Pamela A. Davol, 76 Mildred Avenue, Swansea,
MA 02777-1620
pdavol@labbies.com
To understand tricuspid valve dysplasia (TVD), it is first important to know a bit about the anatomy of the canine heart. The canine heart, like the human heart, is divided into two halves. The right side of the heart receives oxygen depleted blood from the tissues of the body and pumps this blood into the lungs through the pulmonary artery. After becoming oxygenated in the lungs, the blood returns to the left side of the heart through the pulmonary veins where it is then pumped to the tissues of the body by way of the aorta.
Each half of the heart is subdivided into an upper and lower chamber. The upper chamber, called the atrium, receives the blood and then passes the blood to the lower chamber called the ventricle. The ventricle then pumps the blood to its destination. To prevent backflow of the blood from the ventricle to the atrium, the heart is equipped with valves that allow blood to flow in only one direction. There are two atrioventricular valves which control blood flow between the atria and the ventricles: the tricuspid valve which is located between the right atrium and right ventricle and the mitral valve which is located between the left atrium and left ventricle.
In the canine, the tricuspid valve is made up of two irregularly shaped flaps composed of connective tissue. The tissue of the flaps is connected to the papillary muscle of the ventricle by tendon-like cords called chordae tendineae. As the right atrium contracts, blood passes through the tricuspid valve into the right ventricle. When the ventricle contracts, some blood flows backward, pushing upward against the flaps of the valve causing them to meet and form a barrier which prohibits the blood from re-entering the upper chamber. The chordae tendineae prevent the flaps from opening backward into the atrium which would break the seal and thus allow backflow of the blood.
During embryonic development, the flaps of the tricuspid valve are adhered to the wall of the ventricle and cellular degeneration must occur to free the flaps. When this cellular degeneration fails to take place, the flaps remain secured to the ventricular wall preventing proper function of the valve. This malformation of the valve is known as tricuspid valve dysplasia and results in regurgitation of blood back into the atrium. This abnormal blood flow increases the work load of the right-side of the heart resulting in enlargement of the right atrium and ventricle which eventually leads to right-sided congestive heart failure.
Although TVD is a congenital disorder, meaning that the condition is present from birth, many puppies with TVD do not show any clinical symptoms and appear healthy. Eventually, a cardiac murmur is detected upon examination or the dog may suddenly develop signs of right-sided congestive heart failure: fluid retention, cool extremities, and exercise intolerance.
Echocardiogram (ultrasound) is the preferred method for diagnosing TVD. By this method, adhesion of the tricuspid valve to the ventricular wall is easily visualized and allows a definitive diagnosis. Electrocardiography (EKG) and radiography (X-Rays) are other methods for diagnosing TVD. Labrador retrievers with TVD frequently have atrial arrythmias, abnormalities of the heart beat, associated with the enlargement of the atrium which can be detected by EKG. Additionally, x-rays usually clearly demonstrate right-sided enlargement of the heart.
Survival of dogs with TVD is dependent on the extent to which the normal function of the valve is compromised. The more severe the condition, the greater the amount of blood regurgitation and the resulting enlargement of the right side. Surprisingly, however, many dogs with severe TVD exhibit no symptoms until they are in congestive heart failure. Once symptoms of congestive heart failure occur, the affected dog usually succumbs rapidly to the condition. Treatment is limited to controlling symptoms secondary to the failing heart. Exercise should be restricted to avoid overtaxing the already burdened heart. Diuretics can be administered to control fluid retention and digoxin can be administered to regulate atrial arrythmia, if present. Despite clinical intervention, the average life expectancy for dogs with TVD is 1-3 years.
TVD is a congenital abnormality and is not acquired, therefore, prevention is limited to controlling for genetic predisposition to the disorder. Because TVD has been identified in puppies within the same litters, it is suspected that TVD may be an inherited abnormality. At this time, however, mode of inheritance is unknown. Currently, researchers at the Institute of Genetic Disease Control at UC-Davis have established a registry for Labrador retrievers diagnosed with TVD in hopes of determining prevalence within the breed and the mode of inheritance of this disorder.
In the meantime, to reduce the occurence of TVD in future progeny, dogs being used for breeding who come from lines with higher risk for TVD (i.e. a grandparent, parent or littermate diagnosed with TVD) should be screened by echocardiogram to be free of TVD prior to breeding.
Famula
TR, Siemens LM, Davidson AP, Packard M. Evaluation of the genetic basis of
tricuspid valve dysplasia in Labrador Retrievers. Am J Vet Res 2002
Jun;63(6):816-20.
Lamb
CR, Boswood A, Volkman A, Connolly DJ. Assessment of survey radiography as a method for
diagnosis of congenital cardiac disease in dogs. J Small Anim Pract 2001 Nov;42(11):541-5
Tricuspid Dysplasia: A Cardiologist's Perspective by Lori Siemens, DVM, DACVIM
Institute for Genetic Disease Control: Registry for TVD (and other genetic disorders)
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