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use recreational drugs (同)do drugs
administer a drug to; "They drugged the kidnapped tourist" (同)dose
a substance that is used as a medicine or narcotic
a drug used to treat an abnormal heart rhythm (同)antiarrhythmic_drug, antiarrhythmic medication

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『薬』,薬品,薬剤 / 『麻薬』,麻酔剤 / 〈人〉‘に'薬(特に麻酔剤)を与える / 〈飲食物〉‘に'(麻酔薬・毒薬などの)薬を混ぜる

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/10/04 16:44:46」(JST)

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Phases of a cardiac action potential. The sharp rise in voltage ("0") corresponds to the influx of sodium ions, whereas the two decays ("1" and "3", respectively) correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions. The characteristic plateau ("2") results from the opening of voltage-sensitive calcium channels.

Antiarrhythmic agents are a group of pharmaceuticals that are used to suppress abnormal rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.

Many attempts have been made to classify antiarrhythmic agents.. The problem arises from the fact that many of the antiarrhythmic agents have multiple modes of action, making any classification imprecise.

Vaughan Williams classification

The Vaughan Williams classification was introduced in 1970.^[1]

With regards to management of atrial fibrillation, Class I and III are used in rhythm control as medical cardioversion agents while Class II and IV are used as rate control agents.

There are five main classes in the Vaughan Williams classification of antiarrhythmic agents:

Class I agents interfere with the sodium (Na⁺) channel.
Class II agents are anti-sympathetic nervous system agents. Most agents in this class are beta blockers.
Class III agents affect potassium (K⁺) efflux.
Class IV agents affect calcium channels and the AV node.
Class V agents work by other or unknown mechanisms.

Overview table

Class	Known as	Examples	Mechanism	Clinical uses in cardiology ^[2]
Ia	fast-channel blockers-affect QRS complex	Quinidine Procainamide Disopyramide	(Na⁺) channel block (intermediate association/dissociation)	Ventricular arrhythmias prevention of paroxysmal recurrent atrial fibrillation (triggered by vagal overactivity) procainamide in Wolff-Parkinson-White syndrome
Ib	Do not affect QRS complex	Lidocaine Phenytoin Mexiletine Tocainide	(Na⁺) channel block (fast association/dissociation)	treatment and prevention during and immediately after myocardial infarction, though this practice is now discouraged given the increased risk of asystole ventricular tachycardia
Ic		Encainide Flecainide Propafenone Moricizine	(Na⁺) channel block (slow association/dissociation)	prevents paroxysmal atrial fibrillation treats recurrent tachyarrhythmias of abnormal conduction system. contraindicated immediately post-myocardial infarction.
II	Beta-blockers	Propranolol Esmolol Timolol Metoprolol Atenolol Bisoprolol	beta blocking Propranolol also shows some class I action	decrease myocardial infarction mortality prevent recurrence of tachyarrhythmias
III		Amiodarone Sotalol Ibutilide Dofetilide Dronedarone E-4031	K⁺ channel blocker Sotalol is also a beta blocker^[3] Amiodarone has Class I, II, III & IV activity	In Wolff-Parkinson-White syndrome (sotalol:) ventricular tachycardias and atrial fibrillation (Ibutilide:) atrial flutter and atrial fibrillation
IV	slow-channel blockers	Verapamil Diltiazem	Ca²⁺ channel blocker	prevent recurrence of paroxysmal supraventricular tachycardia reduce ventricular rate in patients with atrial fibrillation
V		Adenosine Digoxin Magnesium Sulfate	Work by other or unknown mechanisms (Direct nodal inhibition).	Used in supraventricular arrhythmias, especially in Heart Failure with Atrial Fibrillation, contraindicated in ventricular arrhythmias. Or in the case of Magnesium Sulfate, used in Torsades de Pointes.

