Cardiopathological Observation on a Case of Persistent Ventricular Tachycardia in a Pony Mare.

Motomura, Noboru; Nakamura, Takashi; Kiryu, Keiji; Haramaki, Shigeyuki; Too, Kimehiko

doi:10.1292/jvms.54.1213

Cited by 8 publications

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“…In our previous observations of 19 young Thoroughbred racehorses between 1 year and 3 months and 5 years and 11 months old that exhibited no arrhythmias [19], the area of the AV conduction system indicated no fibrosis, fibroplasia or arteriosclerosis. Furthermore, in support of our previous case report [25], the myocardial fibrosis located close to the BBs in the present study coincided with that detected in a 20-year-old pony mare with persistent VT that led to cardiac arrest. In the case of racehorses, it is reasonable to suppose that there is a relationship between the genesis of instantaneous death and the fibrotic and/or fibroplastic lesions in the areas of the AV bundle and BBs, regardless of age [25,27], in the same way that there is a relationship between instantaneous death and congenital abnormalities in the human heart [3,26].…”

Section: Discussionsupporting

confidence: 93%

“…Furthermore, in support of our previous case report [25], the myocardial fibrosis located close to the BBs in the present study coincided with that detected in a 20-year-old pony mare with persistent VT that led to cardiac arrest. In the case of racehorses, it is reasonable to suppose that there is a relationship between the genesis of instantaneous death and the fibrotic and/or fibroplastic lesions in the areas of the AV bundle and BBs, regardless of age [25,27], in the same way that there is a relationship between instantaneous death and congenital abnormalities in the human heart [3,26]. Humans with LBB and/or RBB block who have no clinical evidence of cardiovascular disease have an increased risk of developing overt cardiovascular disease and SCD [5,9,11,23].…”

Section: Discussionsupporting

confidence: 93%

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Pathologic and Electrocardiographic Findings in Sudden Cardiac Death in Racehorses.

Kiryu

Motomura

Kashida

et al. 1999

The Journal of Veterinary Medical Science

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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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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Pathologic and Electrocardiographic Findings in Sudden Cardiac Death in Racehorses.

Kiryu

Motomura

Kashida

et al. 1999

The Journal of Veterinary Medical Science

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“…Of other published case reports, the aetiology of VT was not definitively determined, and myocardial fibrosis and/or myocarditis were most often implicated (Machida et al . ; Traub‐Dargatz et al . ; Coudry et al .…”

Section: Discussionmentioning

confidence: 99%

Treatment of sustained monomorphic narrow‐complex ventricular tachycardia in a 16‐year‐old Arab mare with a constant rate of infusion of lidocaine and oral propranolol

Bradley

Whelchel

Clay

et al. 2016

Equine Veterinary Education

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Summary A 16‐year‐old Arab mare was referred for treatment of a tachydysrhythmia detected on electrocardiogram by the referring veterinarian. Monomorphic, narrow‐complex ventricular tachycardia (VT) was confirmed by electro‐cardiogram in a normal base‐apex configuration. Subsequent diagnostic testing, including echocardiography and measurement of plasma cardiac troponin concentration, did not reveal a definitive cause for the dysrhythmia. Conversion of VT to ventricular bigeminy occurred following treatment with magnesium sulfate and lidocaine hydrochloride, administered intravenously. Treatment with orally administered propranolol subsequently led to conversion to sinus rhythm with intermittent ventricular premature complexes (VPCs). Oral prednisolone treatment was also initiated to address the possibility that VT resulted from underlying myocarditis. The mare was discharged with oral propranolol, a tapering course of prednisolone, and exercise restriction. Follow‐up cardiac examination 6 weeks later revealed persistent, intermittent VPCs and reversion to VT occurred during exercise. Sinus rhythm with intermittent VPCs was re‐established following the administration of lidocaine. The mare was again discharged with oral propranolol therapy, which was subsequently replaced with oral sotalol. Sudden death occurred 4 weeks later but a post mortem examination was not performed.

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“…7e10 Primary cardiac diseases may include cardiomyopathy, myocarditis, endocarditis and pericarditis. 11,12 Primary cardiac disease as a consequence of a viral respiratory infection is a potential complication reported in horses and is a possible cause of the arrhythmia in this horse. 3,13 The initial history supports viral respiratory infection.…”

Section: Discussionmentioning

confidence: 99%

Resolution of sustained narrow complex ventricular tachycardia and tachycardia-induced cardiomyopathy in a Quarter Horse following quinidine therapy

Stern

Barnett

Lahmers

et al. 2012

Journal of Veterinary Cardiology

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Cardiopathological Observation on a Case of Persistent Ventricular Tachycardia in a Pony Mare.

Cited by 8 publications

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Pathologic and Electrocardiographic Findings in Sudden Cardiac Death in Racehorses.

Pathologic and Electrocardiographic Findings in Sudden Cardiac Death in Racehorses.

Treatment of sustained monomorphic narrow‐complex ventricular tachycardia in a 16‐year‐old Arab mare with a constant rate of infusion of lidocaine and oral propranolol

Resolution of sustained narrow complex ventricular tachycardia and tachycardia-induced cardiomyopathy in a Quarter Horse following quinidine therapy

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