Myxomatous Mitral Valve Disease

Myxomatous mitral valve disease (MMVD) is a common cause of congestive heart failure in small-breed dogs, but the cause is unknown. Serotonin signaling is thought to play a role in canine MMVD development; however, the source of serotonin is unclear. Normally, serotonin is stored in platelets and circulating plasma levels of serotonin are low. Serotonin is released into circulation after platelet adhesion and activation. 

This study compared serotonin concentration in plasma and platelets of normal, healthy small-breed dogs predisposed to MMVD and of dogs with naturally occurring MMVD. Small-breed, client-owned dogs weighing <10 kg and ≥6 years of age (n = 43) were matched by age, breed, and size and divided into a healthy control group and a group with echocardiographic evidence of MMVD. Median plasma serotonin and platelet serotonin concentrations were not significantly different between healthy dogs and dogs with MMVD.

Although male dogs had higher levels of plasma serotonin concentrations than did female dogs, there was no correlation between plasma or platelet serotonin concentration and age, echocardiographic indices, or platelet count. Results showed low levels of plasma serotonin concentration in normal dogs and dogs with MMVD; this suggests that circulating plasma serotonin is an unlikely source of serotonin contributing to MMVD pathogenesis. It has been suggested that platelet activation on damaged mitral valves may induce serotonin release into the circulation. However, more evidence is needed. 

This is another in a long line of studies attempting to identify the underlying cause of MMVD, an important cause of cardiac disease in dogs. So far, we have been unable to identify an underlying cause or prevent or delay disease progression. There is a theory that serotonin signaling and release from platelets may play a role; an enzymatic pathway involved in serotonin synthesis was found to be increased in dogs with naturally occurring MMVD. This study compared serotonin levels in plasma and platelets of dogs with and without MMVD and found no correlation to serotonin levels and echocardiographic indices of MMVD presence or increasing severity. Thus, the clinical importance or underlying involvement of serotonin signaling is still unknown, and this paper illustrates the ongoing frustration of trying to understand the underlying mechanism.—Amara Estrada, DVM, DACVIM (Cardiology)