Class I agents

The class I antiarrhythmic agents interfere with the sodium channel. Class I agents are grouped by what effect they have on the Na⁺ channel, and what effect they have on cardiac action potentials.

Class I agents are called Membrane Stabilizing agents. The 'stabilizing' word is used to describe the decrease of excitogenicity of the plasma membrane which is brought about by these agents. (Also noteworthy is that a few class II agents like propranolol also have a membrane stabilizing effect.)

Class I agents are divided into three groups (Ia, Ib and Ic) based upon their effect on the length of the action potential.^[4]^[5]

Ia lengthens the action potential (right shift)
Ib shortens the action potential (left shift)
Ic does not significantly affect the action potential (no shift)

Class Ia
Class Ib
Class Ic

Class II agents

Class II agents are conventional beta blockers. They act by blocking the effects of catecholamines at the β₁-adrenergic receptors, thereby decreasing sympathetic activity on the heart. These agents are particularly useful in the treatment of supraventricular tachycardias. They decrease conduction through the AV node.

Class II agents include atenolol, esmolol, propranolol, and metoprolol.

Class III agents

Class III

Class III agents predominantly block the potassium channels, thereby prolonging repolarization.^[6] Since these agents do not affect the sodium channel, conduction velocity is not decreased. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. (The re-entrant rhythm is less likely to interact with tissue that has become refractory). Drugs include: bretylium, amiodarone, ibutilide, sotalol, dofetilide, and dronedarone. Inhibiting potassium channels, slowing repolarization, results in slowed atrial-ventricular myocyte repolarization. Class III agents have the potential to prolong the QT interval of the EKG.

Class IV agents

Class IV agents are slow calcium channel blockers. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.

Class IV agents include verapamil and diltiazem.

Other agents

Since the development of the original Vaughan-Williams classification system, additional agents have been used that don't fit cleanly into categories I through IV.

Agents include:

Digoxin, which decreases conduction of electrical impulses through the AV node and increases vagal activity via its central action on the central nervous system, via indirect action, leads to an increase in Acetyl Choline production, stimulating M3 receptors on AV node leading to an overall decrease in speed of conduction.
Adenosine^[7]
Magnesium sulfate, an antiarrhythmic drug, but only against very specific arrhythmias ^[8] which has been used for torsades de pointes.^[9]^[10]

Sicilian Gambit classification

Another approach, known as the "Sicilian Gambit", placed a greater approach on the underlying mechanism.^[11]^[12]^[13]

It presents the drugs on two axes, instead of one, and is presented in tabular form. On the Y axis, each drug is listed, in approximately the Vaughan Williams order. On the X axis, the channels, receptors, pumps, and clinical effects are listed for each drug, with the results listed in a grid. It is therefore not a true classification in that it does not aggregate drugs into categories.^[14]

