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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/06 23:07:10」(JST)

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Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic drugs to facilitate emergence of new arrhythmias.

Types of proarrhythmia

According to the Vaughan Williams classification (VW) of antiarrhythmic drugs, there are 3 main types of Proarrhythmia during treatment with various antiarrhythmic drugs for Atrial Fibrillation or Atrial flutter:

Ventricular proarrhythmia

Torsades de pointes (VW type IA and type III drugs)
Sustained monomorphic ventricular tachycardia (usually VW type IC drugs)
Sustained polymorphic ventricular tachycardia/ventricular fibrillation without long QT (VW types IA, IC, and III drugs)

Atrial proarrhythmia

Conversion of atrial fribrillation to flutter (usually VW type IC drugs or amiodarone). May be a desired effect.
Increase of defibrillation threshold (a potential problem with VW type IC drugs)
Provocation of recurrence (probably VW types IA, IC and III drugs). It is rare.

Abnormalities of conduction or impulse formation

Sinus node dysfunction, atrioventricular block (almost all drugs)
Accelerate conduction over accessory pathway (digoxin, intravenous verapamil, or diltiazem)
Acceleration of ventricular rate during atrial fibrillation (VW type IA and type IC drugs).

Increased risk

Presence of structural heart disease, especially LV systolic dysfunction.
Class IC agents.
Increased age.
Females.

Clinical pointers

Class IA drugs

Dose independent, occurring at normal levels.
Follow QT interval, keep ms.

Class IC drugs

May be provoked by increased heart rate.
Exercise stress tests after loading.

Class III drugs

Dose dependent.
Follow bradycardia, prolonged QT closely.

External links

Roden DM (August 1998). "Mechanisms and management of proarrhythmia". Am. J. Cardiol. 82 (4A): 49I–57I. doi:10.1016/S0002-9149(98)00472-X. PMID 9737654.

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English Journal

Propafenone-Induced Syncope and Atrial Pacemaker.

Wagner V, Nényei Z, Tomcsányi J.SourceDepartment of Cardiology of St. John of God Hospital, Budapest, Hungary.
Pacing and clinical electrophysiology : PACE.Pacing Clin Electrophysiol.2013 Jul 11. doi: 10.1111/pace.12204. [Epub ahead of print]
PMID 23844932

The genetics of pro-arrhythmic adverse drug reactions.

Petropoulou E, Jamshidi Y, Behr ER.SourceHuman Genetics Research Centre, Division of Biomedical Sciences, St George's Hospital Medical School, London, SW17 0RE, UK.
British journal of clinical pharmacology.Br J Clin Pharmacol.2013 Jul 9. doi: 10.1111/bcp.12208. [Epub ahead of print]
Ventricular arrhythmia induced by drugs (proarrythmia) is an uncommon event, whose occurrence is unpredictable but potentially fatal. The ability of a variety of medications to induce these arrhythmias is a significant problem facing the pharmaceutical industry. Genetic variants have been shown to p
PMID 23834499

A history of the role of the hERG channel in cardiac risk assessment.

Rampe D, Brown AM.SourceDisposition, Safety, and Animal Research, Sanofi, Inc., Route 202-206, Bridgewater, NJ 08807, United States. Electronic address: david.rampe@sanofi.com.
Journal of pharmacological and toxicological methods.J Pharmacol Toxicol Methods.2013 Jul-Aug;68(1):13-22. doi: 10.1016/j.vascn.2013.03.005. Epub 2013 Mar 26.
The human ether-a-go-go-related gene (hERG, Kv11.1) K(+) channel plays an important role in cardiac repolarization. Following its cloning and expression it was established that inhibition of this channel was the molecular mechanism for many non-antiarrhythmic drugs that produce torsades de pointes a
PMID 23538024