1.Acquired chronic valvular disease (endocardiosis) 1. Acquired chronic valvular disease (endocardiosis)

Incidence

Acquired atrioventricular valvular endocardiosis is the most common canine heart condition accounting for over 70% of cases, with a reported overall incidence of 17-40%. The disease is most prevalent in small to medium size dogs in the last third of their life, males are more often affected than females (1.5: 1) and it increases both in frequency and severity with increasing age.

One study reported severe disease to be present in 58% of dogs over 9 years of age, and endocardiosis lesions were present in all dogs over 13 years of age (Whitney 1974). The author concluded that the frequency of occurrence and the severity of the valvular lesions increased with increasing age (Table 2.1 and Table 2.2).

Endocardiosis is rarely reported in cats.

Aetiopathogenesis

The cause of the valvular lesions seen in endocardiosis is unknown, but natural ageing processes have been suggested by some authors, either:

(1) associated with ageing changes in the collagen fibres of the valves, or
(2) valve injury progressing to a degenerative lesion.

It is commonly believed that chronic valvular disease begins in the first third of life, progresses to cause valvular incompetence in the second third of life, and may be associated with congestive heart failure in the last third of life, though most dogs are likely to develop cardiac compensation and not progress to exhibit clinical signs of failure.



Gross lesions

Greyish-white nodules or plaques on the valves, with weakening and thickening of the chordae tendinae. Jet lesions on the atrium.

Lesions most often involve the left atrioventricular valve (mitral) and less commonly the right atrioventricular (tricuspid) valve (see Plate 1). The aortic and pulmonary valves are rarely affected.



Histopathology

Various changes have been described including:

(1) myxomatous changes
(2) deposition of hyaline (fibrinoid) material
(3) fibrous and elastic proliferation
(4) mucoid degeneration.


There is proliferation of the spongiosa layer of the valve with increased amounts of matrix containing glycosaminoglycans (GAGs).



Pathophysiology

The valvular lesions result in:

(1) inadequate closure of the valves during systole with regurgitation of blood into the atrium
(2) volume overload of atrium and ventricule
(3) compensatory atrial and ventricular dilatation
(4) myocardial hypertrophy
(5) myocardial failure (eventually)
(6) pulmonary oedema (due to pulmonary vein compression)
(7) left mainstem bronchus compression (causes a cough)
(8) bronchoconstriction (if pulmonary oedema present)
(9) dysrhythmias (due to stretching of chamber wall)
(10) rupture of the atrium with haemopericardium (rare)
(11) rupture of the chordae tendinae.


Endocardiosis results in 'backward' failure or left-sided heart failure initially.



History

Exercise intolerance and coughing are the most frequent owner comOften there is a history of weight loss (even if the dog is still overweight).



Clinical findings
(1) systolic murmur present on auscultation, and localisable to the site of the mitral and/or tricuspid valve
(2) a precordial thrill may be palpable
(3) sinus tachycardia sometimes with dysrhythmias
(4) pulse deficit (sometimes).



Treatment

Preload reducers, e.g. salt restriction, diuretics and vasodilators. Cardiac inotropes, e.g. cardiac glycosides.