Seek and ye shall find: cardiac arrhythmias in the horse.

Cardiac rhythm irregularities are a source of concern for horse-owners and veterinarians alike. Our relationship with the horse is close, physically and aesthetically, and safety is an ever-present concern. Add issues of litigation, public perception and animal welfare, and the result is a heady brew! It doesn’t matter how likely or unlikely it is that a rhythm disturbance will cause any problems; the mere mention of such an issue is alarming. The idea of a horse collapsing and dying grabs everyone’s attention, even more so if it actually happens! Arguably, no horse is safe to ride, but none of us wants to increase the risk unnecessarily. Aside from real danger where real danger exists, we are likely always to err on the side of caution. Advising owners of horses with rhythm disturbances not to work or ride a horse is a simple and direct solution, which keeps everyone safe. Unfortunately, it also deprives owners and riders of a pursuit in which they may have invested heavily in terms of money, effort, time and emotion. It also denies the horse the opportunity to express its true genetic potential. These are heavy prices if concern is, in fact, unwarranted. This is, in part, why the paper by Verheyen et al. [1] in this issue of Equine Veterinary Journal is likely to raise questions. For example, is atrial fibrillation (AF) a ‘dangerous’ arrhythmia in horses, and are the ventricular rhythm disturbances identified in this and other recent studies anything to do with AF, or a potential cause of collapse or sudden death? It is clear that we have a great deal to learn, both about AF and about ventricular rhythm disturbances in the horse. It is also clear from the absence of clear explanations on post mortem examination of horses that do die suddenly, especially at exercise [2], that whatever the underlying causes may be, ventricular arrhythmias are likely to be one very significant immediate and possible cause. The human literature supports this interpretation and is an excellent starting point [3], but simple reliance on this source alone is not sufficient. Aside from the inherent dangers of extrapolation, feeling a little unsteady when you weigh 75 kg does not compare with having a 500 kg exercising horse with someone on its back start to feel woozy! We need to look more closely and gain a much better understanding. What role does AF, the most frequent clinically significant arrhythmia in the horse, play in this discussion? The first reference to equine AF in the literature (Lewis 1911) [4] compared the arrhythmia with similar disturbances of the human heart. Since the late 1940s, at least one paper addressing AF in the horse has been published almost every year, and in recent years, several. Atrial fibrillation is still the subject of a huge amount of controversy and research. In human medicine, it has been described as ‘. a growing public health problem . ’ with ‘. enormous socioeconomic implications’ as the population ages and the number of cases continues to rise [5]. It is self-evident; we still have a lot to learn about this important rhythm disturbance, in all species. We fully understand neither the genesis and maintenance of AF, nor its natural history and the relationships between causation, predisposition and prognosis [6,7]. Clinical management in humans is controversial; should we emphasise rate or rhythm control, and what are the best strategies in either case? Atrial fibrillation frequently accompanies organic heart disease in humans, may connote underlying genetic disease, becomes more frequent with age, and is generally viewed as a guarded prognostic indicator in most circumstances [6]. The relationship in humans between AF and stroke (resulting from left atrial thrombus formation and embolism) is also a huge concern [8]. Clearly, in humans AF is not a trivial diagnosis. Horses also develop AF in association with organic heart disease [9], but in most the arrhythmia is classified as ‘lone’ (unaccompanied by identifiable organic disease) and carries a good prognosis if cardioversion can be achieved [10,11]. Ongoing work in our laboratory has revealed clear evidence of genetic contributions in North American Standardbred pacers, but clinical manifestations do not appear to differ from other cases of AF. There is presently no evidence that genetically predisposed horses experience any other consequences, and they are often very talented racehorses! In fact, there appears to be no immediate danger in lone equine AF, and the primary concern is performance inconsistency and economic impact rather than safety or mortality. Horses with lone AF may experience a significant reduction in performance, depending on their use, but at work they do not typically collapse, they simply tire rapidly. The majority respond to treatment and, in young horses at least, usually return to normal performance. Horses with AF do not experience atrial thrombus formation and thromboembolism. In short, AF seems to be a very benign arrhythmia in the horse, whose greatest significance for performance and racehorses relates to reduced work capacity, necessitating treatment or retirement. In show horses, the diagnosis is often an incidental finding in animals whose performance has raised no cause for concern. There are references in the literature to weakness, incoordination and collapse with AF [9]; however, in these cases and in this author’s clinical experience, these are most often animals with coexisting conditions or underlying primary organic cardiovascular disease, where superimposition of arrhythmia was sufficient to cause clinical signs. There have been occasional concerns raised in the racing press regarding the safety of horses diagnosed with AF [12], but no evidence has been presented of practical impacts. There is, however, legitimate concern about the effect of inconsistent performances on betting [12,13]. While nobody would advocate subjecting horses with AF to intense work, this circumstance does arise on occasion with racehorses that develop the arrhythmia during maximal effort. The picture is quite consistent, however, in that affected horses simply slow down and finish well back. The experience of most clinicians attending a horse with lone AF would lead them to offer a moderately good prognosis without raising major safety issues. Most would advise owners of otherwise normal, sane riding horses to avoid intense work or stressful circumstances until the horse had been successfully converted. This would most often be on the assumption that if the horse did ‘get its knickers into a knot’ it might be less well balanced than usual, something to which the findings of Verheyen et al. might add gravitas [1]. After treatment, it would be ‘back to work,’ with fingers crossed that the horse did not turn out to be one of the approximately 20% that, sooner or later, relapse. So, what happened with the horses in the study by Verheyen et al., and what clinical significance must we attach to their findings? [1] Insights might be gained from a critical evaluation of the methodologies employed. If you work regularly with horses on a lunge line, you may have concerns about a horse galloping. The circle needs to be huge to do this at all safely (for horse and conductor), and there is always a grave danger of the horse simply flying off. Also, with the exception of the occasional horse that insists on galloping at every opportunity, you have to ‘get after’ a horse to persuade it to maintain a gallop on a lunge line. How were the horses in the study induced to maintain the speed and gait? Did the procedure involved cause any of the horses unusual anxiety [14], and was the response episodic or sustained? Were the horses working maximally or simply stimulated maximally? Was the resultant autonomic response typical of that encountered during normal maximal effort? What would have happened if horses without AF had been subjected to the same protocol? Our own work with racing Standardbreds strongly suggested the inciting factor in very similar rhythm disturbances to be sudden introduction of vagal tone during intense sympathetic activity, rather than the catecholamine/sympathetic response that preceded it [15]. In this scenario, the exercise rhythm disturbances encountered by Verheyen et al. could be a reflection of autonomic instability [16] and not of AF per se, i.e. they would reflect the experimental protocol. After all, this study was not controlled. Given that brief episodes of excitement at rest or the walk could induce similar instability, the same mechanism may have been at play here, also. There were no clinical signs. The difference was that in this study, somebody was watching! It is, perhaps, of relevance that in Verheyen et al.’s Figure 2, the upper and lower quartiles suggest greater variance at elevated rates (faster bs_bs_banner