We then started isoproternol up to 10mcg/min with no induction of atrial tachycardia or atrial fibrillation. Within several seconds of ablation, there was complete cessation of tachycardia. We decided to ablate in this region, which was anatomically on the mid posterior wall of the left atrium at the os of the left superior pulmonary vein. The left superior pulmonary vein demonstrated the earliest potentials 40msec in advance of the surface p wave (Figure 3). The circular catheter was then placed at the os of each pulmonary vein. We then accessed the left atrium through a standard double trans-septal access. We performed electro-anatomic mapping in the right atrium with demonstration of late activation times. The patient was taken to the electrophysiologic laboratory. Figure 2 is a continuous strip from a Holter tracing (lead II).
He was interested in catheter ablation due to intolerance of medications, and was referred to our facility.įigure 1 is a 12-lead ECG demonstrating bursts of atrial tachycardia. This study noted “disorganized atrial activity with earliest activation in the left atrium consistent with atrial fibrillation/flutter.” Given the left sided location, the treating physicians decided to pursue medical management with beta blockers and a class Ic antiarrhythmic. He underwent electrophysiologic study at an outside institution.
The patient did not demonstrate signs or symptoms of heart failure, and regularly exercised. Further diagnostic testing included a 2D echocardiogram demonstrating evidence of globally depressed left ventricular (LV) function with an ejection fraction (EF) of 33%. Prior Holter monitoring demonstrated episodes of atrial fibrillation as well as an atrial tachycardia. A 50-year old-male is referred to our electrophysiologic service for evaluation of palpitations.
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