Key result
Medical therapies such as ACE inhibitors and spironolactone derive their benefit in canine degenerative mitral valve disease by interrupting or suppressing maladaptive neurohormonal responses.
Understanding neurohormonal mechanisms in canine degenerative mitral valve disease provides a pathophysiological basis for therapies like ACE inhibitors and spironolactone.
Supports neurohormonal blockade in canine DMVD; leaves open optimal dosing and timing via prospective trials.
Neurohormonal systems play a critical role in canine degenerative mitral valve disease (DMVD). DMVD results in mitral regurgitation, which reduces forward cardiac output and increases intracardiac pressures. These changes trigger neurohormonal responses that ultimately result in maladaptive cardiac remodelling, congestion and heightened morbidity and mortality. Medical therapies such as ACE inhibitors and spironolactone derive their benefit by interrupting or suppressing these neurohormonal responses. Thus, knowledge of neurohormonal mechanisms can lead to a better understanding of how to treat DMVD.
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Mark A. Oyama (2009) conducted a review in canine degenerative mitral valve disease. ACE inhibitors and spironolactone was evaluated. Medical therapies such as ACE inhibitors and spironolactone derive their benefit in canine degenerative mitral valve disease by interrupting or suppressing maladaptive neurohormonal responses.
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