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<p>Exercise-associated sudden death (EASD), defined as acute collapse and death in an apparently healthy racehorse during or within ~1&#xa0;h after exercise, is currently among the top concerns in the racing industry. Cases of EASD with no cause of death identified at necropsy are frequently presumed to be of cardiac origin. In such cases, in addition to a regular necropsy, a cardiac examination protocol is performed that includes a detailed gross examination and microscopic evaluation of 11 regions of the heart. Very often this protocol is unrewarding because there are no microscopic lesions to explain the presumed cardiac event. Here we describe the necropsy of a 3-year-old, Thoroughbred gelding that collapsed a few minutes after a workout. The heart was grossly unremarkable, but significant histologic lesions that included multifocal to diffuse cardiomyocyte degeneration and necrosis, lymphoplasmacytic myocarditis, and myocardial fibroplasia were found, particularly in the right and left ventricular free walls and in the interventricular septum. Other lesions included severe pulmonary edema and congestion, splenic congestion, an open castration wound with localized suppurative inflammation and bacteria in the scrotum, and lymphoplasmacytic interstitial nephritis. We believe that the cardiac lesions were severe and extensive enough to have contributed to death. A cause for such lesions was not definitively identified, but it is possible that the infected castration wound predisposed to myocarditis. This case serves as an example of the use of the cardiac examination protocol to map and evaluate lesions in EASD cases.</p>

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Case report: exercise-associated sudden death in a Thoroughbred racehorse with cardiac lesions

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  • 发表日期：

    2026年7月4日

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  • Hernando Daniel Acevedo,
  • Francisco Uzal,
  • Jeff Blea,
  • Eileen Henderson,
  • Akinyi Nyaoke,
  • Carlos Omar Schild,
  • Javier Asin

摘要

Exercise-associated sudden death (EASD), defined as acute collapse and death in an apparently healthy racehorse during or within ~1 h after exercise, is currently among the top concerns in the racing industry. Cases of EASD with no cause of death identified at necropsy are frequently presumed to be of cardiac origin. In such cases, in addition to a regular necropsy, a cardiac examination protocol is performed that includes a detailed gross examination and microscopic evaluation of 11 regions of the heart. Very often this protocol is unrewarding because there are no microscopic lesions to explain the presumed cardiac event. Here we describe the necropsy of a 3-year-old, Thoroughbred gelding that collapsed a few minutes after a workout. The heart was grossly unremarkable, but significant histologic lesions that included multifocal to diffuse cardiomyocyte degeneration and necrosis, lymphoplasmacytic myocarditis, and myocardial fibroplasia were found, particularly in the right and left ventricular free walls and in the interventricular septum. Other lesions included severe pulmonary edema and congestion, splenic congestion, an open castration wound with localized suppurative inflammation and bacteria in the scrotum, and lymphoplasmacytic interstitial nephritis. We believe that the cardiac lesions were severe and extensive enough to have contributed to death. A cause for such lesions was not definitively identified, but it is possible that the infected castration wound predisposed to myocarditis. This case serves as an example of the use of the cardiac examination protocol to map and evaluate lesions in EASD cases.