Atrial fibrillation (AF) is the most common clinically relevant arrhythmia in horses, with a reported prevalence up to 2.5%. The pathophysiology has mainly been investigated in experimental animal models and human medicine, with limited studies in horses. Atrial fibrillation results from the interplay between electrical triggers and a susceptible substrate. Triggers consist of atrial premature depolarizations due to altered automaticity or triggered activity, or local (micro)reentry. The arrhythmia is promoted by atrial myocardial ion channel alterations, Ca handling alterations, structural abnormalities, and autonomic nervous system imbalance. Predisposing factors include structural heart disease such as valvular regurgitation resulting in chronic atrial stretch, although many horses show so-called ‘lone AF’ or idiopathic AF in which no underlying cardiac abnormalities can be detected using routine diagnostic techniques. These horses may have underlying ion channel dysfunction or undiagnosed myocardial (micro)structural alterations. Atrial fibrillation itself results in electrical, contractile and structural remodelling, fostering AF maintenance. Electrical remodelling leads to shortening of the atrial effective refractory period, promoting reentry. Contractile remodelling consists of decreased myocardial contractility, while structural remodelling includes the development of interstitial fibrosis and atrial enlargement. Reverse remodelling occurs after cardioversion to sinus rhythm, but full recovery may take weeks to months depending on duration of AF. The clinical signs of AF depend on the aerobic demands during exercise, ventricular rhythm response and presence of underlying cardiac disease. In horses with so-called ‘lone AF’, clinical signs are usually absent at rest but during exercise poor performance, exercise-induced pulmonary hemorrhage, respiratory distress, weakness or rarely collapse may develop.
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