ABSTRACT. Five racehorses in apparently normal condition succumbed to sudden cardiac death (SCD) during or shortly after intensive training exercise. Cardiopathologic examination was performed. In 1 of the 5 horses, the use of an electrocardiogram (ECG) recording taken continuously for 440 sec enabled us to analyze some of the arrhythmias in the terminal event of SCD. The ECG tracing exhibited the R-on-T phenomenon following a pair of ventricular premature contractions (VPCs). The phenomenon rapidly degenerated into ventricular fibrillation, which led to cardiac arrest. In all 5 horses cardiopathologic examination revealed the following lesions: (i) foci of myocardial fibrosis in the right atrium located close to the sinoatrial (SA) node, (ii) fibrotic and/or fibroplastic changes in the upper portion of the interventricular septum, including the atrioventricular (AV) conduction system, and (iii) arterio-and arteriolosclerosis of the SA and AV node vessels. Pathogenetically, the process by which the focal lesions of myocardial ischemia secondary to vascular sclerosis progressed into fibrosis and/or fibroplasia could play a major role in the genesis of arrhythmias. Presumably the fibrotic and/or fibroplastic changes in the area of the AV bundle and its bundle branches are closely related to the onset of fatal ventricular arrhythmias such as VPCs, deteriorating into ventricular fibrillation. SCD in training and racing Thoroughbred horses appears to be due to arrhythmia.-KEY WORDS: arrhythmia, equine, heart, pathology, sudden death.J. Vet. Med. Sci. 61(8): 921-928, 1999 matter what conclusions have been drawn thus far about human SCD, the precise relationship between the prodromal signs (including fatal arrhythmias) and the pathologic condition is still controversial [3,5,8,9,11,23,26,36]. This paper reports the cardiopathologic changes found in 5 racehorses that had been in apparently normal condition when they succumbed to SCD or instantaneous death during or shortly after intensive training exercise. It also describes the terminal electrocardiographic events in 1 of the 5 animals. MATERIALS AND METHODSNecropsy of the 5 racehorses in this study (Table 1) was performed as soon as possible after SD, usually within 3 hr. Fortuitously, when horse 1 fell and lay down suddenly shortly after a training exercise, it was possible to record an electrocardiogram (ECG). For the ECG recording, a baseapex lead was used [29]; the positive electrode was positioned over the apex-beat area of the heart and the negative electrode over the cardiac base. The recording was performed continuously over the 400-sec terminal event of the SD, at a paper speed of 25 or 50 mm/sec. So that we could analyze the arrhythmias, the onset of the R-on-T phenomenon was set up as a 0-sec point, and the beginning point of the recording was calculated back to 370 sec (Table 2). For measurements of the Q-T interval, 5 successive intervals with sinus rhythm were randomly taken from the ECG tracing, mainly at a paper speed of 50 mm/sec. The corrected Q-...

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Summary Two hundred and eighty‐five apparently healthy Holstein dairy cows were evaluated serially for atrial fibrillation (AF) over an 18‐month period. AF was noted in 7 cows with an incidence of 2.5%. No particular disease conditions were noted in any case at the time of onset of AF and thereafter. In Cases 1, 2 and 3, arrhythmia developed 30 to 40 days postpartum and persisted thereafter. In Case 4, AF developed 28 days postpartum and lasted for 2 days before spontaneous conversion to normal sinus rhythm. In Cases 5 and 6, AF occurred 2 days after the animals ceased lactation and disappeared spontaneously within a few days. In Case 7, AF developed just before calving and reverted to normal sinus rhythm spontaneously on the 2nd day postpartum. Thus, 3 animals (Cases 1, 2 and 3) exhibited established AF whereas the remaining 4 animals (Cases 4, 5, 6 and 7) demonstrated paroxysmal AF, suggesting that different causative factors may be involved in the genesis of AF in the 7 cases presented here. The genesis of the AF in these cases which had no underlying disease conditions may be interpreted as an increased load imposed on the heart, increased sympathetic tone, or increased vagal tone.

Five racehorses were selected at the time of necropsy during a 4-year period involving about 500 thoroughbred horses. The 5 horses suddenly weakened during races and trailed in. Electrocardiographically, 3 of the 5 animals exhibited paroxysmal atrial fibrillation (AF) at rest, shortly after the races. Ten days to three months later, the 5 revealed exercise-induced ventricular premature contractions (VPCs) on the radiotelemetric electrocardiogram. Cardio pathologically focal lesions of myocardial fibrosis were observed in each of the horses. The fibrotic lesions in all 5 cases were located in a vicinity of the sinoatrial node with the anter o lateral region of right atrium. Fibroplastic lesions also were observed in the atrioventricular junction including the upper portion of the interventricular septum. In addition, there were sclerotic changes of the intramyocardial microvasculature within and around both the fibrotic and fibroplastic lesions. Cardiopathologically, there were no absolute criteria for differential diagnosis to make the 3 horses with paroxysmal AF from the 5 with exerciseinduced VPCs. However, the fibrotic and fibroplastic lesions secondary to myocardial ischemia might play an important role, presumably in creating a suitable background for the initiation of ectopic arrhythmias via automaticity and reentry mechanism, leading to an arrhythmogenic condition that gives rise to paroxysmal AF associated with exercise-induced VPCs.

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