Valvular Endocardiosis
Incidence:
The most common cardiovascular lesion in dogs. In dogs over 9 years old 97% show lesions, of which approximatley 40% are clinically significant.
Often found at post mortem as an incidental age related change.
Aetiology is not currently known but breeds affected include chondrodystrophoid breeds E.g. Pomeranian. Males show a significantly higher prevalence of disease than females.
Potential genetic influence based on connective tissue degeneration. The disease appears similar to prolapsed mitral valve syndrome in humans which is associated with abnormalities in collagen metabolism.
Pathology:
The pathological lesion occurs when collagen in the fibrosa layer of the valve leaflet degenerates and loose fibrelastic tissue and glycosaminoglycans are laid down in the spongiosa layer. This is mucoid or myxomatous degeneration. Endocardiosis is a sterile degenerative disease so no inflammatory infiltrate will be present, perhaps only a few chronic inflammatory cells E.g. lymphocytes. The valve leaflet becomes thickened, the edges often rolling in on themselves. The lesions progress from small nodular areas to larger plaques to make the valve incompetent. Large lesions result in distortion of the valve leaflets and potentially rupture of the chordae tendinae.
In most cases the mitral valve is affected, the tricuspd valve is less commonly involved and the semilunar valves even less commonly involved. Incompetent valves allow mitral regurgitation and left atrial dilation. The regurgitant jet applies damaging forces on the atrial endocardium which may result in endocardial mineralisation and in extreme cases may facilitate left atrial rupture and haemopericardium.
Cinical Signs:
The eventual sequale of endocardiosis is left sided heart failure. The resultant increase in pressure within the pulmonary circulation will be seen as pulmonary oedema.
The enlarged left atrium compresses the left main stem bronchus inducing a soft, moist cardiac cough. A cough is usually the first presenting sign noticed by the owner. Exercise intolerance and dyspnoea may also be evident.
A harsh pansystolic murmur will often be evident, more intense over the left heart apex. A mid-systolic click may indicate the prolapse of AV-valves into the atria. The left atrium enlargement will be clearly visible on radiographs and is identifiable on ECG.
Complications:
Further to the left sided heart failure the heart may not be able to adequately perfuse the coronary circulation resulting in focal myocardial necrosis and then fibrosis. This will impair conduction within the myocardium and potentially induce arrhythmias and further heart failure. In these cases syncope may be seen due to the arrhythmia.