antiarrhythmic

• adj.

• 抗不整脈の

• n.

• 抗不整脈薬

関

anti-arrhythmia agent、antiarrhythmic agent、antiarrhythmic drug、antiarrhythmics

　

WordNet

1. a drug used to treat an abnormal heart rhythm (同)antiarrhythmic_drug, antiarrhythmic medication

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/02/06 22:11:52」(JST)

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The cardiac action potential

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.

Singh Vaughan Williams classification

The Singh Vaughan Williams classification, introduced in 1970 based on the seminal work of Bramah N. Singh in his doctoral thesis at Oxford where Vaughan Williams was his advisor and on subsequent work by Singh and his colleagues in the United States, is one of the most widely used classification schemes for antiarrhythmic agents. This scheme classifies a drug based on the primary mechanism of its antiarrhythmic effect. However, its dependence on primary mechanism is one of the limitations of the Singh-VW classification, since many antiarrhythmic agents have multiple action mechanisms. Amiodarone, for example, has effects consistent with all of the first four classes. Another limitation is the lack of consideration within the Singh-VW classification system for the effects of drug metabolites. Procainamide—a class Ia agent whose metabolite N-acetyl procainamide (NAPA) has a class III action—is one such example. A historical limitation was that drugs such as digoxin and adenosine – important antiarrhythmic agents – had no place at all in the VW classification system. This has since been rectified by the inclusion of class V.^{[citation needed]}

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

There are five main classes in the Singh 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
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 atrial fibrillation
Ic		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 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.

• 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

There is a popular mnemonic to remember the class I agents:

Class Ia	Disopyramide, Quinidine, Procainamide	Double Quarter Pounder Police Department Questions (Procainamide, Disopyramide, Quinidine)
Class Ib	Lidocaine, Mexiletine, Tocainide	Lettuce, Mayo, Tomato The Little Man (Tocainide, Lidocaine, Mexiletine)
Class Ic	Moricizine, Flecainide, Propafenone	More Fries Please. (note there are two "M"s in the mnemonic, but moricizine and more can clarify which is which) For Pushing Ecstasy (Flecainide, Propafenone, Encainide)

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. 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: 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 ("Class V")

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.

Some sources use the term "Class V". However, they are more frequently identified by their precise mechanism.

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.
• Adenosine
• Magnesium sulfate, which has been used for torsades de pointes.

Sicilian Gambit classification

Another approach, known as the "Sicilian Gambit", placed a greater approach on the underlying mechanism.

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.

See also

• Action potential
  • Cardiac action potential
• Cardiac Arrhythmia Suppression Trial (CAST)
• Electrocardiogram
• Proarrhythmic agent

References

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

• Antiarrhythmic drug use in patients <65 years with atrial fibrillation and without structural heart disease.

• Allen LaPointe NM1, Dai D2, Thomas L2, Piccini JP2, Peterson ED2, Al-Khatib SM2.
• The American journal of cardiology.Am J Cardiol.2015 Feb 1;115(3):316-22. doi: 10.1016/j.amjcard.2014.11.005. Epub 2014 Nov 13.
• Little is known in clinical practice about antiarrhythmic drug (AAD) use in patients with atrial fibrillation (AF) (particularly younger ones) who do not have structural heart disease. Using the MarketScan database, we identified patients <65 years without known coronary artery disease or heart
• PMID 25491240

• Marine n-3 PUFAs modulate IKs gating, channel expression, and location in membrane microdomains.

• Moreno C1, de la Cruz A2, Oliveras A3, Kharche SR4, Guizy M2, Comes N3, Starý T4, Ronchi C5, Rocchetti M5, Baró I6, Loussouarn G6, Zaza A5, Severi S4, Felipe A3, Valenzuela C1.
• Cardiovascular research.Cardiovasc Res.2015 Feb 1;105(2):223-32. doi: 10.1093/cvr/cvu250. Epub 2014 Dec 11.
• AIMS: Polyunsaturated fatty n-3 acids (PUFAs) have been reported to exhibit antiarrhythmic properties. However, the mechanisms of action remain unclear. We studied the electrophysiological effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on IKs, and on the expression and locatio
• PMID 25497550

• Measurements of the left atrium and pulmonary veins for analysis of reverse structural remodeling following cardiac ablation therapy.

