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Massai de Castro-Castalia
Dilated cardiomyopathy (DCM) is an idiopathic, genetic, or familial myocardial disease characterized by cardiac dilatation and reduced myocardial contractility.
Histological lesions include absence of inflammation, attenuated wavy fibres, loss of myocytes, and the presence of increased myocardial fibrosis. Coronary arteries are normal and the valves unremarkable, except in older dogs with concurrent mitral or tricuspid valve endocardiosis. Deficiency of metabolic substrates (such as L-carnitine or taurine) is found in a minority of dogs, but the exact cause and effect relationship between these substrates and DCM is incompletely understood. There is no published evidence for deficiency of co-enzyme Q10 in this disorder.
The onset of myocardial failure and limited cardiac output is followed by an assault of neuro-hormones and cytokines released to support arterial blood pressure. However, neuro-hormonal activation is associated with further myocardial damage. The left ventricular ejection fraction continues to decrease, the heart dilates, and ventricular diastolic dysfunction can be recognized by detailed echo-cardiographic studies. Secondary atrio-ventricular valvular regurgitation often develops leading to murmur of mitral or tricuspid regurgitation.
Renal retention of sodium and water combines with reduced left ventricular performance to produce CHF. Arrhythmias can occur at any time during the course of disease. Syncope, sudden cardiac death, or CHF are potential consequences of these events. Frequently, biventricular CHF is precipitated by development of AF in a dog with previously “compensated” DCM.
Dilated cardiomyopathy occurs most often in middle-aged, male, large and giant breed dogs, can affect dogs of any age; males are predisposed or more likely to be affected at a young age.
It is assumed that there is a familial proneness to DCM and/or it may be carried in some bloodlines, although the precise genetic basis has not been as yet demonstrated.
The four most common clinical presentations of DCM are:
Typical symptoms in advanced cases of DCM include exercise intolerance and clinical signs of CHF. There can be marked weight loss and cachexia. Syncope related to ventricular arrhythmia or neuro-cardiogenic syncope (inappropriate bradycardia and vasodilatation) may be referred. Clinical signs of left-sided CHF include tachypnea, respiratory distress, and coughing related to pulmonary oedema. Right-sided CHF is characterized by jugular pulses and jugular venous distension, hepatomegaly, and ascites. Biventricular failure includes the above findings along with pleural effusion. Auscultation may reveal atrial and ventricular gallops, systolic murmurs, or arrhythmias.
The arterial blood pressure usually is normal owing to vasoconstriction and neuro-hormonal activation, but will be decreased in profound DCM with cardiogenic shock. The intensity of the first heart sound and strength of the arterial pulse are often diminished, indicating reduced LV contractility and stroke volume. Crackles of pulmonary oedema or a pleural fluid line may be evident.
Unfortunately for many owners DCM seems to be becoming a critical disease in Bullmastiffs that is appearing more and more often in youngest dogs and females! The reason seems to be linked to a shortfall in selective breeding on one side; yet this disease can be easily screened in youngsters and these should be sold under restricted agreements, to ensure they will not be bred from and the owners perfectly aware of the risks and the need for early and continued preventive treatment.
The good news is that DCM has not been diagnosed in any of the “CASTRO-CASTALIA” Bullmastiffs until now.
(Original text written by Christina of Lima-Netto and Federico Baudin specifically for this web page and protected with Copyright. Not even whole can be reproduced not partially by any way, without Castro-Castalia's express assent in writing)
LAS FOTOGRAFIAS SON MERAMENTE ILUSTRATIVAS NO UNA INDICACION DE QUE LOS EJEMPLARES PADEZCAN DICHA ENFERMEDAD.