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Excerpt # 1 From International Symposium On Chronic Cardiac Valve Disease (Cvd) In The Cavalier King |
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Written by Myra Ehrman, RN, BA, BS, MScN
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MAY 16, 1998, Material under Copyright by the Cavalier King Charles Spaniel Club, U.S.A., Inc. Reproduced with Permission. Content Selected by Myra Ehrman, RN, BA, BS, MScN, on behalf of the Health Education Committee, CKCSCC
The following Introduction is included in a package of materials documenting the symposium.
The Cavalier King Charles Spaniel Club, U.S.A. Inc (CKCSC, USA) has, for a long time, been aware of the high incidence of chronic cardiac valve disease in the Cavalier King Charles Spaniel, just as have Cavalier clubs in other countries, particularly the United Kingdom and Sweden.
Our membership has continuously been appraised of the findings and suggestions have been made to breeders of means of curtailing the incidence and perhaps reducing the severity of the disease.
In this "The Year of the Heart" in which CKCSC, USA is instituting a number of programs geared toward the study and control of chronic cardiac valve disease, this symposium was organized in order to bring together international experts to present data and provide guidelines for breeders.
We urge our members to follow their recommendations, and hope that we will attain our goal of bringing the prevalence, the age of onset, and the severity of the disease to the levels seen in other breeds of dogs.
From James W. Buchanan, DVM, M Med Sci, School of Veterinary Medicine, University of Pennsylvania.
The pathology of mitral valve disease can be grouped into primary and secondary changes. Primary pathology of the valve includes thickening, prolapse, and elongation and rupture of the chordae tendineae. Valve thickening has been proposed as a criterion of disease that could be useful in cardiac screening, but I have seen dogs with ruptured chordae tendineae, mitral insufficiency, and congestive failure, that did not have very thick valves. If you seen valve thickening, it is real. If you do not see thickening it does not necessarily mean it is a normal valve.
A normal mitral valve contains two principle layers, the thicker fibrosa and the thinner spongiosa. The fibrosa is a dense collagen layer that is continuous with the chordae tendineae. It provides most of the strength of the valve. The spongiosa is a loose connective tissue layer that is relatively pliable and weak. It allows the opposing valve edges to adapt to each other and form a tight seal. In chronically diseased canine valves the fibrous layer is thin and its collagen fibers are dispersed and separated by increased amounts of spongiosa-like material. This process is called myxomatous transformation. It causes variable amount of thickening, initially at the points of insertion of the chordae tendineae and later through the valve. The myxomatous change weakens the valve and allows portions of it to bulge upward toward the left atrium giving the valve a knobby appearance. Lengthening or stretching of the chordae tendineae also occurs and allows further upward bulging (prolapse) of the valve leaflet. Often one or more of the chordae tendineae break and cause the tip of the leaflet to flip upward resulting in worsening of the valve leak.
Secondary pathology of mitral valve disease includes cardiac dilatation and hypertrophy, left atrial jet lesions and left atrial rupture. As a consequence of a leaky mitral valve, an excessive amount of blood goes back and forth between the left ventricle and left atrium, causing both chambers to enlarge (dilate). The enlargement puts greater tension on the walls of these chambers and the heart muscle gets thicker (hypertrophy) in order to compensate for the increased workload. The area where the valve attaches (the annulus) also may dilate and this will increase the severity of the valve leak.
"Jet lesions" are raised white fibrous ridges on the endocardium of the left atrium that result from regurgitant jets of blood striking the endocardium each time the heart contracts. The repeated trauma to the left atrium also can lead to myocardial damage and arrhythmias that, coupled with a rise in atrial pressure, results in atrial enlargement and rupture in some cases. In a significant number of Cavaliers, more so than in other breeds, the left atrium ruptures in one or more places. This rupture may extend through part of the thickness of the atrial wall, or it may completely penetrate and bleed into the pericardial sac, causing cardiac tamponade and cardiac arrest. This is a unique complication that does not occur in other species, including humans. It suggests that there is a specific weakness of the atrial wall that occurs in dogs, particularly in Cavaliers.
I want to describe a radiographic method that we use for evaluating heart size. We call it the vertebral heart size (VHS). On a lateral radiograph we place over the heart a piece of paper, with one corner of the paper at the lower edge of the trachea. The length of the heart (long axis), from the base of the atrium to the tip of the apex, is marked on the paper. We then turn the paper, place the same corner on the front edge of the heart and mark the width of the heart (short axis). The paper corner is then placed at the front of the 4th thoracic vertebra, and the lengths of the long and short axes are recorded as the number of vertebrae between the corner and the marked axes. The VHS is the sum of the two measurements. A heart that measures 5.8 vertebrae in the long axis and 4.4 vertebrae in the short axis would be designated as having a VHS of 10.2v.
In 100 normal dogs the average VHS was 9.7v, with a range of 8.5 to 10.6v. In 12 Cavaliers without heart disease the average VHS was 9.9, with a range of 8.8 to 10.8v. That is slightly larger than other breeds, but the difference is not significant.
I think any heart measuring over 11v is beginning to enlarge. We also use this system to monitor progressive enlargement. An example is a Cavalier that came in at 6 years of age with a grade 3 systolic murmur and a 10.5v heart. When it came back six months later, his heart had increased to 11.7v, and the left atrium was prominent. Six months later the heart measured 13.3v, and both the atrium and ventricle were quite large. Two months after that he had a huge 13.6v heart. At this point the dog was only 7 years old. Our radiologists now routinely write the VHS in their reports. Any one who receives report of a 9.5v heart will know that the heart is not enlarged. But if the VHS is 12 or 13v there is cardiac enlargement.
The Cavaliers have been an interesting group for us to look at, but we would like very much to look at them because they are nice dogs, rather than just being heart disease cases. Thank you.
Disclaimer: Your veterinarian is the most qualified person to answer all of the questions you have about your pet's health. Nothing in this article should be construed as medical advice regarding any individual animalís condition.
© Copyright April 11, 1999.
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