Heart rhythm characterisation during unexplained transient loss of consciousness in dogs.

The identification of the heart rhythm during an episode of transient loss of consciousness (TLOC) is considered the reference standard method to elucidate the underlying aetiology. This study aimed to characterise heart rhythm in dogs during TLOC using Holter and external loop recorder monitoring. We retrospectively reviewed 24-h Holter monitoring and external loop recorder tracings from 8084 dogs. Heart rhythms from dogs that experienced TLOC during the recording was analysed to identify rhythm disturbances that occurred during episodes of TLOC. Electrocardiograms (ECGs) were subsequently categorised into Type 1 (ventricular arrest), Type 2 (sinus bradycardia), Type 3 (no/slight rhythm variations), and Type 4 (tachycardia). Transient LOC was documented in 92 dogs over 230 episodes of TLOC. Percentage of cases with ECGs compatible with each classification were as follows: 72.1%, Type 1; 6.1%, Type 2; 20.9%, Type 3; and 0.9%, Type 4. Cardiac rhythm during the TLOC could have been a consequence of a neurocardiogenic mechanism in 46.7% cases, while intrinsic rhythm disturbances of the sinus node or of the atrioventricular node were diagnosed in 31.5% cases. In two cases, tachycardia was the possible cause of the TLOC. ECG patterns in dogs presenting with multiple TLOC episodes were completely reproducible during each episode. TLOC in dogs was primarily caused by ventricular arrest. Most dogs with TLOC had electrocardiographic finding suggestive of a reflex or neurally-mediated syncope, but one third had an ECG more suggestive of a conduction disorder. Distinguishing these two entities could help inform diagnostic, therapeutic, and prognostic plans.

Ventricular tachycardia in English bulldogs with localised right ventricular outflow tract enlargement.

OBJECTIVES: To describe the electrocardiographic characteristics of ventricular tachycardia arising from the right ventricular outflow tract and the particular association between this arrhythmia and the presence of localised right ventricular outflow tract enlargement in English bulldogs. METHODS: Five English bulldogs were referred with a history of syncope or cardiogenic shock. In all dogs, 12-lead surface ECG, thoracic radiograph and echocardiography were collected. In all but one dog 24-hours Holter monitoring and signal-averaged ECGs was examined and in one dog electrophysiological study and radiofrequency catheter ablation of the VT substrate was performed. RESULTS: Documented arrhythmias included a single sustained monomorphic wide QRS tachycardia in four dogs, and an alternans of two different monomorphic forms in one dog. Mean QRS duration during tachy-cardia was 91·6 ±9·83 milliseconds. QRS complexes manifested a left bundle branch block morphology and an inferior axis (81 ±13·73°). R wave notching was present in the caudal (inferior) leads in three tachy-cardias. Lead I was negative in 3 of 6, positive in 1 of 6 and isodiphasic in 2 of 6. Lead aVL was negative in 5 of 6 and positive in 1 of 6. Signal-averaged electrocardiograms revealed late potentials in three dogs. Echocardiography showed a localised right ventricular outflow tract enlargement in all dogs. Cardiac map-ping established two sites of origin of ventricular tachycardia within the right ventricular outflow tract in one dog: caudal free-wall and cranial-septal. CLINICAL SIGNIFICANCE: The presence of a localised right ventricular outflow tract enlargement and ventricular tachycardia with left bundle branch block morphology could suggest segmental arrhythmogenic right ven-tricular cardiomyopathy in the English bulldog.