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药物对除颤能力的影响。

Effect of drugs on defibrillation capacity.

作者信息

Dopp Anna Legreid, Miller John M, Tisdale James E

机构信息

Extension Services in Pharmacy, University of Wisconsin-Madison School of Pharmacy, Madison, WI 53705-2222, USA.

出版信息

Drugs. 2008;68(5):607-30. doi: 10.2165/00003495-200868050-00004.

Abstract

Over 300,000 people die of sudden cardiac death (SCD) in the US annually. Implantable cardioverter-defibrillators (ICDs) have been shown to be more effective than antiarrhythmic drugs for the prevention of SCD in specific susceptible populations. Many patients in whom ICDs have been implanted receive concomitant therapy with antiarrhythmic drugs, for the purpose of reducing the frequency of appropriate and inappropriate defibrillation shocks. Drugs may influence defibrillation capacity and therefore influence the function of ICDs. The objective of this article is to review and update the literature regarding the effects of drugs on defibrillation capacity.A literature search was performed using PubMed (1966 to December 2007) to identify clinical studies, case reports and animal studies describing the effects of drugs on defibrillation capacity. Search terms included: antiarrhythmic drugs; cardiovascular drugs; amiodarone; sotalol; flecainide; propafenone; dofetilide; ibutilide; beta-blockers; lidocaine; procainamide; N-acetylprocainamide; mexiletine; disopyramide; moricizine; calcium channel blockers; defibrillation threshold; defibrillation energy requirements; defibrillation energy changes; defibrillation efficacy; implantable cardioverter defibrillators; and external defibrillators. Evidence from clinical studies indicates that amiodarone may increase defibrillation threshold (DFT). In addition, some data indicate that drugs including lidocaine, mexiletine, moracizine (moricizine), verapamil, venlafaxine and anaesthetic agents may increase DFT. In contrast, agents including sotalol, dofetilide and beta-adrenergic receptor antagonists (beta-blockers) may reduce DFT. Propafenone and procainamide appear to have minimal effect on DFT. For those antiarrhythmic drugs with both sodium and potassium channel blockade (e.g. amiodarone), the effect of sodium channel blockade predominates, resulting in an increase in DFT. Numerous drugs may affect defibrillation capacity. These effects must be considered when managing patients who have an ICD and require concomitant pharmacotherapy.

摘要

在美国,每年有超过30万人死于心源性猝死(SCD)。对于特定的易感人群,植入式心脏复律除颤器(ICD)已被证明在预防SCD方面比抗心律失常药物更有效。许多植入ICD的患者同时接受抗心律失常药物治疗,目的是减少适当和不适当的除颤电击次数。药物可能会影响除颤能力,进而影响ICD的功能。本文的目的是回顾和更新关于药物对除颤能力影响的文献。

使用PubMed(1966年至2007年12月)进行文献检索,以识别描述药物对除颤能力影响的临床研究、病例报告和动物研究。检索词包括:抗心律失常药物;心血管药物;胺碘酮;索他洛尔;氟卡尼;普罗帕酮;多非利特;伊布利特;β受体阻滞剂;利多卡因;普鲁卡因胺;N - 乙酰普鲁卡因胺;美西律;丙吡胺;莫雷西嗪;钙通道阻滞剂;除颤阈值;除颤能量需求;除颤能量变化;除颤效果;植入式心脏复律除颤器;以及体外除颤器。临床研究证据表明,胺碘酮可能会增加除颤阈值(DFT)。此外,一些数据表明,包括利多卡因、美西律、莫雷西嗪(moracizine)、维拉帕米、文拉法辛和麻醉剂在内的药物可能会增加DFT。相比之下,包括索他洛尔、多非利特和β肾上腺素能受体拮抗剂(β受体阻滞剂)在内的药物可能会降低DFT。普罗帕酮和普鲁卡因胺对DFT似乎影响最小。对于那些同时具有钠通道和钾通道阻滞作用的抗心律失常药物(如胺碘酮),钠通道阻滞作用占主导,导致DFT升高。许多药物可能会影响除颤能力。在管理患有ICD且需要同时进行药物治疗的患者时,必须考虑这些影响。

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