References

^ Vaughan Williams EM. "Classification of anti-arrhythmic drugs." In: Symposium on Cardiac Arrhythmias, Sandfte E, Flensted-Jensen E, Olesen KH eds. Sweden, AB ASTRA, Södertälje, 1970;449-472.
^ Unless else specified in boxes, then ref is: Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.
^ Kulmatycki KM, Abouchehade K, Sattari S, Jamali F (May 2001). "Drug-disease interactions: reduced beta-adrenergic and potassium channel antagonist activities of sotalol in the presence of acute and chronic inflammatory conditions in the rat". Br. J. Pharmacol. 133 (2): 286–94. doi:10.1038/sj.bjp.0704067. PMC 1572777. PMID 11350865.
^ Milne JR, Hellestrand KJ, Bexton RS, Burnett PJ, Debbas NM, Camm AJ (February 1984). "Class 1 antiarrhythmic drugs—characteristic electrocardiographic differences when assessed by atrial and ventricular pacing". Eur. Heart J. 5 (2): 99–107. PMID 6723689.
^ Trevor, Anthony J.; Katzung, Bertram G. (2003). Pharmacology. New York: Lange Medical Books/McGraw-Hill, Medical Publishing Division. p. 43. ISBN 0-07-139930-5.
^ Lenz TL, Hilleman DE, Department of Cardiology, Creighton University, Omaha, Nebraska. Dofetilide, a New Class III Antiarrhythmic Agent. Pharmacotherapy 20(7):776–786, 2000. (Medline abstract)
^ Conti JB, Belardinelli L, Utterback DB, Curtis AB (March 1995). "Endogenous adenosine is an antiarrhythmic agent". Circulation 91 (6): 1761–7. doi:10.1161/01.cir.91.6.1761. PMID 7882485.
^ Brugada P (July 2000). "Magnesium: an antiarrhythmic drug, but only against very specific arrhythmias". Eur. Heart J. 21 (14): 1116. doi:10.1053/euhj.2000.2142. PMID 10924290.
^ Hoshino K, Ogawa K, Hishitani T, Isobe T, Eto Y (October 2004). "Optimal administration dosage of magnesium sulfate for torsades de pointes in children with long QT syndrome". J Am Coll Nutr 23 (5): 497S–500S. doi:10.1080/07315724.2004.10719388. PMID 15466950.
^ Hoshino K, Ogawa K, Hishitani T, Isobe T, Etoh Y (April 2006). "Successful uses of magnesium sulfate for torsades de pointes in children with long QT syndrome". Pediatr Int 48 (2): 112–7. doi:10.1111/j.1442-200X.2006.02177.x. PMID 16635167.
^ "The 'Sicilian Gambit'. A new approach to the classification of antiarrhythmic drugs based on their actions on arrhythmogenic mechanisms. The Task Force of the Working Group on Arrhythmias of the European Society of Cardiology". Eur. Heart J. 12 (10): 1112–31. October 1991. PMID 1723682.
^ Vaughan Williams EM (November 1992). "Classifying antiarrhythmic actions: by facts or speculation". J Clin Pharmacol 32 (11): 964–77. doi:10.1002/j.1552-4604.1992.tb03797.x. PMID 1474169.
^ "Milestones in the Evolution of the Study of Arrhythmias". Retrieved 2008-07-31. ^{[dead link]}
^ Fogoros, Richard N. (1997). Antiarrhythmic drugs: a practical guide. Oxford: Blackwell Science. p. 49. ISBN 0-86542-532-9.

UpToDate Contents

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1. 心房細動患者における洞調律維持のための抗不整脈剤：推奨 antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation recommendations
2. 心筋活動電位および抗不整脈剤の作用 myocardial action potential and action of antiarrhythmic drugs
3. 心房細動患者における洞調律維持のための抗不整脈薬：臨床試験 antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation clinical trials
4. I群抗不整脈薬の主な副作用 major side effects of class i antiarrhythmic drugs
5. 心房細動における洞調律の維持：カテーテルアブレーションおよび抗不整脈薬の比較 maintenance of sinus rhythm in atrial fibrillation catheter ablation versus antiarrhythmic drug therapy

English Journal

Catheter ablation for ventricular tachycardia in structural heart disease.

