[Show abstract][Hide abstract] ABSTRACT: This study compared a biphasic waveform with a conventional monophasic waveform for cardioversion of atrial fibrillation (AF).
Biphasic shock waveforms have been demonstrated to be superior to monophasic shocks for termination of ventricular fibrillation, but data regarding biphasic shocks for conversion of AF are still emerging.
In an international, multicenter, randomized, double-blind clinical trial, we compared the effectiveness of damped sine wave monophasic versus impedance-compensated truncated exponential biphasic shocks for the cardioversion of AF. Patients received up to five shocks, as necessary for conversion: 100 J, 150 J, 200 J, a fourth shock at maximum output for the initial waveform (200 J biphasic, 360 J monophasic) and a final cross-over shock at maximum output of the alternate waveform.
Analysis included 107 monophasic and 96 biphasic patients. The success rate was higher for biphasic than for monophasic shocks at each of the three shared energy levels (100 J: 60% vs. 22%, p < 0.0001; 150 J: 77% vs. 44%, p < 0.0001; 200 J: 90% vs. 53%, p < 0.0001). Through four shocks, at a maximum of 200 J, biphasic performance was similar to monophasic performance at 360 J (91% vs. 85%, p = 0.29). Biphasic patients required fewer shocks (1.7 +/- 1.0 vs. 2.8 +/- 1.2, p < 0.0001) and lower total energy delivered (217 +/- 176 J vs. 548 +/- 331 J, p < 0.0001). The biphasic shock waveform was also associated with a lower frequency of dermal injury (17% vs. 41%, p < 0.0001).
For the cardioversion of AF, a biphasic shock waveform has greater efficacy, requires fewer shocks and lower delivered energy, and results in less dermal injury than a monophasic shock waveform.
Journal of the American College of Cardiology 06/2002; 39(12):1956-63. DOI:10.1016/S1062-1458(02)00955-8 · 16.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Compared with monophasic defibrillation, biphasic defibrillation is associated with less myocardial stunning and earlier activation of sodium channels. We therefore hypothesised that earlier sodium channel activation would result in earlier restoration of the first sinus beat following elective DC cardioversion.
Adults undergoing elective DC cardioversion were randomised to receive either monophasic or biphasic escalating transthoracic shocks. The ECG was recorded electronically during defibrillation and the time from delivery of the shock to restoration of the first sinus beat, measured from the beginning of the 'P' wave, was calculated.
Seventy four patients were studied. Data were unavailable from 18 patients. There was no demographic difference between groups. Median time to the first sinus beat following monophasic defibrillation (n=25) was 3.66 s (95% CI 2.55-4.61 s) and following biphasic defibrillation (n=33) was 2.21s (95% CI 1.76-2.56 s; P<or=0.0001). Linear regression confirmed that the waveform was an independent predictor of time to restoration of sinus rhythm; P<0.0001. The final defibrillation energy level used to achieve cardioversion was not an independent predictor of time to restoration of sinus rhythm; P=0.49.
Biphasic defibrillation for elective DC cardioversion achieved more rapid restoration of the first sinus beat compared with a monophasic waveform. Waveform, but not energy level that achieved defibrillation, was an independent predictor of time to restoration of the first sinus beat. The mechanism for this may be related to the earlier reactivation of sodium channels associated with the biphasic waveform.
[Show abstract][Hide abstract] ABSTRACT: Conversion of atrial fibrillation and flutter to sinus rhythm results in a transient mechanical dysfunction of atrium and atrial appendage, termed atrial stunning. Atrial stunning has been reported with all modes of conversion of atrial fibrillation and flutter to sinus rhythm including both transthoracic and low energy internal electrical, pharmacological, and spontaneous cardioversion, and conversion by overdrive pacing and by radiofrequency ablation. Atrial stunning is a function of the underlying arrhythmia becoming apparent at the restoration of sinus rhythm, not the function of the mode of conversion, and does not develop after the unsuccessful attempts of cardioversion or the delivery of electric current to the heart during rhythms other than atrial fibrillation or flutter. Tachycardia-induced atrial cardiomyopathy, cytosolic calcium accumulation, and atrial hibernation are the suggested mechanisms of atrial stunning. Atrial stunning is at maximum immediately after cardioversion and improves progressively with a complete resolution within a few minutes to 4-6 weeks depending on the duration of the preceding atrial fibrillation, atrial size, and structural heart disease. Atrial stunning causes postcardioversion thromboembolism despite restoration of sinus rhythm. Duration of anticoagulation therapy after successful cardioversion should depend on the duration of atrial stunning. Lack of improvement in cardiac output and functional recovery of patients immediately after cardioversion is attributed to the atrial stunning. Verapamil, acetylstrophenathidine, isoproterenol, and dofetilide have been reported to protect from atrial stunning in animal and small human studies. Right atrium stunning is less marked and improves earlier than that of left atrium, resulting in a differential atrial stunning explaining the rare occurrence of pulmonary edema after cardioversion.
International Journal of Cardiology 01/2004; 92(2-3):113-28. DOI:10.1016/S0167-5273(03)00107-4 · 4.04 Impact Factor
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