Endocardiosis is the most common cause of heart failure in small breed dogs and the most common cause of heart failure in dogs in general. Therapy is initiated once clinical signs of heart failure are present as well as consistent imaging studies which reveal in most cases significant left atrial enlargement with or without pulmonary edema. Which treatments are appropriate will depend on which signs of heart failure are manifested.

Angiotensin Converting Enzyme Inhibitors (ACE inhibitors)

These medications have proven to be one of the most significant breakthroughs in cardiac therapeutics for both humans and our small animal patients. Though there are many cardiac medications available, few have been shown to prolong life. ACE inhibitors not only prolong the lifespan of our cardiac patients in heart failure, but they also improve their quality of life. Quality of life is a vital issue in veterinary medicine, since owners can resort to euthanasia if the pet is perceived to be suffering or not living a good quality life anymore.

ACE inhibitors have a variety of effects in heart failure. One of the hallmarks of heart failure is thought to be activation of the Renin-Angiotensin-Aldosterone System (RAAS). This certainly does apply to dogs with dilated cardiomyopathy (DCM). It does not seem to be as uniform in dogs with valvular heart disease, however. It has been shown that use of diuretics such as furosemide or marked salt restriction can lead to activation of the RAAS. Activation of the RAAS leads to vasoconstriction, water and salt retention. Angiotensin II (AT-II) is also thought to play a role in cardiac remodelling, a process that leads to progressive cardiac dysfunction. This may relate more to local concentrations of AT-II rather than circulating blood levels.

Effects of ACE Inhibitors in Congestive Heart Failure

A variety of studies have looked at the affects of ACE inhibitors in patients with symptomatic heart failure.^1-4 In dogs with marked heart failure from mitral valve disease, life expectancy more than doubled with ACE inhibitors when compared to placebo. This applies to both enalapril and benazapril. In dogs with DCM enalapril had the same effect. Statistically it was not possible to show the same benefit with benazapril, though this may have related more to the small size of the group investigated rather than any true differences between the medications. The ability to exercise is also significantly improved as is the patient's overall well-being when these medications were given.

There is little doubt that a dog with congestive heart failure should be placed on an ACE inhibitor unless it absolutely cannot tolerate the drug. This is especially true if diuretics are being used or is a salt restricted diet has been prescribed. Adverse side effects are rare in dogs. The greatest concern is the development of azotemia. This usually only occurs when diuretics and/or salt restriction are concurrently being used and can often resolve when the diuretic dose is reduced. In fact in some studies renal values improved in those dogs that were receiving an ACE-I in comparison to placebo.

When to Start a Patient on an ACE inhibitor

The question arises whether to start using these medications in dogs with heart disease without clinical signs. Goal of starting these medications early would be to slow the progressive changes associated with heart disease and prolong the amount of time till heart failure develops. It appears that this does occur in humans, however in humans one of the most common causes of heart failure is myocardial infarction, a disease where progressive cardiac remodelling plays a significant role in future decompensation. Until recently there was little data to guide veterinarians in this regard. A recent publication has looked at this important question in detail. The study was a prospective, placebo-controlled double blind study involving 229 Cavalier King Charles Spaniels with mitral valve disease that had no evidence of heart failure.⁵ The dogs were evaluated by physical examination, electrocardiography and radiographs. The dogs were randomized to either receive placebo or enalapril at standard dosages. The study revealed that patients with cardiomegaly or louder murmurs progressed more rapidly to heart failure. The study however failed to show any preventive benefit from using enalapril in these asymptomatic dogs, whether or not cardiomegaly was present at enrolment. There are obvious limitations to this study in that only one breed and only 1 ACE inhibitor was studied. Nonetheless, given the scope of the study, similarity in progression of valvular endocardiosis in dogs and the similar effects various ACE inhibitors it is likely that this study does apply to most dogs with mitral valve disease.

Unlike dogs with mitral valve disease, the situation in dogs with dilated cardiomyopathy may be dramatically different. This may because RAAS activation is more pronounced in DCM. A study in Dobermans tried to determine if early therapy was able to slow the progression of DCM and positively influence lifespan. The study group consisted of dogs with evidence of DCM such as increased left ventricular diameter, decreased contractility and arrhythmias without having clinical signs.⁶ Administering enalapril in the occult phase was able to significantly prolong lifespan and increase the time to onset of congestive heart failure. Overall it is recommended to start an ACE inhibitor in dogs suspected of having DCM as early as possible, independent of whether or not they have evidence of decompensation.