Treatment of Resistant Atrial Fibrillation

Zarembski, Dawn G.; Nolan, Paul E.; Slack, Marion; Caruso, Anthony C.

doi:10.1001/archinte.1995.00430170081010

Cited by 56 publications

(4 citation statements)

References 45 publications

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“…In rhythm control therapy, amiodarone has shown relatively favorable efficacy, but it sometimes has serious extracardiac adverse effects such as lung fibrosis. [1][2][3][4] Bpd was recently reported as effective for AF and AFL. 5,[9][10][11][12] It has also multi-ion channel blocking effects similar to amiodarone, but fewer extra-cardiac adverse effects.…”

Section: Discussionmentioning

confidence: 99%

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Clinical Evaluation of Adverse Effects During Bepridil Administration for Atrial Fibrillation and Flutter

Yasuda

Nakazato

Sasaki

et al. 2006

Circ J

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Background Bepridil hydrochloride (Bpd) has attracted attention as an effective drug for atrial fibrillation (AF) and atrial flutter (AFL). However, serious adverse effects, including torsade de pointes (Tdp), have been reported. Methods and Results Adverse effects of Bpd requiring discontinuation of treatment were evaluated. Bpd was administered to 459 patients (361 males, 63±12 years old) comprising 378 AF and 81 AFL cases. Mean left ventricular ejection fraction and atrial dimension (LAD) were 66±11% and 40±6 mm, respectively. Adverse effects were observed in 19 patients (4%) during an average follow-up of 20 months. There was marked QT prolongation greater than 0.55 s in 13 patients, bradycardia less than 40 beats/min in 6 patients, dizziness and general fatigue in 1 patient each. In 4 of 13 patients with QT prolongation, Tdp occurred. The major triggering factors of Tdp were hypokalemia and sudden decrease in heart rate. There were no differences in the clinical backgrounds of the patients with and without Tdp other than LAD and age, which were larger and older in the patients with Tdp. Conclusion Careful observation of serum potassium concentration and the ECG should always be done during Bpd administration, particularly in elderly patients. (Circ J 2006; 70: 662 -666)

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Section: Discussionmentioning

confidence: 99%

“…In rhythm control therapy, amiodarone shows favorable efficacy by multi-ion channel blocking, -receptor blocking and also partly by reverse remodeling. [1][2][3][4] However, it has serious extra-cardiac adverse effects including lung fibrosis.…”

mentioning

confidence: 99%

Clinical Evaluation of Adverse Effects During Bepridil Administration for Atrial Fibrillation and Flutter

Yasuda

Nakazato

Sasaki

et al. 2006

Circ J

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“…Mean time of conversion to sinus rhythm was lower with class IC than with amiodarone [52,62], but they were similarly effective and equally welltolerated [63]. Sotalol is rather ineffective for AF conversion but it is effective to slow down the ventricular response to AF [64,65].…”

Section: Pharmacological Conversion -Restoration Of Sinus Rhythmmentioning

confidence: 93%

“…In patients with paroxysmal or chronic AF refractory to other ADs amiodarone provided sinus rhythm maintenance in 53-79% of patients after a follow-up time of about 15-22 months, suggesting a superior efficacy [61,63,88]. In the Canadian Trial of Atrial Fibrillation (CTAF) study, amiodarone was more effective than sotalol or propafenone at maintaining sinus rhythm in patients with either paroxysmal or persistent AF, but adverse effects resulting in drug withdrawal occurred more frequently in those treated with amiodarone [77].…”

Section: Maintenance Of Sinus Rhythm: Prevention Of Recurrencesmentioning

confidence: 99%

Pharmacological Approaches in the Treatment of Atrial Fibrillation

Tamargo¹,

Caballero²,

Delpón

2004

CMC

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Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with substantial cardiovascular morbidity and mortality. The arrhythmia can be initiated and/or maintained by rapidly firing foci, single- and multiple-circuit reentry. Once initiated, AF alters atrial electrical and structural properties (atrial remodeling) in a way that promotes its own maintenance and recurrence and may alter the response to antiarrhythmic drugs. Thus, initial episodes of paroxysmal (self-terminating) AF lengthens to the point where the arrhythmia becomes persistent (requires cardioversion to restore sinus rhythm) and permanent. AF usually requires a trigger for initiation and a favorable electrophysiological and/or anatomical substrate for maintenance. The substrate includes both cardiovascular (coronary artery disease, valvular heart disease, heart failure, hypertension, dilated cardiomyopathy) and non cardiovascular diseases (thyrotoxicosis, pulmonary diseases). Accordingly, the initial step in patients with AF requires a careful assessment of symptoms and identification of underlying reversible triggers and potentially modifiable underlying structural substrate and treat them aggressively. In contrast to other cardiac arrhythmias, antiarrhythmic drugs (ADs) are the mainstay of therapy. Long-term treatment of AF is directed to restore and maintain the sinus rhythm with class I and III ADs (rhythm-control) or to allow AF to persist and ensure that the ventricular rate is controlled (rate-control) with atrioventricular nodal blocking drugs (digoxin, beta-blockers, verapamil, diltiazem) and prevent thromboembolic complications with anticoagulants. However, the long-term efficacy of ADs for preventing AF recurrence is far from ideal, because of limited efficacy (AF recurs in at least one-half of the patients) and potential side effects, particularly proarrhythmia. Thus, the choice of the appropriate AD will depend on the temporal pattern of the arrhythmia, the presence of associated diseases, easy of administration and adverse effects profile, particularly the risk of proarrhythmia. The recent finding that angiotensin converting enzyme inhibitors and beta-blockers reduce the incidence of AF in patients post myocardial infarction with left ventricular dysfunction confirmed the importance of targeting the underlying arrhythmogenic substrate. This review focuses on the mechanisms underlying AF and the mechanism of action and the efficacy and safety profile of the ADs used in the treatment of atrial fibrillation. The advantages and disadvantages of rhythm and rate control, the role pill in a pocket concept and the role of the new ADs are dicussed.

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