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.