Effect of the vein of Marshall on arrhythmia recurrence after PV reconnection: an in-silico study
H Hosseini, P Martinez Diaz, E Zappon, C H Roney, G Plank, J Bayer, E VigmondAbstract
Background
Pulmonary vein isolation (PVI) is the cornerstone treatment of atrial fibrillation (AF). However, reconnection following wide antral circumferential ablation (WACA) is one of the main reasons for recurrent atrial arrhythmias (AA). To overcome this problem, ethanol infusion, to ablate the Vein of Marshall (VM), has shown promising results as an adjunct therapy. The role of the VM in AA initiation remains unelucidated.
Purpose
To evaluate the effect of the VM on the recurrence of AA after PV reconnection using computer simulations.
Methods
Biatrial bilayer meshes were created from CT scans of ten patients undergoing PVI. Electroanatomical data were collected, and low voltage areas (<0.5 mV) were defined as fibrotic and mapped back to the CT geometry. After constructing shells of the LA and RA, sub-anatomical structures, the coronary sinus(CS), and VM were added. The VM was an offshoot of the CS terminating between the left PVs and was electrically connected to the LA along its length every 10 mm. We used a modified human atrial myocyte model to include AF remodeling. WACA ablation was implemented as a contiguous set of 2 mm diameter non-conductive points encircling the left PVs. Reconnection was modelled by restoring each point one by one back to its original underlying conductive tissue. To induce arrhythmia, we administered a sinus node beat followed by five ectopic beats from the LSPV. An arrhythmia lasting more than 10 seconds was considered sustained. Tachycardia cycle length (TCL) was calculated over 42 different points on the right atrium (RA )and left atrium (LA). The monodomain formula was solved using the openCARP simulator.
Results
In 294 simulations with the VM, 88 sustained arrhythmias were induced with a mean TCLRA and TCLLA of 205±38.4ms, and 200±43.3ms, respectively. Without the VM, only 30 sustained arrhythmias were induced with a TCLRA and TCLLA equal to 386±89.1ms, and 188±57.2ms, respectively. During the initiation of the reentries the VM acts as a bridge to facilitate conduction block. The combination of the VM and WACA makes an anatomical substrate which can connect the inside and outside of WACA as a slow-fast pathway which results in a figure of eight AA. The VM also played an important role in the initiation of perimitral atrial flutters. Moreover, the VM and Bachmann’s bundle serve as two principal interatrial conduction routes, enabling the initiation of biatrial flutter. Most reentries were atrial flutters with a 85% occurrence with the VM, and a 93% occurrence without the VM.
Conclusion
The presence of the VM increases the rate of recurrence of AA in patients with incomplete WACA. Our results show that after the initiation of arrhythmia, WACA acts as an anatomical non-conductive area, which becomes the main pathway of induced reentry. Most of the induced AA in models with and without VM were roof-dependent atrial flutters. Ablation of the VM is important for reducing recurrent AA.Figure 1