LAA=left atrial appendage; RIPV=right inferior PV; RSPV=right superior PV.
Figure 5. Pre- and post-PFA maps of the left atrium and the PVs with histology at 3 months of follow-up. 3D maps created pre-(A, B), immediately post-PFA (D, E), and 3 months post-PFA (G, H), along with the corresponding intracardiac electrograms (C, F, I) demonstrating electrical isolation of the right superior (RSPV) and inferior (RSPV) and left PVs (LPV).J, Subgross histology illustrating complete, circumferential and transmural fibrous replacement of the cardiac sleeve around the LPV.K, Subgross histology of the RSPV demonstrating full-thickness, circumferential fibrous replacement (blue staining, yellow outline) of the cardiac sleeve. Moreover, the treatment extended to involve the myocardium from the posterior wall of the right atrium and a small branch of the pulmonary artery (PA). L, Photomicrograph (hematoxylin and eosin) demonstrating acute contraction band degeneration of cardiac myocytes consistent with PFA.
Figure 6. Histology of lesions created using PFA. A, Sections of right superior pulmonary vein (RSPV) illustrating a circumferential, transmural PFA lesion (arrow). A normal phrenic nerve (arrow) following PFA depicted both on gross (B) and histologic examinations(C) after deliberately performing PFA adjacent to this structure. As illustrated, no phrenic nerve injury has occurred and the nerve is completely intact. D and E, Sections of RSPV and right inferior pulmonary vein (RIPV) demonstrating circumferential ablation following PFA. F, Depicts a higher magnification ofpanel D, demonstrating an area of transmural ablation (arrow) around the circumference of the RSPV. G, Represents a higher magnification of panel D, demonstrating transmural fibrous replacement of the muscular sleeve around the RSPV (arrow). H,Histologic representation demonstrating fibrous replacement of the muscular sleeve (outlined) of the left common pulmonary vein (LPV).I and J, illustrate higher magnifications ofpanel H, showing transmural ablation (arrows) and replacement fibrosis of the muscular sleeve of the LPV with normal surrounding epicardial fat and sparing of the nerve and artery.
Figure 7. Assessment for embolic events following PFA. Gross and histologic examination of the porcine brain (A, B), the rete mirabile (C, D), and the kidneys (G, H) following PFA of the atria, the atrial appendages, and the pulmonary veins using the CRC EP system showed no evidence of embolization. Additionally, MRI was also performed to radiologically investigate for embolic events. As shown, compared to baseline/pre-PFA (E), no gross or radiological abnormalities suggestive of cerebral embolization/events were encountered in any of the animals on MRI, 1 week post-PFA(F). DWI=diffusion-weighted imaging; FLAIR=fluid attenuated inversion recovery; GRE=gradient recalled echo T2-weighted; PD=proton density-weighted imaging; T1=T1-weighted.
Figure 8. Histologic examination of the esophagus following PFA performed within the adjacent IVC. A, Sections of porcine esophagus depicting normal tissue without evidence of injury or lesions following PFA. B, Acute PFA-related changes (outlined) in the esophageal muscular layer within 2 h of PFA with complete resolution during follow-up by 3 weeks.
Supplemental Figure. Assessment of chest contraction acceleration during following PFA. Absolute chest contraction acceleration recorded during PFA in the left atrium, the PVs, and the left atrial appendage (LAA). As seen, pulsed field applications delivered at anatomical locations immediately adjacent to the left and right phrenic nerves (e.g., right superior PV or deep within the LAA) was accompanied by prominent phrenic nerve capture, yielding acceleration levels of 5–9 m/s2. Conversely, PFA using the same waveform parameters performed at anatomical sites far enough from phrenic nerves (e.g., left PV or posterior wall) yielded no measurable chest contractions with an absolute mean acceleration of 0.05 m/s2 indiscernible from background noise.