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Circulatory System
Congenital and Inherited Anomalies of the Cardiovascular System
Mitral Valve Dysplasia
Pathophysiology
Clinical Findings and Treatment
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Sections in Veterinary Professionals
  • Behavior
  • Circulatory System
  • Clinical Pathology and Procedures
  • Digestive System
  • Emergency Medicine and Critical Care
  • Endocrine System
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Chapters in Circulatory System
  • Hematopoietic System Introduction
  • Anemia
  • Blood Groups and Blood Transfusions
  • Blood Parasites
  • Canine Malignant Lymphoma
  • Erythrocytosis and Polycythemia
  • Hemostatic Disorders
  • Leukocyte Disorders
  • Lymphadenitis and Lymphangitis
  • Cardiovascular System Introduction
  • Congenital and Inherited Anomalies of the Cardiovascular System
  • Heart Disease and Heart Failure
  • Heartworm Disease
  • Bovine High-Mountain Disease
  • Thrombosis, Embolism, and Aneurysm
Topics in Congenital and Inherited Anomalies of the Cardiovascular System
  • Overview of Congenital and Inherited Anomalies of the Cardiovascular System
  • Anomalies of Derivatives of the Aortic Arches
  • Outflow Tract Obstructions
  • Septal Defects
  • Peritoneopericardial Diaphragmatic Hernia (PPDH)
  • Tetralogy of Fallot
  • Mitral Valve Dysplasia
  • Mitral Stenosis
  • Tricuspid Dysplasia
  • Ectopic Heart
  • Miscellaneous Congenital Cardiac Abnormalities
 
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Mitral Valve Dysplasia

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Congenital malformation of the mitral valve complex (mitral valve dysplasia) is a common congenital cardiac defect in cats. Canine breeds predisposed are Bull Terriers, German Shepherds, and Great Danes. Mitral valve dysplasia results in mitral insufficiency and systolic regurgitation of blood into the left atrium. Any component of the mitral valve complex (valve leaflets, chordae tendineae, papillary muscles) may be malformed, and often more than one component is defective.

Fig. 5

Mitral valve dysplasia, dog. Illustration by Dr. Gheorghe Constantinescu.

Pathophysiology

Malformation of the mitral valve complex results in significant valvular insufficiency. Chronic mitral regurgitation leads to volume overload of the left heart, which results in dilatation of the left ventricle and atrium. When mitral regurgitation is severe, cardiac output decreases, which results in signs of cardiac failure. Severe mitral regurgitation can also result in pulmonary venous congestion and left-sided CHF. Dilatation of the left-sided chambers predisposes affected animals to arrhythmias. In some cases, malformation of the mitral valve complex causes a degree of valvular stenosis as well as insufficiency (see Congenital and Inherited Anomalies of the Cardiovascular System: Mitral Stenosis).

Clinical Findings and Treatment

Clinical signs correlate with the severity of the defect. Affected animals usually display signs of left-sided CHF. A holosystolic murmur of mitral regurgitation is prominent at the left cardiac apex. A diastolic heart sound (gallop rhythm) is present in some cases. Affected animals may have a precordial thrill over the left cardiac apex. Electrocardiography may demonstrate atrial arrhythmias (atrial premature complexes, atrial fibrillation), especially in severely affected animals. There may also be evidence of both left atrial (widened P waves) and left ventricular enlargement. Thoracic radiographs may demonstrate severe left atrial enlargement. Left ventricular enlargement and pulmonary venous congestion can also be noted. Echocardiography demonstrates malformation of the mitral valve complex (fused chordae tendineae and thickened, immobile valve leaflets, abnormal appearance to the papillary muscles) and left atrial and ventricular dilatation. Doppler echocardiography demonstrates severe mitral regurgitation. If present, mitral stenosis can be identified (see Congenital and Inherited Anomalies of the Cardiovascular System: Mitral Stenosis).

Prognosis for animals with clinical signs and severe disease is poor. Mildly affected animals may remain free of clinical signs for several years. For therapy of progressive left-sided CHF, see Heart Disease and Heart Failure: Management.

Last full review/revision April 2012 by Davin Borde, DVM, DACVIM

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