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PubMed2005

Therapies for the prevention of stroke and other vascular events in atrial fibrillation and atrial flutter.

Stroke is the major clinical cause of atrial fibrillation (AF). Treatments to reduce the risk of stroke and other vascular events are an important part of AF management. Oral anticoagulation is effective against stroke and has an acceptable risk of adverse events (primarily bleeding). Acetylsalicylic acid is less effective than oral anticoagulants but better tolerated. Anticoagulants are recommended for AF patients with risk factors for stroke.

Atrial Fibrillation↗
PubMed1988

Long-term oral propafenone therapy for suppression of refractory symptomatic atrial fibrillation and atrial flutter.

Sixty patients who had recurrent episodes of symptomatic atrial fibrillation or flutter, or both, and who had failed one to five prior drug trials were treated with open label oral propafenone hydrochloride. On a mean maximal tolerated dose of 795 +/- 180 mg/day, actuarial estimates of the percent of individuals free of recurrences of symptomatic atrial fibrillation/flutter during propafenone treatment were: 1 month, 54%; 3 months, 44% and 6 months, 40%. No individual baseline characteristic achieved statistical significance as a correlate of poor response to propafenone. Drug-related adverse reactions were reported in 22% of patients but were severe enough to require termination of propafenone in only 5%. Thus, oral propafenone is a useful and well tolerated drug for long-term suppression of symptomatic recurrences of atrial fibrillation/flutter despite a history of unresponsiveness to prior antiarrhythmic drug treatment.

Actuarial Analysis↗
PubMed2002

Electrophysiological response of the right atrium to ibutilide during typical atrial flutter.

BACKGROUND: The efficacy of ibutilide in conversion of atrial fibrillation and flutter (AFL) has been demonstrated. However, its electrophysiological effects on human atria have not been fully studied. METHODS AND RESULTS: Twelve patients with typical AFL were studied. Electrograms were recorded from the anterolateral right atrium, His bundle position, and coronary sinus. During AFL, we measured the conduction time, CTi, through the isthmus between the tricuspid annulus and eustachian ridge and the conduction time, CTni, through the remainder of the right atrium. Resetting response curves and atrial effective refractory periods were determined with single extrastimuli delivered in the tricuspid annulus-eustachian ridge isthmus. After infusion of ibutilide (2 mg over 15 minutes), AFL cycle length (CL) increased from 260+/-30 to 295+/-39 ms (P<0.0003) because of an increase in either CTi, CTni, or both. Effective refractory periods increased from 149+/-16 to 208+/-26 ms (P<0.001). AFL CL variability increased, with a rightward shift of the resetting response curves and loss of full excitability. In 8 patients, AFL was terminated by atrial overdrive pacing after ibutilide at CLs equal to or longer than those that were not effective at baseline, which was caused by orthodromic block in the tricuspid annulus-eustachian ridge isthmus or was associated with development of transient rapid rhythms around newly formed sites of intra-atrial conduction block. CONCLUSIONS: Ibutilide causes prolongation of AFL CL and increased CL variability by abolishment of a fully excitable gap. Ibutilide may facilitate pace termination of AFL by development of new short-lived reentry around functional blocks.

Adult↗
PubMed2002

[Current strategies of pharmacological and non-pharmacological treatment in atrial fibrillation and atrial flutter].

The current information regarding mechanistic understanding of atrial fibrillation(AF) and flutter(AFL) is reviewed, and the recent development in both pharmacological and non-pharmacological treatment for AF and AFL is also introduced. For the antiarrhythmic therapy, the effectiveness and safety of new class III drugs(ibutilide and azimilide) in the termination and prophylactic therapy are focused. In the non-pharmacological section, several ablative strategies including electrical isolation of PV-LA interface for focal AF, 'Ablate and Pace' therapy and AV nodal modification for drug-refractory tachycardic AF, and so-called 'Hybrid' therapy are introduced. It is emphasized that the newly developed 3-dimensional mapping system is useful to determine the appropriate target site of ablation for atypical AFL.

Atrial Fibrillation↗
PubMed2002

Ablation of atrial flutter: block (isthmus conduction) or not a block, that is the question?

It is important to identify residual slow conduction and minimize the chance of resumption of conduction after right atrial isthmus ablation to reduce the chance of recurrence of atrial flutter (AFL). The aim of this article is to discuss the best possible way of confirming a bi-directional isthmus conduction (BIC) block after ablation of an isthmus-dependent AFL. A combination of activation and double potential mapping seems to be the most practical way of acutely confirming the BIC block.

Journal Article↗