked shocks [5]. online at http://ccforum.com/series/ Antiarrhythmic drugs that may be used include amio- annualupdate2017. Further information about the darone, lidocaine, and nifekalant ([5, 6]; Table 1). The Annual Update in Intensive Care and Emergency ILCOR guidelines recommend the use of amiodarone as Medicine is available from http://www.springer.com/ first‐choice treatment for adult patients with refractory series/8901. VF/pVT to improve the rate of return of spontaneous circulation (ROSC) [5, 6]. Lidocaine and nifekalant are recommended as alternatives to amiodarone in the treat- Background ment of refractory VF/pVT in adult patients. However, ‐ ‐ Out of hospital cardiac arrest (OHCA) affects approxi- as mentioned in the knowledge gap section of the latest mately 300,000 people in the United States, 280,000 resuscitation guidelines [5], existing evidence is not people in Europe and 110,000 people in Japan each year enough to suggest that amiodarone is superior to lidocaine – [1 3].
    [Show full text]
  • Cross-Tumoral Phase 2 Clinical Trial Exploring Crizotinib (PF-02341066) in Patients with Advanced Tumors Induced by Causal Alterations of ALK And/Or MET ("CREATE")
    EORTC Avenue E. Mounierlaan 83/11 Brussel 1200 Bruxelles België – Belgique Tel: +32 2 774 16 11 e-mail: [email protected] www.eortc.org EORTC Network of Core Institutions (NOCI) Cross-tumoral phase 2 clinical trial exploring crizotinib (PF-02341066) in patients with advanced tumors induced by causal alterations of ALK and/or MET ("CREATE") EORTC protocol 90101 (EudraCT number 2011-001988-52) (NCT01524926) Study Coordinator: Patrick Schöffski Protocol Date of PRC Amendment reference version approval/notification N° Classification Outline December 03, 2010 ---- ---- 1.0 July 27, 2011 ---- ---- 2.0 February 08, 2012 1 Scientific 3.0 May 15, 2012 2 Scientific 4.0 March 28, 2014 3 Scientific 5.0 June 04, 2014 4 Scientific 6.0 March 26, 2015 5 Scientific 7.0 April 21, 2015 6 Scientific 8.0 August 17, 2015 7 Scientific 9.0 February 25, 2016 8 Scientific 9.1 April 13, 2016 9 Administrative 10.0 February 06, 2017 10 Scientific Version 10.0 / February 06, 2017 Copyright EORTC 2017 EORTC-90101 CREATE Contact addresses Writing Committee: P. Schöffski, University Hospitals Leuven, Leuven, Belgium EORTC Headquarters team, Brussels, Belgium Study Coordinator: Patrick Schöffski Phone: +32 16 346900 E-mail: [email protected] Clinical Research Sandrine Marreaud Physician: Phone: +32 2 774 16 85 E-mail: [email protected] Clinical Scientist: Angélique Deleersnijder Phone: +32 2 774 10 35 E-mail: [email protected] Project Manager: Dominiek Staelens Phone: +32 2 774 15 34 E-mail: [email protected] Data Manager: Tiana
    [Show full text]
  • Stembook 2018.Pdf
    The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 WHO/EMP/RHT/TSN/2018.1 © World Health Organization 2018 Some rights reserved. This work is available under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 IGO licence (CC BY-NC-SA 3.0 IGO; https://creativecommons.org/licenses/by-nc-sa/3.0/igo). Under the terms of this licence, you may copy, redistribute and adapt the work for non-commercial purposes, provided the work is appropriately cited, as indicated below. In any use of this work, there should be no suggestion that WHO endorses any specific organization, products or services. The use of the WHO logo is not permitted. If you adapt the work, then you must license your work under the same or equivalent Creative Commons licence. If you create a translation of this work, you should add the following disclaimer along with the suggested citation: “This translation was not created by the World Health Organization (WHO). WHO is not responsible for the content or accuracy of this translation. The original English edition shall be the binding and authentic edition”. Any mediation relating to disputes arising under the licence shall be conducted in accordance with the mediation rules of the World Intellectual Property Organization. Suggested citation. The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances. Geneva: World Health Organization; 2018 (WHO/EMP/RHT/TSN/2018.1). Licence: CC BY-NC-SA 3.0 IGO. Cataloguing-in-Publication (CIP) data.
    [Show full text]
  • A Abacavir Abacavirum Abakaviiri Abagovomab Abagovomabum
    A abacavir abacavirum abakaviiri abagovomab abagovomabum abagovomabi abamectin abamectinum abamektiini abametapir abametapirum abametapiiri abanoquil abanoquilum abanokiili abaperidone abaperidonum abaperidoni abarelix abarelixum abareliksi abatacept abataceptum abatasepti abciximab abciximabum absiksimabi abecarnil abecarnilum abekarniili abediterol abediterolum abediteroli abetimus abetimusum abetimuusi abexinostat abexinostatum abeksinostaatti abicipar pegol abiciparum pegolum abisipaaripegoli abiraterone abirateronum abirateroni abitesartan abitesartanum abitesartaani ablukast ablukastum ablukasti abrilumab abrilumabum abrilumabi abrineurin abrineurinum abrineuriini abunidazol abunidazolum abunidatsoli acadesine acadesinum akadesiini acamprosate acamprosatum akamprosaatti acarbose acarbosum akarboosi acebrochol acebrocholum asebrokoli aceburic acid acidum aceburicum asebuurihappo acebutolol acebutololum asebutololi acecainide acecainidum asekainidi acecarbromal acecarbromalum asekarbromaali aceclidine aceclidinum aseklidiini aceclofenac aceclofenacum aseklofenaakki acedapsone acedapsonum asedapsoni acediasulfone sodium acediasulfonum natricum asediasulfoninatrium acefluranol acefluranolum asefluranoli acefurtiamine acefurtiaminum asefurtiamiini acefylline clofibrol acefyllinum clofibrolum asefylliiniklofibroli acefylline piperazine acefyllinum piperazinum asefylliinipiperatsiini aceglatone aceglatonum aseglatoni aceglutamide aceglutamidum aseglutamidi acemannan acemannanum asemannaani acemetacin acemetacinum asemetasiini aceneuramic
    [Show full text]