Macintyre CJ1, Sapp JL2.Author information 1Heart Rhythm Service, Cardiology Division, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, Nova Scotia, Canada.2Heart Rhythm Service, Cardiology Division, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, Nova Scotia, Canada. Electronic address: john.sapp@cdha.nshealth.ca.AbstractThe management of ventricular tachyarrhythmias has changed significantly over the past several decades. The advent of readily available implantable cardioverter defibrillators (ICDs) has had the greatest effect, with important mortality effects in patients with ventricular tachycardia and structural heart disease. ICDs have been shown to reduce sudden death in patients with ischemic and nonischemic cardiomyopathies; evidence of adverse consequences of ICD shocks, however, is mounting. In addition to the negative effects on patient-reported quality of life, anxiety, and depression, frequent ventricular arrhythmias and ICD shocks have also been associated with increased mortality. It is therefore important to identify and implement effective ventricular tachycardia-suppressive strategies. Antiarrhythmic drugs represent one such method, but are challenged by unfavourable side effect profiles and proarrhythmic risk. Catheter ablation of ventricular tachycardia is now a well-accepted intervention, which has been demonstrated to reduce recurrent arrhythmias. Questions persist regarding the optimal role for ablation compared with drug therapy.
The Canadian journal of cardiology.Can J Cardiol.2014 Feb;30(2):244-6. doi: 10.1016/j.cjca.2013.11.015. Epub 2013 Nov 20.
The management of ventricular tachyarrhythmias has changed significantly over the past several decades. The advent of readily available implantable cardioverter defibrillators (ICDs) has had the greatest effect, with important mortality effects in patients with ventricular tachycardia and structural
PMID 24373758

Antibiotic-induced Cardiac Arrhythmias.

Abo-Salem E, Fowler JC, Attari M, Cox CD, Perez-Verdia A, Panikkath R, Nugent K.Author information Department of Cardiovascular Diseases, University of Cincinnati, Cincinnati, OH, USA.AbstractThis review aims to clarify the underlying risk of arrhythmia associated with the use of macrolides and fluoroquinolones antibiotics. Torsades de pointes (TdP) is a rare potential side effect of fluoroquinolones and macrolide antibiotics. However, the widespread use of these antibiotics compounds the problem. These antibiotics prolong the phase 3 of the action potential and cause early after depolarization and dispersion of repolarization that precipitate TdP. The potency of these drugs, as potassium channel blockers, is very low, and differences between them are minimal. Underlying impaired cardiac repolarization is a prerequisite for arrhythmia induction. Impaired cardiac repolarization can be congenital in the young or acquired in adults. The most important risk factors are a prolonged baseline QTc interval or a combination with class III antiarrhythmic drugs. Modifiable risk factors, including hypokalemia, hypomagnesemia, drug interactions, and bradycardia, should be corrected. In the absence of a major risk factor, the incidence of TdP is very low. The use of these drugs in the appropriate settings of infection should not be altered because of the rare risk of TdP, except among cases with high-risk factors.
Cardiovascular therapeutics.Cardiovasc Ther.2014 Feb;32(1):19-25. doi: 10.1111/1755-5922.12054.
This review aims to clarify the underlying risk of arrhythmia associated with the use of macrolides and fluoroquinolones antibiotics. Torsades de pointes (TdP) is a rare potential side effect of fluoroquinolones and macrolide antibiotics. However, the widespread use of these antibiotics compounds th
PMID 24428853

Antiarrhythmic drug therapy for maintaining sinus rhythm early after pulmonary vein ablation in patients with symptomatic atrial fibrillation.

Sohns C, von Gruben V, Sossalla S, Bergau L, Seegers J, Lüthje L, Vollmann D, Zabel M.Author information Department of Cardiology and Pneumology, Heart Center, Georg-August-University of Göttingen, Göttingen, Germany; Division of Imaging Sciences and Biomedical Engineering, King's College London, London, UK.AbstractAIMS: The optimal pharmacological treatment for patients early after ablation of atrial fibrillation (AF) is still not clear. We analyzed if concomitant antiarrhythmic drug (AAD) therapy significantly alters early recurrence of AF/atrial tachycardia (AT) following pulmonary vein ablation (PVA).
Cardiovascular therapeutics.Cardiovasc Ther.2014 Feb;32(1):7-12. doi: 10.1111/1755-5922.12052.
AIMS: The optimal pharmacological treatment for patients early after ablation of atrial fibrillation (AF) is still not clear. We analyzed if concomitant antiarrhythmic drug (AAD) therapy significantly alters early recurrence of AF/atrial tachycardia (AT) following pulmonary vein ablation (PVA).METHO
PMID 24138075