• Rettmann ME1, Holmes Iii DR1, Breen JF2, Ge X1, Karwoski RA1, Monahan KH3, Bahnson TD4, Packer DL3, Robb RA1; CABANA Pilot Imaging Investigators.
• Computer methods and programs in biomedicine.Comput Methods Programs Biomed.2015 Feb;118(2):198-206. doi: 10.1016/j.cmpb.2014.11.001. Epub 2014 Nov 13.
• RATIONALE AND OBJECTIVES: Geometric analysis of the left atrium and pulmonary veins is important for assessing reverse structural remodeling following cardiac ablation therapy. Most volumetric analysis techniques, however, require laborious manual tracing of image cross-sections. Pulmonary vein diam
• PMID 25476706

• Targeting cardiac potassium channels for state-of-the-art drug discovery.

• Walsh KB1.
• Expert opinion on drug discovery.Expert Opin Drug Discov.2015 Feb;10(2):157-69. doi: 10.1517/17460441.2015.983471. Epub 2014 Nov 15.
• INTRODUCTION: Cardiac K(+) channels play a critical role in maintaining the normal electrical activity of the heart by setting the cell resting membrane potential and by determining the shape and duration of the action potential. Drugs that block the rapid (IKr) and slow (IKs) components of the dela
• PMID 25400064

Japanese Journal

• Electrophysiological Effects of the Antiarrhythmic Drug Bepridil on the Guinea-Pig Pulmonary Vein Myocardium

• Takahara Akira,Takeda Kiyoshi,Hagiwara Mihoko [他]
• Biological & pharmaceutical bulletin 36(2), 311-315, 2013-02-00
• NAID 40019558673

• Potential Antiarrhythmic Effect of Methyl 3,4,5-Trimethoxycinnamate, a Bioactive Substance from Roots of Polygalae Radix : Suppression of Triggered Activities in Rabbit Myocytes

• Zhao Zhenghang,Fang Minfeng,Xiao Dandan [他]
• Biological & pharmaceutical bulletin 36(2), 238-244, 2013-02-00
• NAID 40019558475

• 抗不整脈薬の催不整脈作用と対策 (特集 心房細動 : 診断・治療の最新動向) -- (心房細動の治療)

• 小林 義典
• 日本臨床 71(1), 79-85, 2013-01-00
• NAID 40019536402

• リズムコントロールの薬剤選択 (特集 心房細動 : 診断・治療の最新動向) -- (心房細動の治療)

• 笹野 哲郎,平尾 見三
• 日本臨床 71(1), 67-71, 2013-01-00
• NAID 40019536375

Related Links

• Antiarrhythmic | definition of antiarrhythmic by Medical dictionary

antiarrhythmic [an″te-ah-rith´mik] 1. preventing or alleviating cardiac arrhythmias. 2. an agent that has this effect. an·ti·ar·rhyth·mic (an'tē-ă-ridh'mik), Combating an arrhythmia. Synonym(s): antidysrhythmic antiarrhythmic /an·ti·ar·rhyth ...

• Antiarrhythmic - definition of antiarrhythmic by The Free ...

an·ti·ar·rhyth·mic (ăn′tē-ə-rĭth′mĭk, ăn′tī-) adj. Preventing or alleviating irregularities in the force or rhythm of the heart. n. An antiarrhythmic drug. Thesaurus Antonyms Related Words Synonyms Legend: Noun 1. antiarrhythmic - a drug ...

• Antiarrhythmic | Define Antiarrhythmic at Dictionary.com

antiarrhythmic an·ti·ar·rhyth·mic (ān'tē-ə-rĭð'mĭk, ān'tī-) adj. Preventing or alleviating irregularities in the force or rhythm of the heart. n. An antiarrhythmic substance, such as lidocaine.

Related Pictures

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★リンクテーブル★

リンク元

「抗不整脈」

「抗不整脈」

　　[★]

英

antiarrhythmic

関

抗不整脈薬