A Hybrid Approach to the Cure of Atrial Fibrillation <br />

History The patient was a 61-year-old retired male with a history of persistent AF for 7 years. His arrhythmic events were initially paroxysmal but had progressed to persistent AF. He had previously failed sotalol and propafenone. He also had mild coronary artery disease, hypertension, obesity, and hyperlipidemia. His echocardiogram revealed a left atrium (LA) size of 6.0 cm and mild mitral regurgitation (MR). Three weeks earlier he had undergone endocardial catheter-based AF ablation with ostial isolation of all four pulmonary veins, left inferior pulmonary vein (LI)-mitral isthmus line, roof line ablation, and cavotricuspid isthmus line ablation. At hospital discharge he was in sinus rhythm, which he maintained for just eight days before reverting back to AF. He was subsequently brought in for a TEE and cardioversion, and following this, the addition of amiodarone and warfarin. He maintained sinus rhythm for two days but reverted back to AF. He was increased to amiodarone 400 mg a day, but still had AF despite cardioversion. He was initiated on diltiazem 360 mg daily for rate control. He was then referred to electrophysiologist Dr. Srijoy Mahapatra in the Atrial Fibrillation Center at the University of Virginia. During his clinic visit he reported significant fatigue and a strong sense of an irregular heartbeat, and felt better when in sinus rhythm. He requested further treatment, with the hope of maintaining sinus rhythm long term. The patient was offered three treatment options: 1) continue amiodarone and undergo another attempt at cardioversion; 2) undergo another attempt at endocardial ablation; or 3) undergo surgical ablation with a Mini-Maze approach. He chose the surgical option, and was referred to Dr. Gorav Ailawadi, a cardiovascular surgeon. The thorascopic Mini-Maze was originally developed by Dr. Randall Wolf at the University of Cincinnati.¹ The procedure is a minimally invasive, off-pump, epicardial bipolar radiofrequency ablation. The procedure consists of: ablation of the ganglionic plexi (GP) of the left atrium (Figures 1A and 1B), isolation of the pulmonary veins (Figure 2), division of the ligament of Marshall (LOM), and amputation of the left atrial appendage in order to decrease the potential for left-sided clot formation and the risk for subsequent stroke. The GP of the left atrium, found in the epicardial fat pad regions, have increasingly become targets during AF ablation procedures. Excessive nerve activity is believed to be responsible for the initiation and sustaining of AF. Ablation of these GP regions in the left heart has resulted in denervation and elimination of AF.² The ligament of Marshall is the remnant of the left common cardinal vein, and contains nerve trunks and ganglia.³Surgical Procedure Per their protocol, Drs. Ailawadi and Mahapatra were both in attendance for the surgical procedure. After informed consent was obtained, general anesthetic was administered and the TEE probe was inserted. The patient was placed in the right lateral decubitus position, and the left chest was prepped and draped. Dr. Ailawadi made separate 2-10 mm incisions and a third 6 cm incision. It is important to note that the ribs are not spread during this procedure to minimize postoperative pain. The pericardium was carefully opened, avoiding injury to the phrenic nerve. The left-sided pulmonary veins were identified. A space was created between the left superior pulmonary vein and the PA. The ligament of Marshall was identified and divided. At this point, atrial mapping and stimulation were performed by Dr. Mahapatra. Entrance block was not present for the left superior vein, indicating a break in the original endocardial ablation line. Positive GP, identified by high-frequency stimulation with an ablation pen (AtriCure, Inc., West Chester, Ohio), are those in which a vagal response is found, resulting in a heart rate decrease by as much as 50%. Ganglia L7 exhibited a positive response. Dr. Ailawadi now used the dissector to encircle the left superior and inferior veins. A bipolar ablation clamp (AtriCure, Inc.) was passed carefully around the left-sided pulmonary veins, and the jaws of the clamp were closed. Four separate bipolar radiofrequency ablation lines were created. Next, with the ablation pen, GP re-mapping and stimulation were performed. No positive ganglia were found, and entrance block was obtained for the left pulmonary veins. The superior portion of the left atrium was dissected and subsequently ablated across to the right side to create a roof line lesion. Block was confirmed. The left atrial appendage was excised. An 8 mm chest tube was then inserted and the skin was closed. Next the patient was placed in the left lateral decubitus position and the right chest was prepped and draped. Dr. Ailawadi made similar incisions on the right side. The phrenic nerve was identified and the pericardium was opened. The oblique sinus was opened, and the right superior pulmonary vein and right PA were separated under direct visualization. Dr. Mahapatra performed atrial mapping and stimulation, which revealed a positive response at ganglia R1, R3, R5, R7, and R9. A lighted dissector was again used to encircle the right-sided veins followed by the ablation clamp, creating four separate bipolar burns on the left atrium. A connecting lesion from the right side across the roof of the left atrium was performed with the pen. Using TEE guidance, an additional lesion was created with the pen to the mitral annulus. The GP were re-mapped; those found to be positive were ablated, and the right pulmonary veins were confirmed to have entrance block. At the conclusion of these ablations, the patient was in atrial flutter and was successfully cardioverted on the initial attempt into a sinus rhythm. An 8 mm chest tube was placed in the right side and skin was closed. Post-Op The patient was admitted to the postoperative unit after the procedure and was extubated that day. On post-operative day 1, he began ambulating and was started on Toradol for pain control. IV fluids were discontinued and his diet was advanced. He was moved to a general care floor. By the third day, both chest tubes were removed. The chronicity of the patient’s AF led to the preoperative plan that the patient should undergo a percutaneous atrial flutter ablation procedure. On post-op day 4, the patient was brought to Dr. Mahapatra in the electrophysiology lab, where it was noted that the patient did not have block across his atrial flutter line. Thus, Dr. Mahapatra performed a repeat cavotricuspid isthmus line and and SVC isolation. Near the conclusion of the procedure, while isoproterenol at 20 micrograms was being infused and with aggressive pacing, AF was induced. The patient was cardioverted electrically and returned to a sinus rate of 60 bpm. He was re-started on warfarin and amiodarone, and discharged on post-operative day 5. Follow-up One month later, the patient was seen in follow-up in the CV surgery clinic. He was free of AF and atrial flutter. His beta blocker was being stopped, but he was continued on amiodarone and warfarin. Activity restrictions were lifted and he was planning to begin cardiac rehabilitation. At two months, he remained in sinus rhythm as noted on a one-month monitor and his amiodarone was stopped. He continues to be followed in the AF clinic. Conclusion The expertise of both electrophysiology and surgery led to a probable cure for this patient’s AF. At the time of this writing, the patient remains free of AF and continues to do well.