Symmetrical recovery time course between impedance and intramyocardial temperature after bipolar radiofrequency ablation; Role of impedance monitoring to estimate temperature rise.

INTRODUCTION: During radiofrequency (RF) ablation, impedance monitoring has been used to avoid steam-pop caused by excessive intramyocardial temperature (IMT) rise. However, it is uncertain why the impedance decline is related to steam-pop and whether the impedance decline is correlated to IMT. METHODS: Twenty-one bipolar ablations (40 W, 30-g contact, 120 s) were attempted for seven perfused porcine myocardium. Immediately after ablation, a temperature electrode was inserted into the mid-myocardial portion, and the recovery process of impedance and its correlation to IMT were assessed. RESULTS: Transmural lesion was created in all 21 applications but steam-pop occurred in 5/21 applications with large impedance decline. In the 16 applications without steam-pop, impedance and IMT soon after ablation were 97.2 ± 4.0 Ω and 66.1 ± 4.8 °C, respectively. Reasonably high linear correlation was demonstrated between the maximum IMT after ablation and impedance differences before and after ablation. Recovery processes of the decreased impedance and the elevated IMT fit well to each equation of the single exponential decay function and showed symmetric shapes with no statistical difference of time constant (100.1 ± 34.5 s in impedance vs. 108.7 ± 27.3 s in IMT) and half-time of recovery (144.5 ± 49.8 s in impedance vs. 156.9 ± 39.4 s in IMT). Recovered impedance after ablation (104.8 ± 3.9 Ω) was 5.1 ± 2.0 Ω smaller than that before ablation (109.9 ± 2.7 Ω), suggesting several factors other than IMT rise participate in impedance decline in RF ablation. CONCLUSIONS: Recovery of impedance and IMT after ablation well correlated, which supports the usefulness of impedance monitoring for safe RF ablation.

Impedance-decline-guide power control long application time bipolar radiofrequency catheter ablation.

INTRODUCTION: Bipolar (BIP) radiofrequency (RF) ablation creates deep myocardial lesions but ideal energy application modes to treat ventricular arrhythmias originating from deep inside the thick myocardium have not been well established. An experimental study was performed to clarify whether high power and long application time BIP ablation were performable by impedance-decline-guide power control (PC) and whether it could create transmural lesions in the thick ventricle with a minimum risk of steam-pop. METHODS AND RESULTS: Perfused porcine ventricle (18.4 ± 2.3 mm) was placed in an experimental bath and BIP ablation (50 W) for 120 s was attempted with catheter contact of 30-g using two protocols; fixed power (FP) and impedance-decline-guide PC. In the latter protocol, BIP ablation was started from 50 W, while the energy was decreased to 40-20 W according to the impedance decline during RF ablation. FP ablation was attempted in 30 applications and the transmural lesion was created in all 30, although steam-pop occurred in 16/30 applications (53%). Low minimum impedance, large total impedance decline (TID), and %-TID were associated with the steam-pop occurrence. PC ablation was attempted in another 21 applications, and the transmural lesion was created in all 21 without steam-pop. PC ablation was superior to FP ablation (21/21 vs. 14/30, p < .001) in the creation of a transmural lesion without resulting in steam-pop. CONCLUSIONS: High power and long application time BIP ablation seems to be feasible according to the impedance-decline-guide approach, which could create transmural lesions in thick porcine ventricles with minimal risk of steam-pop.

Impedance decrement indexes for avoiding steam-pop during bipolar radiofrequency ablation: An experimental study using a dual-bath preparation.

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.

Bepridil Inhibits Premature Ventricular Complexes Induced by Cardio-Sympathetic Nerve Stimulation in a Canine Experimental Model.

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 SG-stimulations 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.

Enhanced arrhythmogenic potential induced by renal autonomic nerve stimulation: Role of renal artery catheter ablation.

BACKGROUND: Renal artery catheter ablation has been reported as a possible therapeutic option for drug-refractory ventricular arrhythmias (VAs) associated with structural heart diseases. OBJECTIVE: To further clarify its therapeutic background, we examined the relationship between electrical nerve stimulation (ENS)-induced blood pressure (BP) elevation and occurrence of VAs by using an acute canine model of renal artery ablation. METHODS: Using a decapolar electrode catheter, ENS was successively applied from the distal, mid, and proximal segments of the renal artery in 8 beagles. The same ENS was repeated after accomplishment of radiofrequency ablation at the ostial site of the renal artery by using an irrigation catheter. RESULTS: Before ablation, ENS increased BP from 140 ± 11/77 ± 11 to 167 ± 20/98 ± 16 mm Hg and heart rate from 100 ± 21 to 131±33 beats/min as well as induced VAs in 20 of the 45 ENS applications. Occurrence of VAs was associated with a greater magnitude of sympathetic nerve augmentation, and VAs were more frequently observed by ENS at the distal (67%) rather than mid/proximal segments of the renal artery (33%). Renal artery ablation was accomplished without any angiographic stenosis, and ENS-induced BP elevation, heart rate acceleration, and VAs occurrence were attenuated not only at the close segment (proximal) but also at the remote segments (mid/distal) of the renal artery. CONCLUSION: The renal autonomic nerves are considered as one of the therapeutic targets for suppression of frequent VAs because its activation has arrhythmogenic potential and induces premature ventricular beats.

Therapy-Resistant Ventricular Arrhythmias Developed More Often in Advanced Than in Therapeutic Mild Hypothermic Condition.

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°C).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°C, VF tended to be inducible more frequently (1/11 at 37°C, 1/11 at 32°C, and 5/11 hearts at 28°C), and some VFs at 28°C 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.