Background
- The mechanism of esophageal thermal injury (ETI; esophageal mucosal injury and periesophageal nerve injury leading to gastric hypomotility) remains unknown when using a high-power short-duration (HP-SD) setting. This study sought to evaluate the characteristics of esophageal injuries in atrial fibrillation (AF) ablation using a high-power short-duration (HP-SD) setting.
Methods
- After exclusion of 5 patients with their esophagus at the right portion of left atrium (LA) and 21 patients with additional ablations such as box isolation and/or low voltage ablation in LA posterior wall, 271 consecutive patients (62 ± 10 years, 56 women) who underwent pulmonary vein isolation (PVI) by radiofrequency catheter ablation were analyzed. In the 101 patients, a HP-SD setting at 45-50 W with an Ablation Index module® was used (HP-SD group). In the remaining 170 patients before introduction of the HP-SD setting, a conventional power setting of 20-30 W with contact force monitoring was used (Conventional group). We performed esophagogastroduodenoscopy after PVI in all patients and investigated the incidence and characteristics of ETI.
Results
- Although the incidence of ETI was significantly higher in the HP-SD group compared to the Conventional group (37% vs. 22%, P = 0.011), the prevalence of esophageal lesions did not differ between the groups (7% vs. 8%). Multivariate logistic regression analysis revealed that the use of the HP-SD setting (odds ratio: 6.09, P < 0.001), and the parameters that suggest anatomical proximity surrounding the esophagus, were independent predictors of ETI. However, the majority of ETI in the HP-SD group was gastric hypomotility, and the thermal injury was limited to the shallow layer of the periesophageal wall using the HP-SD setting.
Conclusions
- Although the use of the HP-SD setting was a strong predictor of ETI, it could avoid deeper thermal injuries that reach the esophageal mucosal layer.
Intravenous injection of pravastatin prevents impaired NO-dependent vasodilation and Rac1/NAD(P)H oxidase-mediated-ROS generation by blocking the down-regulation of Akt/eNOS pathways and the full activation of unprocessed RhoA and Rac1 in vivo.
Background
Both endocardial trigger elimination and epicardial substrate modification are effective in treating ventricular fibrillation (VF) in Brugada syndrome. However, the primary approach and the characteristics of patients who respond to endocardial ablation remain unknown.
Methods
Among 123 symptomatic Brugada syndrome patients (VF, 63%; syncope, 37%), ablation was performed in 21 VF/electrical storm patients, the majority of whom were resistant to antiarrhythmic drugs.
Results
Careful endocardial mapping revealed that 81% of the patients had no specific findings, whereas 19% of the patients, who experienced the most frequent VF episodes with notching of the QRS in lead V
1
, had delayed low-voltage fractionated endocardial electrograms. Ablation of VF triggers followed by endocardial substrate modification was performed in the right ventricular outflow tract in 85% of the cases and in the right ventricle in 15%. VF triggers could not be completely eliminated in 1 patient and VF became noninducible in 14 (88%) patients among 16 patients who underwent VF induction with normalization of Brugada-type ECG in 3. During follow-up (56.14±36.95 months), VF recurrence was observed in 7 patients. Importantly, all patients who had nothing of QRS in lead V
1
did not respond to endocardial ablation despite presence of VF-triggering ectopic beats during ablation.
Conclusions
With careful documentation of VF-triggering ectopic beats and detailed endocardial mapping, endocardial VF trigger elimination followed by endocardial substrate modification has an excellent long-term outcome, whereas presence of QRS notching in lead V
1
was associated with high VF recurrence suggesting epicardial substrate ablation as effective initial approach.
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