Synchronized biatrial arrhythmias: Anatomic differences in biatrial versus bicaval orthotopic heart transplants drive arrhythmogenic sequelae

Michael C. Downey MD , Edwin Zishiri MD
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Abstract

A 37-year-old male with a history of familial Titin (TTN) gene mutation and orthotopic heart transplant (OHT) 20 years prior presented for evaluation of persistent atrial arrhythmias, including atrial fibrillation and atrial flutter. Despite the lower risk for atrial fibrillation in OHT patients due to surgical anastomosis isolating the pulmonary veins, biatrial OHT, which preserves the native atrial connection (unlike bicaval OHT), allows for arrhythmogenesis on both the donor and recipient atrial sides. This patient's case illustrates a unique arrhythmic mechanism where electrical reentry between residual and transplanted atrial myocardium resulted in multiple distinct atrial tachycardias. Intracardiac electrograms revealed sinus rhythm along with atrial tachycardia, particularly in the posterior left atrium and the right atrium. High-density voltage mapping identified significant scarring along the anterior and lateral right atrium, likely due to the prior recipient-to-donor right atrial anastomosis. A narrow gap of viable tissue indicated electrical reconnection across the suture line, facilitating multiple micro-reentrant circuits. Radiofrequency ablation (RFA) was performed to interrupt this excitable gap, isolating the native and donor atrial tissues. The RFA lesion set transected the anastomosis site and extended to the cavo-tricuspid isthmus, reestablishing electrical isolation. This case highlights the importance of understanding the biatrial OHT anatomy for targeted electrophysiologic interventions, selective placement of reference electrodes/catheters for mapping, and the need for careful consideration of electrical reconnection across surgical anastomoses to prevent arrhythmogenesis.
同步双房心律失常:双房与双腔原位心脏移植的解剖差异驱动心律失常的后遗症
一位37岁男性,20年前有家族性Titin (TTN)基因突变和原位心脏移植(OHT)史,提出评估持续性心房心律失常,包括心房颤动和心房扑动。尽管由于手术吻合隔离肺静脉,OHT患者房颤的风险较低,但双房OHT保留了原有的心房连接(与双腔OHT不同),允许供体和受体心房侧发生心律失常。该患者的病例说明了一种独特的心律失常机制,残留和移植心房心肌之间的电再入导致多重明显的心房心动过速。心内电图显示窦性心律伴房性心动过速,尤见于左后心房和右心房。高密度电压测绘发现沿右心房前部和外侧有明显的疤痕,可能是由于先前的受体-供体右心房吻合所致。活组织的狭窄间隙表明电重新连接穿过缝合线,促进多个微可入电路。射频消融(RFA)被用来中断这种可兴奋的间隙,分离原生和供体心房组织。RFA病变组横切吻合口并延伸至腔-三尖峡,重建电隔离。本病例强调了了解双房OHT解剖对靶向电生理干预的重要性,选择性放置参考电极/导管进行测绘,以及仔细考虑外科吻合口电重连以防止心律失常的必要性。
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