Dofetilide Reduces the Frequency of Ventricular Arrhythmias and Implantable Cardioverter Defibrillator Therapies

Baquero, Giselle A.; Banchs, Javier E.; DePalma, Sondra M.; Young, Sallie K.; Penny-Peterson, Erica; Samii, Soraya; Wolbrette, Deborah L.; Naccarelli, Gerald V.; González, Mario D.

doi:10.1111/j.1540-8167.2011.02183.x

Cited by 48 publications

(21 citation statements)

References 31 publications

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“…A more recent study in 30 ICD recipients with drug-refractory VT/VF episodes showed a significant reduction in both monthly ventricular arrhythmia episodes (from 1.8 ± 4.5 to 1.0 ± 3.5, P = 0.006) and monthly ICD therapies (from 0.9 ± 1.4 to 0.4 ± 1.7, P = 0.037) after treatment with dofetilide. In addition, 83% of patients had complete suppression of VT/VF during their first month of treatment [60]. …”

Section: Discussionmentioning

confidence: 99%

Current and Emerging Antiarrhythmic Drug Therapy for Ventricular Tachycardia

Williams

Viswanathan

2013

Cardiol Ther

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Ventricular arrhythmias, including ventricular fibrillation (VF) and sustained ventricular tachycardia (VT), are the principal causes of sudden cardiac death in patients with structural heart disease. While coronary artery disease is the predominant substrate associated with the development of VT, these arrhythmias are known to occur in a variety of disorders, including dilated cardiomyopathy, valvular and congenital heart disease, and cardiac ion channelopathies such as the long QT syndrome. In a minority of patients, VT occurs in the absence of structural heart disease. Despite the established mortality benefit of the implantable cardioverter defibrillator (ICD) in patients at risk of lethal arrhythmias, recurrent VT/VF events continue to be a source of morbidity and impaired quality of life in such patients. Antiarrhythmic therapy is indicated in select patients to treat symptomatic VT episodes, to reduce the incidence of ICD shocks, and potentially to improve quality of life and reduce hospitalizations related to cardiac arrhythmia. The primary adverse effects of antiarrhythmic medications are related to both cardiac and extracardiac toxicity, including the risk of proarrhythmia. Current drug therapy for ventricular arrhythmia has been limited by suboptimal efficacy in many patients, resulting in recurrent VT/VF events, and by drug toxicity or intolerance leading to discontinuation in a large percentage of patients. Amiodarone and sotalol are the principal agents used in the chronic treatment of VT. In addition, dronedarone and dofetilide, agents approved for the treatment of atrial fibrillation, and ranolazine, an antianginal agent, have been demonstrated to be protective against ventricular arrhythmia in small clinical studies. Finally, advances in basic electrophysiology have uncovered new molecular targets for the treatment of ventricular arrhythmia, and pharmacologic agents directed at these targets may emerge as promising VT treatments in the future. The roles of these current and emerging therapies for the treatment of VT in humans will be summarized in this review.

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Section: Discussionmentioning

confidence: 99%

Current and Emerging Antiarrhythmic Drug Therapy for Ventricular Tachycardia

Williams

Viswanathan

2013

Cardiol Ther

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“…58 Although dofetilide has only been studied in randomized controlled trials for atrial fibrillation, dofetilide may be an option for patients with VT, because there has been an association noted between dofetilide use and lower rates of VT and appropriate ICD therapy in patients with secondary prevention ICDs. 59 Ranolazine is a late sodium channel blocker that has been shown to decrease VT episodes within the first week after myocardial infarction, 60 and the ongoing (RAID) Ranolazine Implantable Cardioverter-Defibrillator Trial will answer the question about the benefit of ranolazine in preventing appropriate ATP, ICD shocks, or death in primary and secondary prevention ICD patients (NCT01215253). 61 When using antiarrhythmic medications in patients who have received ATP therapy, it is important to remember the effects of the antiarrhythmic medications on defibrillation thresholds.…”

Section: Medications For Treatment and Prevention Of Ventricular Tachmentioning

confidence: 99%

Management of Pace-Terminated Ventricular Arrhythmias

Pokorney

Al‐Khatib

2015

Cardiac Electrophysiology Clinics

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“…Another clinical trial documented a decrease in the frequency of defibrillation shocks in patients with an ICD and recurrent VT and VF receiving adjuvant therapy with dofetilide. Dofetilide decreases the frequency of VT/VF and ICD shocks even when other AADs including amiodarone have failed 55 .…”

Section: Role Of Antiarrhythmic Drugs In Patients With Icdsmentioning

confidence: 99%

Class I and III antiarrhythmic drugs for prevention of sudden cardiac death and management of postmyocardial infarction arrhythmias. A review

Vrána

Pokorný²,

Marcián³

et al. 2013

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The aim of the present paper is to review the evolution of concepts regarding the use of Class I and III antiarrhythmic drugs (AADs) in myocardial infarction over the past four decades. Methods. Results of animal experiments carried out by the authors and papers published between 1970 and 2012 in journals and the PubMed search system were used. Results. Animal experiments carried out as early as the 1970s showed that Class IB and IC AADs lose their antiarrhythmic effect and electrically destabilize ventricles in the very early phase of myocardial ischemic focus formation. The cause of this is interaction between Class IB and IC AADs as well as Class III AADs with sympathetic neural activation (SNA) of the heart in the early phase of myocardial ischemia. Given the extremely high and uneven distribution of noradrenaline in tissue, SNA results in dispersion of the depolarization and repolarization processes in the ventricles. The clinical sequels of the interaction between the effects of AADs and SNA are as follows: the antiarrhythmic effect of AADs is restored in AMI once SNA has resolved; membrane-destabilization of the ventricles can be restored any time in the presence of randomly occurring SNA not only due to increasing myocardial ischemia but, also, as a result of psychological stress (emotions), and any pre-existing structural heart disease will enhance the pro-fibrillatory effect of a randomly occurring SNA. Conclusions. Despite the above risks, AADs continue to play an irreplaceable role in suppressing post-myocardial arrhythmias and in preventing sudden cardiac death following ICD placement. The risk of AADs' proarrhythmic effect in SNA can be reduced by combining them with beta-blockers. The last recourse when attempting to suppress malignant ventricular tachyarrhythmias is left sympathetic denervation of the heart.

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Dofetilide Reduces the Frequency of Ventricular Arrhythmias and Implantable Cardioverter Defibrillator Therapies

Cited by 48 publications

References 31 publications

Current and Emerging Antiarrhythmic Drug Therapy for Ventricular Tachycardia

Current and Emerging Antiarrhythmic Drug Therapy for Ventricular Tachycardia

Management of Pace-Terminated Ventricular Arrhythmias

Class I and III antiarrhythmic drugs for prevention of sudden cardiac death and management of postmyocardial infarction arrhythmias. A review

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