José Roberto Barreto

Luminal Esophageal Temperature Monitoring With a Deflectable Esophageal Temperature Probe and Intracardiac Echocardiography May Reduce Esophageal Injury During Atrial Fibrillation Ablation Procedures Results of a Pilot Study

Background— Luminal esophageal temperature (LET) monitoring is one strategy to minimize esophageal injury during atrial fibrillation ablation procedures. However, esophageal ulceration and fistulas have been reported despite adequate LET monitoring. The objective of this study was to assess a novel approach to LET monitoring with a deflectable LET probe on the rate of esophageal injury in patients undergoing atrial fibrillation ablation. Methods and Results— Forty-five consecutive patients undergoing an atrial fibrillation ablation procedure followed by esophageal endoscopy were included in this prospective observational pilot study. LET monitoring was performed with a 7F deflectable ablation catheter that was positioned as close as possible to the site of left atrial ablation using the deflectable component of the catheter guided by visualization of its position on intracardiac echocardiography. Ablation in the posterior left atrial was limited to 25 W and terminated when the LET increased 2°C from baseline. Endoscopy was performed 1 to 2 days after the procedure. All patients had at least 1 LET elevation >2°C necessitating cessation of ablation. Deflection of the LET probe was needed to accurately measure LET in 5% of patients when ablating near the left pulmonary veins, whereas deflection of the LET probe was necessary in 88% of patients when ablating near the right pulmonary veins. The average maximum increase in LET was 2.5±1.5°C. No patients had esophageal thermal injury on follow-up endoscopy. Conclusions— A strategy of optimal LET probe placement using a deflectable LET probe and intracardiac echocardiography guidance, combined with cessation of radiofrequency ablation with a 2°C rise in LET, may reduce esophageal thermal injury during left atrial ablation procedures.

Catecholaminergic polymorphic ventricular tachycardia: a current overview.

Catecholaminergic polymorphic ventricular tachycardia occurs in healthy children and young adults causing syncope and sudden cardiac death. This is a familial disease, which affect de novo mutation in 50% of the cases. At least two causative genes have been described to be localized in the chromosome 1; mutation of the ryanodine receptor gene and calsequestrin gene. The classical clinical presentation is syncope triggered by exercise and emotion in children and adolescents with no structural heart disease. Polymorphic ventricular tachycardia during treadmill testing, or after isoproterenol infusion, is the most common feature. Therapeutic options include, beta-blockers, calcium-channel blockers and, an implantable cardioverter defibrillator is indicated in high-risk patients. Risk stratification of this disease is very challenging, since some risk factors proved to be useful in some series but not in others. However, family history of sudden cardiac death and symptoms initiated in very young children are important predictors.

Ablation of idiopathic ventricular tachycardia with left bundle-branch block morphology located in the pulmonary trunk

We report the case of a 26-year-old female patient with palpitations and presyncopes due to nonsustained ventricular tachycardia, who had no structural heart disease. The patient underwent electrophysiological study in an attempt to ablate the arrhythmogenic focus, whose location was determined by using mapping criteria. Because mapping of the right ventricular outflow tract was not successful, the catheter was placed inside the pulmonary artery with satisfactory mapping of the arrhythmogenic focus, and tachycardia was eliminated as soon as radiofrequency was initiated. The patient has remained asymptomatic for 14 months, with no treatment with antiarrhythmic drugs, and no arrhythmias on serial 24-hour Holter.