A pilot study investigating circulating trimethylamine N-oxide and its precursors in dogs with degenerative mitral valve disease with or without congestive heart failure.

Abstract

BACKGROUND: Pathophysiologic mechanisms for the development and progression of degenerative mitral valve disease (DMVD) remain elusive. Increased concentrations of circulating trimethylamine N-oxide (TMAO) and its precursors choline and l-carnitine are associated with the presence and severity of heart disease in people. OBJECTIVES: To determine if differences exist in plasma concentrations of TMAO, choline, or l-carnitine among dogs with DMVD and congestive heart failure (CHF), dogs with asymptomatic DMVD, and healthy control dogs. ANIMALS: Thirty client-owned dogs: 10 dogs with CHF secondary to DMVD, 10 dogs with asymptomatic DMVD, and 10 healthy control dogs. METHODS: A pilot cross-sectional study in which echocardiography was performed and fasting plasma concentrations of TMAO, choline, and l-carnitine (total and fractions) were measured. RESULTS: TMAO (P = .03), total l-carnitine (P = .03), carnitine esters (P = .05), and carnitine esters to free carnitine ratio (E/F ratio; P = .05) were significantly higher in dogs with CHF compared to those with asymptomatic DMVD. TMAO (P = .02), choline (P = .01), total l-carnitine (P = .01), carnitine esters (P = .02), free carnitine (P = .02), and E/F ratio (P = .009) were significantly higher in dogs with CHF compared to healthy controls. CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with CHF secondary to DMVD had higher concentrations of TMAO compared to both asymptomatic DMVD dogs and healthy controls. Larger prospective studies are warranted to determine if TMAO plays a role in the development or progression of DMVD or CHF.