Decanav

Endocardial (Endo) access to the left ventricle (LV) was obtained via the retrograde and transseptal approaches in all patients. Epicardial mapping was performed in all patients, as part of the clinical ablation study. Pericardial puncture was performed using the subxiphoid approach. Substrate maps were created during sinus rhythm, using CARTO 3D mapping system (Biosense Webster, Inc., Diamond Bar, CA, USA). Mapping was performed using a PentaRay (PentaRay, Biosense Webster, Inc.) or DecaNav mapping catheter (DecaNav, Biosense Webster, Inc.) with impedance parameters scaled to ensure tissue contact. Normal myocardium was defined as tissue with a bipolar voltage >1.5 mV, dense scar was defined as a bipolar voltage <0.5 mV, and scar borderzone was defined as a bipolar voltage 0.5–1.5 mV, consistent with previously published data.¹ (link)^,2 (link) Though debate exists regarding the optimal voltage cut-off to define Epi scar⁶ (link)^,7 (link) we sought to use a consistent value for both epicardium and endocardium as previously published,⁸ (link) in order to provide consistency to the APD measurements. Following this, activation mapping was performed if haemodynamically tolerated. Finally areas of late potentials and mid-diastolic potentials were identified.

Decapolar catheters, DecaNav (DecaNav, Biosense Webster, Inc.) were placed epicardially and endocardially and aligned to record across a geometrically opposed transmural area, traversing healthy tissue, scar-borderzone, dense scar, or all three (Figure 1). S₁–S₂ restitution curves were then performed at twice the diastolic capture threshold before clinical ablation, from the endocardium and epicardium in these catheter positions, as previously described.⁹ (link) In each region, steady state was achieved by pacing at basic cycle length of 600 ms for 3 min. Following this an S₁–S₂ protocol was performed beginning with an extra stimulus (S₂) at 1000 ms. The S₁–S₂ coupling interval was then decremented in 50 ms steps until an S₂ of 400 ms, then by 20 ms intervals between 400 and 300 ms, and thereafter, in 5 ms steps until effective refractory period (ERP) of the tissue. At ERP an S₂ stimulus at 10 ms + ERP was applied followed by further decrementing S₂ in steps of 2 ms to confirm ERP. All patients gave informed consent, the study was approved by our regional ethics board (LO10/H0715/19) and complied with the declaration of Helsinki.

Two to four days after the cardiac MRI, a follow-up in vivo electrophysiology (EP) study was performed in a subset of 15 pigs (9 MI and 6 sham). Under general anesthesia, a 12-lead ECG was recorded at 1 kHz as described previously for at least 5 min. Then, the femoral vein, jugular vein, and carotid artery were cannulated with 7–8-Fr vascular sheaths. Standard EP catheters (Decanav Biosense Webster, Belgium) were positioned in the LV, right ventricle (RV), and coronary sinus as previously described (28 (link)). One MI pig was excluded because of a vascular access complication. A ventricular arrhythmia induction protocol was performed by programmed electrical stimulation (PES) from the RV apex (adapted from Refs. 16 (link) and 29 (link)) in eight MI and six sham. To avoid induction of a nonspecific VF, stimulation in the LV and burst pacing were not done. Animals without arrhythmias in this single-site protocol were considered noninducible.
The inducibility of VT/VF as a surrogate of arrhythmia vulnerability was assessed using a scale constructed from the stepwise progression of the PES protocol where the first step (S1 = 600 ms and 1 extrasystole, S2 = 400 ms) was 100% and the last most aggressive step (S1 = 350 ms and 3 extrasystoles, S2 = 200 ms, S3 = 180 ms, S4 = 150 ms) marked noninducibility as 0%, adapted from León et al. (29 (link)).