The most common acquired heart disease in dogs, have a direct relation with the age. They are:

Mitral Valve Disease

 Primary: Abnormal valve (valvular myxomatous degeneration, bacterial endocarditis, valvular tumors, etc.).

 Secondary, the valve is morphologically normal (ventricular geometric alterations in the dilated cardiomyopathy or hypertrophic cardiomyopathy, rupture of tendinous cords, etc.).

Mitral Apparatus

The anatomical structure that regulates the flow of blood through the mitral orifice, is called Mitral apparatus and its function is to keep the valve open fully during diastole to allow proper filling of the ventricle, and close smoothly, without allowing the return of blood during ventricular systole. The most commonly affected in dogs is the valve, which suffers a degenerative process known as valvular myxomatous degeneration (DVM).

Prevalence

 The highest prevalence of acquired heart disease in dogs.

 Incidence increases with age. (8-11 years).

 Canine small breed (less than 20 kg).

 Poodle, Dachshunds, Chihuahua.

 The GLICAV (Latin American Group for Research in Cardiovascular Diseases) found in a sample of 1163 patients, a ratio of 60-40% male / female, 59% were patients without race, the 8% poodle, Cocker Spaniel 4%, 4% Dachshunds and 12% other. The average age of diagnosis was 11 years.

Histological Structure of the Mitral Valve

We can divide the normal mitral valve in four layers, from the atrium to the ventricle are atrialis surface (endocardium, atrial continued) Pars spongiosa, a collection of rare and bundles of collagen fibers and some elastic fibers embedded in a substance fundamental muco-polysaccharides, Pars fibrous skeleton forms the valve, and consists of a dense layer of collagen fibers. Ventricularis surface (endocardium is continuous with the ventricular coating).

Pathophysiology

It is a thickening of the valves mainly affecting the free edge (or coaptation) and the middle third valve. Macroscopically, these lesions are at first punctiform type, then leave together, in small nodules and unite to form larger areas producing an increase in the valve tissue and the retraction of the same. With the evolution of the process there is a failure in coaptation of the valves and start the regurgitation of blood from the ventricle into the atrium, which will produce the cardinal signs of this disease: the murmur.

Histologically characterized by an expansion of the pars spongiosa, which invades and produces a focal disruption of the pars fibrosa, this change in the spongiosa ago to take the appearance of embryonic mesenchymal tissue, which is known as myxomatous tissue. Regurgitation, cardiovascular causes (changes in pressure and volume), which bring into play the cardiovascular compensatory mechanisms (neurohormonal, RAAS, etc).

Etiology

It is unclear, there are several theories about it: a polygenic hereditary factor, based mainly on studies on race and Cavalier King Charles Spaniel and Dachshunds, an abnormality in the biochemical composition of collagen, the "dyscollagenosis", is a disorder in synthesis, content or organization of collagen and several more.

But so far the cause remains unknown, knowing only that myxomatous mitral degeneration is a degenerative process not associated with an inflammatory or infectious agent.

Background and Clinical Diagnosis

The MVD is a chronic disease course and progression. On auscultation, a murmur is determined holosystolic more audible at the mitral area, with dorsal irradiation, cranial and caudal, produced by the sudden passage of blood from the ventricle to the atrium. The patient may not show symptoms, or in more advanced stage with symptoms of cough, dyspnea, fatigue, etc.

Canine Dilated Cardiomyopathy

Is a term designated to describe heart disease characterized by dilation of the atrial and ventricular cardiac chambers, on a unilateral or bilateral and may be primary or secondary. Clinically it is observed, an alteration of contractility, which over time lead to congestive heart failure and the presence of clinical symptoms.

Prevalence

 It affects mainly large dogs (over 20kg).

 Doberman, Boxer, Great Danes, Cocker Spaniel.

 The GLICAV (Latin American Group for Research in Cardiovascular Diseases) found in a sample of 331 dogs, a ratio of 70-30% male / female, 26% were Doberman, German Shepherd 20%, 18% patients without race, 13 % Boxer and 6% Cocker Spaniel). The average age of diagnosis was 9 years.

Etiology

The exact cause is not clearly identified, there are suspicions nutritional deficiencies (taurine, carnitine, etc.), a hereditary component, genetic causes, or is the expression of multiple factors (endocrinopathies, ischemic changes, viral, alteration in the synthesis of cardiac proteins, etc). Although the primary mechanism is idiopathic in most cases.

Pathological and Histopathological Finding

Primarily it should be noted the remarkable cardiomegaly, with increases of chambers and thinning of the walls, which lead to a chronic deterioration of left ventricular geometry, the traction of the papillary muscles and presentation of mitral failure secondary to cardiomyopathy dilated. Histologically it is noteworthy degeneration of myocardial tissue, cell lysis, vacuolization and atrophy of myocytes.

Clinical Signs

The symptoms are variable and often depend on the breed and habits of patients. Dogs that have daily physical activity may have changes in it, exercise intolerance, fatigue or weakness (or syncope for effort) as the first manifestation. Instead sedentary pets, usually presented in advanced stages of consultation and clinical symptoms (cough, dyspnea, etc.). In advanced stages the signs are related to weight loss, weakness, cough and lung congestion and ascites. Frequent presence of arrhythmia in these cases, the most common being atrial fibrillation and ventricular arrhythmias such as isolated extrasystoles in salves or ventricular tachycardia (either continuous or paroxysmal).

Progress in clinical and cachexia, are often very fast (mostly in Doberman and Boxer). Cardiac cachexia is due to several causes such as metabolic disorders, an increase of tumor necrosis factor alpha and pro-inflammatory agents, which together lead to an increased catabolism.

References

References are available upon request.