Equine pulmonary veins demonstrated lower voltage (1.2 vs 3.4 mV, P<0.001) and higher fibrosis (26.1% vs 14.5%, P=0.003) than the left atrium, indicating an arrhythmogenic substrate for AF.
Observational (n=13)
Equine pulmonary veins exhibit structural heterogeneity, lower voltages, and distinct ion channel expression compared to the left atrium, providing a potential substrate for atrial fibrillation initiation.
Absolute Event Rate: 1.2% vs 3.4%
p-value: p=<0.001
Spontaneous pulmonary vein (PV) activity triggers atrial fibrillation (AF) in humans. Although AF frequently occurs in horses, the origin remains unknown. This study investigated the structural and electroanatomical properties of equine PVs to determine the potential presence of an arrhythmogenic substrate. Endocardial three-dimensional (3D) electroanatomical mapping (EnSite Precision) using high-density (HD) catheters was performed in 13 sedated horses in sinus rhythm. Left atrium (LA) access was obtained retrogradely through the carotid artery. Post-mortem, tissue was harvested from the LA, right atrium (RA), and PVs for histological characterisation and quantification of ion channel expression using immunohistochemical analysis. Geometry, activation maps, and voltage maps of the PVs were created and a median of four ostia were identified. Areas of reduced conduction were found at the veno-atrial junction. The mean myocardial sleeve length varied from 28±13 to 49±22 mm. The PV voltage was 1.2±1.4 mV and lower than the LA (3.4±0.9 mV, P<0.001). The fibrosis percentage was higher in PV myocardium (26.1±6.6 %) than LA (14.5±5.0 %, P=0.003). L-type calcium channel (CaV1.2) expression was higher in PVs than LA (P=0.001). T-type calcium channels (CaV3.3), connexin-43, ryanodine receptor-2, and small conductance calcium-activated potassium channel-3 was expressed in PVs. The veno-atrial junction had lower voltages, increased structural heterogeneity and areas of slower conduction. Myocardial sleeves had variable lengths, and a different ion channel expression compared to the atria. Heterogenous properties of the PVs interacting with the adjacent LA likely provide the milieu for re-entry and AF initiation.
Kjeldsen et al. (Sat,) conducted a observational in Atrial fibrillation (n=13). Endocardial 3D electroanatomical mapping and histological characterisation vs. Left atrium was evaluated on Myocardial voltage (p=<0.001). Equine pulmonary veins demonstrated lower voltage (1.2 vs 3.4 mV, P<0.001) and higher fibrosis (26.1% vs 14.5%, P=0.003) than the left atrium, indicating an arrhythmogenic substrate for AF.