Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology · 2016
Paroxysmal atrial fibrillation in seven dogs with presumed neurally-mediated syncope.
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Porteiro Vázquez D M, Perego M, Santos L, Gerou-Ferriani M, Martin M W S, Santilli R A
Аннотация
OBJECTIVES: To document the electrocardiographic findings of vagally-induced paroxysmal atrial fibrillation following a presumed reflex syncopal episode in the dog.
ANIMALS: Seven dogs with a syncopal episode followed by a paroxysm of atrial fibrillation recorded on a 24-hour Holter.
METHODS: Twenty-four hour Holter monitors were retrospectively reviewed, analysing the cardiac rhythm associated with syncopal events. Each recording was analysed from 10 min before the syncopal episode to until 10 min after a normal sinus rhythm had returned.
RESULTS: Nine episodes were recorded in seven dogs, with one patient experiencing three events during one Holter recording. Five of the seven dogs presented with underlying structural heart disease. In two the syncopal episodes occurred following exercise, two associated with coughing and three were during a period of rest. All dogs had documented on the Holter recording a rhythm abnormality during syncope. The most common finding leading up to the syncopal event was development of a progressive sinus bradycardia, followed by sinus arrest interrupted by a ventricular escape rhythm and then ventricular arrest. This was then followed by an atrial fibrillation. The atrial fibrillation was paroxysmal in seven recordings and persistent in two. In two dogs, the atrial fibrillation reorganised into self-limiting runs of atypical atrial flutter.
CONCLUSIONS: This combination of electrocardiographic arrhythmias are probably caused by an inappropriate parasympathetic stimulation initiating a reflex or neurally-mediated syncope, with abnormal automaticity of the sinus node and of the subsidiary pacemaker cells and changes in the electrophysiological properties of the atrial muscle, which promoted the paroxysmal atrial fibrillation.
ANIMALS: Seven dogs with a syncopal episode followed by a paroxysm of atrial fibrillation recorded on a 24-hour Holter.
METHODS: Twenty-four hour Holter monitors were retrospectively reviewed, analysing the cardiac rhythm associated with syncopal events. Each recording was analysed from 10 min before the syncopal episode to until 10 min after a normal sinus rhythm had returned.
RESULTS: Nine episodes were recorded in seven dogs, with one patient experiencing three events during one Holter recording. Five of the seven dogs presented with underlying structural heart disease. In two the syncopal episodes occurred following exercise, two associated with coughing and three were during a period of rest. All dogs had documented on the Holter recording a rhythm abnormality during syncope. The most common finding leading up to the syncopal event was development of a progressive sinus bradycardia, followed by sinus arrest interrupted by a ventricular escape rhythm and then ventricular arrest. This was then followed by an atrial fibrillation. The atrial fibrillation was paroxysmal in seven recordings and persistent in two. In two dogs, the atrial fibrillation reorganised into self-limiting runs of atypical atrial flutter.
CONCLUSIONS: This combination of electrocardiographic arrhythmias are probably caused by an inappropriate parasympathetic stimulation initiating a reflex or neurally-mediated syncope, with abnormal automaticity of the sinus node and of the subsidiary pacemaker cells and changes in the electrophysiological properties of the atrial muscle, which promoted the paroxysmal atrial fibrillation.