Key result
In a canine model, ventricular ICD shocks induced atrial fibrillation depending on shock intensity and timing to the atrial effective refractory period, with distinct upper and lower limits of vulnerability.
Why the study?
Does the timing and intensity of ventricular ICD shocks relative to the atrial effective refractory period affect the induction of atrial fibrillation in a canine model?
Does the timing and intensity of ventricular ICD shocks relative to the atrial effective refractory period affect the induction of atrial fibrillation in a canine model?
p-value: p=<0.05
Ventricular ICD shocks can induce atrial fibrillation if delivered during a specific vulnerable window relative to the atrial effective refractory period, suggesting that avoiding this window may minimize post-shock AF.
Identifies atrial vulnerability window to ventricular shocks in canines; leaves open translation to human ICD programming.
BACKGROUND: Implantable ventricular cardioverter defibrillator (ICD) shocks can cause atrial fibrillation/flutter (AF). This study investigated the pathogenesis of AF after ICD shocks in a canine model. METHODS AND RESULTS: The study was conducted in 8 dogs. In 5 dogs (group 1), truncated exponential (8 ms, 78% tilt) monophasic and biphasic shocks were delivered through a bipolar epicardial (patch) or endocardial lead. After the last S1 of atrial pacing at a cycle length of 350 ms, shocks of 0.1 to 7.6 A (0.005 to 27.7 J) were delivered, timed to the atrial effective refractory period (AERP). Ventricular defibrillation thresholds were also determined. In 3 dogs (group 2), the effect of the open versus closed chest technique on AF induction was tested in the endocardial biphasic shock configuration. AF was induced in all 8 dogs and in all waveforms and configurations. Mean AF duration was 11.5+/-6 s, with a mean ventricular rate of 184+/-37 bpm. Ventricular shocks could induce AF only if they were timed between an AERP of -60 to 40 ms, -40 to 60 ms, -40 to 60 ms, and -20 to 60 ms in the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively. The mean+/-SD of the upper limit of vulnerability (ULV) for AF induction (in J) was 5. 2+/-0.6, 3.5+/-0.4, 5.2+/-1.2, and 2.5+/-0.1 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P<0.05). The lower limit of vulnerability (LLV) was 0.8+/-0.1, 0.8+/-0.1, 0.9+/-0, and 0.6+/-0 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P=NS). The ventricular defibrillation threshold (in J) for all wave forms and configurations was higher than the ULV (P<0. 05). CONCLUSIONS: (1) An atrial LLV and ULV exist for ventricular ICD shock-induced AF; (2) the shock-induced AF is related to both shock intensity and its timing to AERP; and (3) avoiding this atrial window of vulnerability may minimize the risk of post-ICD shock AF.
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Katz et al. (1999) studied Atrial fibrillation/flutter following ICD shocks (n=8). Ventricular ICD shocks vs. Different waveforms and configurations was evaluated on Upper and lower limits of vulnerability for AF induction (p=<0.05). In a canine model, ventricular ICD shocks induced atrial fibrillation depending on shock intensity and timing to the atrial effective refractory period, with distinct upper and lower limits of vulnerability.
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