Safety and Efficacy of Ibutilide in Cardioversion of Atrial Flutter and Fibrillation

The Journal of the American Board of Family Medicine

Madhuri Nair¹  Lekha K. George²  Santhosh K. G. Koshy² 

[1] Department of Medicine, University of Oklahoma at Tulsa, Tulsa (MN);Department of Medicine, University of Tennessee Health Sciences Center, Memphis (LKG, SKGK)

关键词: Antiarrhythmics;    Arrhythmia;    Atrial Fibrillation;    Cardiovascular Disorders;    Cardioversion;    Drug Therapy;    Ibutilide;    Patient Safety;    QT Prolongation;   

DOI  :  10.3122/jabfm.2011.01.080096

学科分类：过敏症与临床免疫学

来源: The American Board of Family Medicine

【 摘 要 】

This article reviews the safety and efficacy of ibutilide for use in patients with atrial fibrillation and flutter. Ibutilide, a class III antiarrhythmic agent, is primarily used for conversion of atrial flutter and fibrillation and is a good alternative to electrical cardioversion. Ibutilide has a conversion rate of up to 75% to 80% in recent-onset atrial fibrillation and flutter; the conversion rate is higher for atrial flutter than for atrial fibrillation. It is also safe in the conversion of chronic atrial fibrillation/flutter among patients receiving oral amiodarone therapy. Ibutilide pretreatment facilitates transthoracic defibrillation and decreases the energy requirement of electrical cardioversion by both monophasic and biphasic shocks. Pretreatment with ibutilide before electrical defibrillation has a conversion rate of 100% compared with 72% with no pretreatment. Ibutilide is also safe and efficient in the treatment of atrial fibrillation in patients who have had cardiac surgery, and in accessory pathway–mediated atrial fibrillation where the conversion rate of ibutilide is as high as 95%. There is up to a 4% risk of torsade de pointes and a 4.9% risk of monomorphic ventricular tachycardia. Hence, close monitoring in an intensive care unit setting is warranted during and at least for 4 hours after drug infusion. The anticoagulation strategy is the same as for any other mode of cardioversion.

• Antiarrhythmics
• Arrhythmia
• Atrial Fibrillation
• Cardiovascular Disorders
• Cardioversion
• Drug Therapy
• Ibutilide
• Patient Safety
• QT Prolongation

In selected patient populations, cardioversion still remains the preferred management for atrial fibrillation and flutter, even though data suggest no survival advantage for rhythm control over rate control.¹ Electrical cardioversion has been the most widely used and the most effective method to restore sinus rhythm in these atrial arrhythmias. However, chemical cardioversion is a good alternative for use in certain patient groups. Chemical cardioversion is less invasive, more cost-effective, and, unlike electrical cardioversion, it does not require sedation.^2–4 The various drugs commonly used for pharmacologic cardioversion are ibutilide, procainamide, propafenone, flecanide, amiodarone, and dofetilide. Among these drugs, ibutilide, dofetilide, flecanide, and propafenone have class I (level of evidence A) indication for their use in pharmacologic cardioversion of atrial fibrillation.⁵ This corresponds to the Strength of Recommendation Taxonomy (SORT) level 1 recommendation. Amiodarone has class IIa (SORT level 2 recommendation), whereas procainamide and quinidine have class IIb (SORT level 3 recommendation) indication for their use in cardioversion of atrial fibrillation.⁵ Digoxin and sotalol do not have proven efficacy when used for this purpose.⁵

Ibutilide—despite its efficacy, which is comparable or superior to other agents—is not widely used, mainly because of physician's lack of awareness about its safety and efficacy profile. This article reviews the safety and efficacy data of ibutilide and also compares it with other antiarrhythmics used for atrial fibrillation and flutter.

Ibutilide, a class III antiarrhythmic drug that was approved by the Food and Drug Administration for use on December 28, 1995, is available only for intravenous use because of its extensive first-pass metabolism. It prolongs repolarization time, action potential duration, and refractory period of atrial and ventricular myocardium through its action as a potassium channel blocker, affecting the rapid component of the cardiac delayed rectifier potassium current.⁶ In addition to this action, ibutilide also activates the slow delayed inward sodium current that occurs early during repolarization.⁶ Ibutilide also increases the refractory period of the accessory pathway, the His-Purkinje system, and the atrioventricular node.⁶

The most common electrocardiography changes caused by ibutilide are mild slowing of the sinus rate and prolongation of QT interval, similar to most other class III antiarrhythmic drugs. The degree of prolongation of QT interval is related to the dose, the rate of infusion, and serum concentration.⁷ The QT interval returns to baseline within 2 to 4 hours after stopping the infusion^8,9; however, PR or QRS intervals are not affected.¹⁰

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