Intrinsic Electrical Remodeling Underlies Atrioventricular Block in Athletes.

[Figure: see text].

First catheter-based high-density endocardial 3D electroanatomical mapping of the right atrium in standing horses.

BACKGROUND: Three-dimensional electroanatomical mapping is of potential interest in equine cardiology to identify arrhythmia mechanisms, characterise electroanatomical substrates and guide ablation strategies. OBJECTIVES: To describe three-dimensional electroanatomical mapping in standing horses. STUDY DESIGN: Research methodology, proof of concept study. METHODS: Four Standardbred horses (2 geldings, 2 mares, median age 4.5 [4-9] years, mean bodyweight 485 [440-550] kg) were sedated and placed in stocks. Via the jugular vein, a high-density multipolar grid catheter (Advisor™ HD Grid Mapping Catheter with EnSite VelocityTM, Abbott Medical) was used for endocardial mapping of the right atrium. The P-wave on the surface ECG was used as a timing reference for simultaneous local activation time- and bipolar voltage-mapping. For a positional reference a 10-pole catheter (Abbott Medical) was placed in the caudal vena cava. RESULTS: Endocardial right atrial mapping guided by the three-dimensional mapping system and local electrograms was successfully performed in all four horses. A median of 32719 [25499-65078] points, covering the entire right atrium, were collected. Three-dimensional electroanatomical mapping provided detailed information about activation patterns and electrogram-characteristics of the sinoatrial node, intervenous tubercle and cavotricuspid isthmus. Additionally, transvenous biopsy forceps connected to the mapping system were visualised on screen to guide biopsy collection. MAIN LIMITATIONS: The feasibility of electroanatomical mapping for the left atrium and in larger breeds requires further study. CONCLUSIONS: High-density three-dimensional electroanatomical mapping of the right atrium is feasible in the standing horse.

Thoracotomy and Pericardiotomy for Access to the Heart in Horses: Surgical Procedure and Effects on Anesthetic Variables.

Thoracotomy is an uncommon procedure in horses but remains essential in a variety of cases of pleuropneumonia, pericarditis, thoracic trauma or diaphragmatic herniation, and for experimental thoracic and cardiac procedures. This study aimed at developing an experimental surgical procedure allowing access to the entire circumference of the heart and describing the effect of thoracotomy on pulmonary gas exchange in these horses. The study consisted of two arms, arm one (undergoing thoracotomy), was a terminal experimental study that included 11 Standardbred horses with experimentally induced (by tachypacing) atrial fibrillation. Arm two consisted of 6 Standardbred horses undergoing anesthesia for reasons unrelated to the present study. These horses functioned as controls. Anesthesia was induced using zolazepam and tiletamine. Anesthesia was maintained with isoflurane in 100% oxygen and ventilation with intermittent positive pressure (IPPV); no positive end-expiratory pressure (PEEP) was performed. Rib resection and pericardiotomy were performed for complete exposure of the entire circumference of the heart. Arterial blood samples were collected prior to, 5 and 30 minutes after puncture of pleura parietalis. In 10 horses, resection of the fifth rib was adequate for exposure of the heart. In one horse, removal of the sixth rib was also necessary. The duration of the surgical procedure (thoracotomy, pericardiotomy) was < 45 minutes. During a thoracotomy, PaO2 decreased significantly (P < .05) from 291.8 ± 82.8 mmHg to 165.2 ± 73.5 mmHg but was not different from normal anesthetized controls. The PaCO2 remained within normal limits. This surgical approach provided access to the entire circumference of the heart.

Molecular Cloning and Functional Expression of the Equine K+ Channel KV11.1 (Ether à Go-Go-Related/KCNH2 Gene) and the Regulatory Subunit KCNE2 from Equine Myocardium.

The KCNH2 and KCNE2 genes encode the cardiac voltage-gated K+ channel KV11.1 and its auxiliary ß subunit KCNE2. KV11.1 is critical for repolarization of the cardiac action potential. In humans, mutations or drug therapy affecting the KV11.1 channel are associated with prolongation of the QT intervals on the ECG and increased risk of ventricular tachyarrhythmia and sudden cardiac death--conditions known as congenital or acquired Long QT syndrome (LQTS), respectively. In horses, sudden, unexplained deaths are a well-known problem. We sequenced the cDNA of the KCNH2 and KCNE2 genes using RACE and conventional PCR on mRNA purified from equine myocardial tissue. Equine KV11.1 and KCNE2 cDNA had a high homology to human genes (93 and 88%, respectively). Equine and human KV11.1 and KV11.1/KCNE2 were expressed in Xenopus laevis oocytes and investigated by two-electrode voltage-clamp. Equine KV11.1 currents were larger compared to human KV11.1, and the voltage dependence of activation was shifted to more negative values with V1/2 = -14.2±1.1 mV and -17.3±0.7, respectively. The onset of inactivation was slower for equine KV11.1 compared to the human homolog. These differences in kinetics may account for the larger amplitude of the equine current. Furthermore, the equine KV11.1 channel was susceptible to pharmacological block with terfenadine. The physiological importance of KV11.1 was investigated in equine right ventricular wedge preparations. Terfenadine prolonged action potential duration and the effect was most pronounced at slow pacing. In conclusion, these findings indicate that horses could be disposed to both congenital and acquired LQTS.