BIP ablation created much deeper lesions as compared to UNIP ablation. Lesion depth could be different depending on experimental preparation, and contact force-controlled DB preparation may be a much more appropriate model for studying the effects of BIP ablation.
Introduction: This experimental study was conducted to explore impedance monitoring for safely performing bipolar (BIP) radiofrequency (RF) ablation targeted to arrhythmia focus. Methods and Results: Using a newly designed dual-bath experimental model, contact-force-controlled (20-g) BIP ablation (50 W, 60 s) was attempted for porcine left ventricle (17.0 ± 2.7 mm thickness). BIP ablation was successfully accomplished for 60 s in 75 of the 89 RF applications (84.3%), whereas audible steam-pop occurred in the other 14 RF applications (15.7%). Receiver operating characteristic analysis demonstrated the optimal predictive values regarding the occurrence of steam-pop as follows; thinner myocardial wall (≤14.8 mm), low minimum impedance (≤89 ohm), greater total impedance decrement (TID) (≤ −25 ohm) and %TID (≤ −22.5%). Greater impedance decrement was not observed immediately preceding the occurrence of steam-pop but appeared around 15 s before. Four steam-pops happened before reaching the optimal predictive values of minimum impedance, whereas all 14 steam-pops developed 11.5 ± 9.2 and 8.1 ± 8.1 s after reaching the optimal predictive values of TID and %TID, respectively. Total lesion depth (endocardial plus epicardial) was 10.7 ± 1.2 mm on average, and was well correlated with TID and %TID. Transmural lesion through the myocardial wall was created in 22 RF applications. Conclusion: Relatively thinner areas of the myocardium are likely to be at greater risk for steam-pop during BIP RF ablation. Lowering the RF application energy to reduce the impedance decrement may help to lessen this risk.
Therapy-resistant ventricular arrhythmias can occur during accidental advanced hypothermic conditions. On the other hand, hypothermic therapy using mild cooling has been successfully accomplished with infrequent ventricular arrhythmia events.To further clarify the therapeutic-resistant arrhythmogenic substrate which develops in hypothermic conditions, an experimental study was performed using a perfusion wedge preparation model of porcine ventricle, and electrophysiological characteristics, inducibility of ventricular arrhythmias, and effects of therapeutic interventions were assessed at 3 target temperatures (37, 32 and 28 ).As the myocardial temperature decreased, myocardial contractions and the number of spontaneous beats deceased. Depolarization (QRS width, stimulus-QRS interval) and repolarization (QT interval, ERP) parameters progressively increased, and dispersion of the ventricular repolarization increased. At 28 , VF tended to be inducible more frequently (1/11 at 37 , 1/11 at 32 , and 5/11 hearts at 28 ), and some VFs at 28 required greater defibrillation energy to resume basic rhythm.An advanced but not a mild hypothermic condition had an enhanced arrhythmogenic potential in our model. In the advanced hypothermic condition, VF with relatively prolonged F-F intervals and a greater defibrillation energy were occasionally inducible based on the arrhythmogenic substrate characterized as slowed conduction and prolonged repolarization of the ventricle.
Sympathetic nerve activity has arrhythmogenic potential for ventricular arrhythmias associated with structural heart diseases. However, a sufficient amount of beta-blockers occasionally cannot be prescribed in some patients. An experimental study was performed to clarify the therapeutic effects of bepridil, a multiple ionic current inhibitor that does not affect beta-adrenergic receptors, for premature beats occurring during enhanced sympathetic nerve activity. Cardio-sympathetic nerve activity was augmented via stellate-ganglion (SG) stimulation in a canine model (n = 8), and the arrhythmogenic potential and anti-arrhythmic effects of bepridil (2 and 4 mg/kg intravenously) were assessed. For safe use, vagal-stimulation-induced slow HR and programmed electrical stimulation were applied to evaluate possible pro-arrhythmic effects of the drug. Heart rate variability (HRV) indexes were used to estimate cardio-autonomic nerve activity. Either side of the SG-stimulation increased BP and HR. Premature beats were induced in 10/16 SGstimulations and it was more frequent in left (8/8) rather than right stimulation (2/8). Following 2 mg/kg drug administration, premature beats were still inducible in 8/16 stimulations (7/8 in left and 1/8 in right), but burden of the premature beats decreased from 87.1 ± 46.8 to 62.1 ± 42.6 beats. After 4 mg/kg administration, premature beats were inducible in one SG-stimulation. Proarrhythmic effects were not observed in all experiments. Steady-state HRV indexes and percent increases in SG-stimulation-induced BP-elevation and HR-acceleration were similar among the 3 periods (before, 2 and 4 mg/kg of the drug). Bepridil may be an option for ventricular arrhythmias developed during enhanced cardio-sympathetic nerve activity with minimal effect on autonomic nerve responses.
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