Efficacy and Safety of Oral Dofetilide in Converting to and Maintaining Sinus Rhythm in Patients With Chronic Atrial Fibrillation or Atrial Flutter

Singh, Steven; Zoble, Robert G.; Yellen, Laurence; Brodsky, Michael A.; Feld, Gregory K.; Berk, Martin R.; Billing, Clare B.

doi:10.1161/01.cir.102.19.2385

Cited by 397 publications

(290 citation statements)

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“…Dofetilide and ibutilide, pure class III AADs, are effective for Atrial Flutter, Typical and Atypical interrupting flutter with a small risk of QT prolongation and torsade de pointes. Class IA and IC AADs are relatively ineffective or have no effect [60][61][62][63][64][65] and can be problematic if they cause a slow atrial flutter rate ≤200/min with 1:1 AV conduction and QRS widening that mimics ventricular tachycardia (see Figure 4). 66,67 Amiodarone may not be very effective at re-establishing sinus rhythm in the acute setting but it does help control ventricular rate.…”

Section: Management Of Atrial Fluttermentioning

confidence: 99%

Atrial Flutter, Typical and Atypical: A Review

Cosío

2017

Arrhythmia &Amp; Electrophysiology Review

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Clinical electrophysiology has made the traditional classification of rapid atrial rhythms into flutter and tachycardia of little clinical use. Electrophysiological studies have defined multiple mechanisms of tachycardia, both re-entrant and focal, with varying ECG morphologies and rates, authenticated by the results of catheter ablation of the focal triggers or critical isthmuses of re-entry circuits. In patients without a history of heart disease, cardiac surgery or catheter ablation, typical flutter ECG remains predictive of a right atrial re-entry circuit dependent on the inferior vena cava–tricuspid isthmus that can be very effectively treated by ablation, although late incidence of atrial fibrillation remains a problem. Secondary prevention, based on the treatment of associated atrial fibrillation risk factors, is emerging as a therapeutic option. In patients subjected to cardiac surgery or catheter ablation for the treatment of atrial fibrillation or showing atypical ECG patterns, macro-re-entrant and focal tachycardia mechanisms can be very complex and electrophysiological studies are necessary to guide ablation treatment in poorly tolerated cases.

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Section: Management Of Atrial Fluttermentioning

confidence: 99%

Atrial Flutter, Typical and Atypical: A Review

Cosío

2017

Arrhythmia &Amp; Electrophysiology Review

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“…For these drugs, available evidence indicates that both torsades risk and QT interval prolongation by the drugs are doserelated. [6][7][8] While these relationships speak to links among drug dose, I Kr block, QT prolongation, and torsades risk, they should not be over-interpreted. Specifically, it is clear that the extent of arrhythmia risk with a given drug dose or degree of QT prolongation varies among individuals, reflecting both known factors such as comedications, pauses, or underlying rhythm 9 as well as undetermined factors, including possible genetic contributors.…”

Section: Variable Arrhythmogenic Potential Of Qt Prolongationmentioning

confidence: 99%

Keep the QT interval: It is a reliable predictor of ventricular arrhythmias

Roden

2008

Heart Rhythm

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The cardiovascular community understands that the QT interval is the surface electrocardiographic representation of ventricular repolarization. However, despite tremendous advances in our understanding of the molecular and cellular basis for cardiac repolarization and its surface ECG representation, clinicians, regulators, and drug developers are increasingly faced with uncertainty over the best way to interpret this parameter. The evidence described below demonstrates that• Prolongation of the QT interval is a reliable predictor of ventricular arrhythmias in some settings, and may be less predictable in others• The arrhythmogenic potential of a given degree of QT prolongation varies among individuals and drugs. Further, the relationship between QT prolongation and arrhythmia susceptibility is non-linear. Multiple mechanisms may underlie QT prolongation, and these may carry different arrhythmogenic potential.• There is little doubt that further understanding of the cellular and molecular mechanisms underlying repolarization hold the promise of developing better indices of the arrhythmogenic potential of abnormalities of repolarization, but that science has not yet matured A caveat: The QT interval is hard to measureMeasuring the QT is hard enough when it is normal, and it is almost impossible to come up with a workable number in the face of common disease-associated ECG changes such as diffuse ST segment changes, inverted T-waves, small or large U-waves, or pauses (see Figure 1). A second problem is rate: while there is absolutely no doubt that action potential durations in ventricular tissue, and the QT interval, are exquisitely dependent on previous cycle length or cycle lengths, the "best" method to correct for rate, and thus allow QT intervals recorded at different rates to be compared, is not known. Indeed, comparing two "rate-corrected" QT values presupposes that whatever the intervention between the two recordings -often a drug -itself has no effect on rate. Further, even if a drug has no direct effect on rate, common conditions for which drugs are prescribed may be associated with increases in heart rate (e.g. due to fever or to autonomic activation); any effective drug may thus affect heart rate indirectly.

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“…The efficacy of oral dofetilide has been assessed in several randomized, placebo-controlled trials. 154,155 At the highest dose of dofetilide tested (500 g twice per day), maintenance of sinus rhythm more than or equal to 350 days occurred in 73% of patients with atrial flutter compared with 40% of patients with AF. Contraindications for dofetilide include creatinine clearance less than 20, hypokalemia, hypomagnesemia, and prolonged QT at baseline.…”

Section: Circulation October 14 2003mentioning

confidence: 99%