Structural and electro-anatomical characterization of the equine pulmonary veins: implications for atrial fibrillation.

This research investigates the structural and electrical properties of a horse’s pulmonary veins to identify potential origins of atrial fibrillation, a common heart condition. The study combines live electrical mapping with post-mortem histological analysis and shows that these veins have areas of reduced electrical conduction and different ion channel expressions, which might create conditions conducive to irregular heartbeat initiation.

Research Objectives and Methods

• The goal of the research was to increase understanding of atrial fibrillation in horses, a heart condition that is common but little understood. The researchers sought to determine whether the pulmonary veins in horses could be a source of this condition.
• To do this, the team performed endocardial three-dimensional electro-anatomical mapping on 13 sedated horses in sinus rhythm using high-density catheters. Sinus rhythm means the horses were in a state of normal heartbeat during the procedure.
• Access to the left atrium for the procedure was obtained retrogradely through the carotid artery.
• After the live horses were assessed, tissue was taken from post-mortem specimens from the left atrium, right atrium, and pulmonary veins. The tissues were then histologically characterized and quantitatively assessed for ion channel expression using immunohistochemical analysis.

Results

• The team was able to create geometry, activation maps, and voltage maps of the pulmonary veins for the sedated horses. They determined the mean length of the myocardial sleeve (a component of the pulmonary vein) and found it to vary from 28 ± 13 to 49 ± 22 mm.
• The pulmonary veins exhibited a lower voltage than the left atrium, indicating a lower level of electrical activity.
• Areas of reduced conduction were discovered at the junction between the veins and atrium (the veno-atrial junction).
• The fibrosis percentage, which indicates the level of scarring or damage, was higher in the vein myocardium than in the left atrium.
• Increased expression of L-type calcium channels (Ca1.2) was noted in the pulmonary veins compared to the left atrium.
• The study also found expression of T-type calcium channels (Ca3.3), connexin-43, ryanodine receptor-2, and small conductance calcium-activated potassium channel-3 in the pulmonary veins.

Conclusions

• The study concluded that the veno-atrial junction, the point where the pulmonary vein transitions to the atrium, showed lower voltages, increased structural heterogeneity, and areas of slower conduction.
• The myocardial sleeves had variable lengths and a different ion channel expression compared to the atria, likely contributing to the conditions that can lead to atrial fibrillation.
• The research suggests that the heterogeneous properties of the pulmonary veins could be influencing the adjacent left atrium and thus creating a potential starting point for atrial fibrillation.