Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog.
Dogs with MMVD frequently develop congestive heart failure after an asymptomatic period. There is significant interest in providing medical intervention during the asymptomatic period in hopes of postponing the development of heart failure, but there is little consensus on the best therapy. Although use of angiotensin converting enzyme (ACE) inhibitors for manipulation of an activated renin angiotensin aldosterone system (RAAS) is an important component of management of congestive heart failure, use of ACE inhibitors in a dog with asymptomatic cardiac enlargement is controversial.
One study performed in Cavalier King Charles Spaniels (CKCS) did not show a benefit. Another study performed with several dog breeds demonstrated a significant increase in number of dogs who were heart failure free at day 500 in the enalapril group compared to placebo. This variable response to ACE inhibitor therapy is also observed in human beings and has been attributed to an intronic polymorphism in the ACE gene.
We have recently demonstrated that dogs also have polymorphisms within the same intron. Dogs homozygous for these polymorphisms have lower baseline ACE activity. We suggest that these dogs may have a weaker response to RAAS activation and subsequently ACE inhibition. If this is the case, families or breeds with this polymorphism may have developed an alternative cardiac compensation system and ACE inhibitors may be of minimal value to them as had been suggested by the study in which a lack of benefit was observed with enalapril in CKCS.