Feasibility and safety of three-dimensional electroanatomical cardiac mapping, mapping-guided biopsy and transseptal puncture in dogs.

Three-dimensional electroanatomical mapping (3D EAM) has expanded radiofrequency catheter ablation applications in humans to almost all complex arrhythmias and has drastically reduced fluoroscopy use, yet its potential in dogs is poorly investigated. The objectives of the current study were to assess the feasibility and safety of 3D EAM of all four heart chambers, 3D EAM-guided biopsies and transseptal puncture in dogs. Eight healthy purpose-bred Beagle dogs. Electroanatomical mapping was performed under general anaesthesia during sinus rhythm using a 22-electrode mapping catheter. Left heart catheterisation was achieved by either retrograde transaortic access (n = 4) or transseptal puncture (n = 4). Successful 3D EAM of the right atrium and ventricle was achieved in all dogs at a median time of 33 (13-40) min and 17 (3-52) min, respectively. Left atrial and ventricular 3D EAM was successful in six and seven dogs, at a median time of 17 (4-27) min and 8 min (4-19 min), respectively. Complications requiring intervention occurred in one dog only and were a transient third degree atrioventricular block and pericardial effusion following transseptal puncture, which was treated by pericardiocentesis. All dogs recovered uneventfully. Fluoroscopy time was limited to a median of 7 min (0-45 min) and almost exclusively associated with transseptal puncture. Three-dimensional EAM of all cardiac chambers, including mapping-guided biopsy and transseptal puncture is feasible in small dogs. Complications are similar to those reported in human patients. This suggests a potential added value of 3D EAM to conventional electrophysiology in dogs with arrhythmias.

Endocardial electro-anatomic mapping in healthy horses: Normal sinus impulse propagation in the left and right atrium and the ventricles.

Understanding the depolarisation pattern of the equine heart under normal physiologic conditions, and its relationship to the surface electrocardiogram (ECG), is of uppermost importance before any further research can be done about the pathophysiology of complex arrhythmias. In the present study, a 3D electro-anatomical mapping system was used to evaluate the qualitative and quantitative depolarisation patterns and correlation to the surface ECG of both the atrial and ventricular endocardium in seven healthy horses in sinus rhythm under general anaesthesia. Bipolar activation maps of the endocardium were analysed. The first atrial activation was located at the height of the terminal crest. Only one interatrial conduction pathway was recognised. The first and second P wave deflections represent the right and left atrial depolarisation, respectively. Bundle of His electrograms could be recorded in 5/7 horses. Left ventricular activation started at the mid septum and right ventricular activation started apically from the supraventricular crest. This was followed by separate depolarisations at the height of the mid free wall. Further ventricular depolarisation occurred in an explosive pattern. Electrically active tissue could be found in all pulmonary veins. In contrast to findings of previous studies, all parts of the ventricular depolarisation contributed to the surface ECG QRS complex. This study provides a reference for the normal sinus impulse endocardial propagation pattern and for conduction velocities in equine atria and ventricles.

The Brugada syndrome: update 2006.

Over the last 14 years - since the Brugada syndrome was first recognized as a distinct clinical/electrocardiographical entity - a considerable number of papers have been published on its various aspects. It has been defined as the combination of a typical ST-segment elevation in the right precordial leads and a predisposition for malignant ventricular arrhythmias occurring in the absence of structural heart disease. From the outset, controversy arose about the diagnostic criteria to be applied. This issue has been clarified since the announcement of a first (2002) and second (2005) consensus report. Our review will discuss the clinical characteristics and different possible pathophysiological mechanisms underlying the specific ECG-abnormalities and susceptibility for malignant arrhythmias. Nowadays, the main issue of discussion revolves essentially around its prognostic features, especially in asymptomatic patients. This review will compare the results of different follow-up studies and yields a possible explanation for the differences in event rates and in the identification of useful sudden-death predictors. Finally, the most recent data concerning new diagnostic techniques, gene identification and future therapeutic options will also be discussed.