3. Dilated cardiomyopathy 3. Dilated cardiomyopathy

Incidence

Dilated cardiomyopathy (DCM) usually occurs in young to middle age dogs (range 6 months to 14 years, mean 4-6 years) of giant breeds, however in the boxer the mean age at presentation is reported to be 8 years (Fox 1988) and so the condition is included in this chapter. In boxers more males are affected than females and there is greater prevalence in some breeding lines.

DCM affects mainly young to middle aged cats, and is often associated with taurine deficiency. Taurine deficiency has been identified as a cause of DCM in cats fed commercial petfoods that failed to maintain satisfacplasma taurine concentrations. It is not considered further here.



Gross pathology

Severe dilatation of all chambers of the heart is characteristic of the condition in most breeds, but this is not true in the boxer. There is thinning of the ventricular walls (unless compensatory hypertrophy is present) and atrophy of papillary muscles and trabeculae. Focal endocardial fibrosis is present.

In boxers there is usually thickening of the atrioventricular valves (mitral, but sometimes the tricuspid or aortic valve).



Histopathology
Myocardial degeneration.



Aetiopathogenesis
The aetiology is unknown in most cases. Metabolic defects have been demonstrated in some species and carnitine-related problems in the myocardium have been reported in some dogs, including boxers with DCM.

Selenium deficiency has been implicated but not proven in some cases as have toxins, infective agents (viruses) and immunological factors.



Pathophysiology
Impaired ventricular contractility leads to reduced ejection volume, though compensatory mechanisms such as increased heart rate may maintain cardiac output for a short period. Reduced renal blood flow stimulates the renin-angiotensin-aldosterone-antidiuretic hormone (ADH) pathway causing sodium and water retention increasing preload and afterload. Increased sympathetic tone also increases preload, and results in peripheral vasoconstruction further reducing cardiac output. Congestive heart failure eventually develops.


Clinical findings
(1) weakness
(2) congestive heart failure
(3) syncope
(4) pale membranes, prolonged capillary refill times
(5) ascites, hepatosplenomaegaly
(6) mitral murmur
(7) weight loss
(8) arrhythmias (atrial fibrillation often - but not in boxers)
(9) cardiomegaly on radiographs
(10) ECG changes.

About one-half of the boxers with DCM have no significant radiographic abnormalities present, and about one-third of boxers are asymptomatic.

ECG changes most typical for the boxer are ventricular premature complexes and paroxysmal ventricular tachycardia.

Endomyocardial biopsy has confirmed carnitine-deficiency in some boxers with DCM, and dietary supplementation may be beneficial.


Treatment