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Degenerative valvular disease common in older dogs
Q. Could you provide a brief review of mitral valve insufficiency in older dogs?
Q. Could you provide a brief review of mitral valve insufficiency in older dogs?
A. Dr. Jonathan Abbott at the 21st American College of Veterinary Internal Medicine Forum in Charlotte, North Carolina, gave an excellent lecture on mitral valve insufficiency in dogs. Some relevant points made in this lecture are provided below.
Degenerative valvular disease exceeds 90 percent incidence in dogs older than 9 years of age and most commonly affects the atrioventricular valves.
The clinical manifestations usually result from mitral valve disease (MVD). The clinical syndrome of severe, clinically apparent mitral valve regurgitation is observed almost exclusively in aged, small breed dogs. The Chihuahua, Miniature Poodle and Toy Poodle, Pomeranian and Miniature Schnauzer are predisposed to the development of clinically consequential mitral regurgitation.
The incidence of degenerative MVD is particularly high in the Cavalier King Charles Spaniel. In dogs of this breed, MVD may be apparent at a very early age and in some individuals, the disease is severe and rapidly progressive.
Gross structural changes of the mitral valve apparatus associated with MVD include nodular distortion of the leaflets as well as lengthening and sometimes rupture of the chordae tendinae.
How does that work?
These structural abnormalities prevent normal coaptation of the mitral valve leaflets and contribute to leaflet prolapse resulting in mitral valve regurgitation. When the mitral valve is incompetent, a portion of the left ventricular stroke volume is ejected retrograde into the left atrium increasing the volume and intracavitary pressure of the left atrium.
The regurgitant volume augments the pulmonary venous return that enters the ventricle during diastole. Mitral regurgitation, therefore, imposes a volume load on the left atrium and the left ventricle; dilation and hypertrophy of the atrium and ventricle follow as a consequence.
Ventricular remodeling causes further distortion of the mitral apparatus, which contributes to progressive worsening of mitral regurgitation. Afterload (the forces that oppose myocardial shortening) is low relative to the size of the ventricle and this, together with the increase in preload results in hyperdynamic ventricular performance. The altered loading conditions associated with mitral regurgitation are generally well tolerated; however, with chronicity myocardial dysfunction can develop.
The reduction in forward stroke volume associated with severe mitral regurgitation results in neuroendocrine activation. Specifically, sympathetic tone is elevated and unopposed by vagal restraint.
Additionally, the products of the renin cascade result in vasoconstriction and renal retention of salt and water. The latter contributes to volume loading of the cardiac chambers. Potentially, ventricular filling pressures rise, resulting in pulmonary venous hypertension and the development of pulmonary edema. Clinical signs of tachypnea, polypnea and cough predictably result from the presence of pulmonary edema.
In some small breed dogs with mitral regurgitation, cough develops in the absence of pulmonary edema. Mechanical compression of the bronchi by the enlarged atrium is likely to be an important causative factor in these cases. Reflex bronchoconstriction and mucus production associated with pulmonary venous distention may also contribute.
Cough is the clinical sign that is observed most commonly in dogs with clinically evident mitral regurgitation. Respiratory distress, syncope and abdominal distention resulting from ascites occasionally prompt veterinary evaluation. When the regurgitant volume is large, ventricular hyperkinesis results in a palpably dynamic precordium. The arterial pulse is often normal although very severe mitral regurgitation may result in a weak pulse. mitral regurgitation results in a systolic murmur that is generally heard best over the left cardiac apex.
It should be recognized that primary respiratory tract disorders, including bronchitis and tracheal collapse, often affect the dog population in which MVD is most common. Because the historical findings of cough and tachypnea are common to heart disease and respiratory tract disease, the clinical presentation of a small breed dogs with respiratory signs and a heart murmur presents a challenge. MVD is a common disorder that exhibits a broad spectrum of severity; only the minority of dogs with MVD develop clinical signs. Inevitably then, there are dogs in whom the heart murmur is incidental to the clinical presentation.
When confronted with an older small breed dog in which the primary complaint is cough, it is important to determine which, of airway disease or cardiac disease, bears the greatest responsibility for the clinical signs.
Although primary respiratory tract disease and cardiac disease can coexist, one of the two often dominates the clinical presentation. In most cases, the case history, physical examination and thoracic radiographic examination provide the information needed to make this important clinical distinction.
A history of months or years of cough that occurs in the absence of dyspnea tends to support a diagnosis of airway disease. When cardiac disease is sufficiently severe that it becomes clinically apparent, it is generally progressive. Therefore, untreated dogs in which cardiac disease plays an important role tend to have a relatively short history; often, the clinical course progresses to include dyspnea.
The character of the dog's cough can also provide some diagnostic information. In general, a loud "hacking" cough is most often associated with diseases that affect the large airways such as extraluminal compression of the mainstem bronchi, chronic bronchitis or collapsing trachea. In contrast, cardiogenic pulmonary edema may cause a soft cough that is often associated with dyspnea.
The body condition of the dog can provide useful clues. Generally, dogs that cough due to heart disease or heart failure are thin. While exceptions certainly occur, obesity suggests that respiratory tract disease is primarily responsible for clinical signs. The vital signs may also be useful in distinguishing dogs that suffer primarily from cardiac disease from those with respiratory disease. Careful examination of the cardiac rate and rhythm is essential.
Healthy dogs often have a respiratory-associated arrhythmia that is evident on auscultation. In accordance with phasic variations in autonomic traffic, the heart rate increases during inspiration and decreases during expiration. This respiratory-induced sinus arrhythmia results primarily from fluctuations in vagal tone. When cardiac performance is impaired, vagal discharge is inhibited and sympathetic tone becomes dominant. Thus, in many dogs with clinical signs related to cardiac disease, tachycardia develops, and there is loss of physiologic respiratory-induced sinus arrhythmia. The clinical finding of respiratory-induced sinus arrhythmia is virtually incompatible with a diagnosis of heart failure and uncommon in dogs with severe heart disease. In contrast, many dogs that cough primarily due to primary respiratory disease have preserved and sometimes accentuated sinus arrhythmia.
In older small-breed dogs, the absence of a cardiac murmur is usually assurance that the cough results from primary respiratory tract disease. When present, the intensity of a cardiac murmur is important. In general, dogs with mild mitral regurgitation have soft murmurs and an increase in the intensity of the murmur typically parallels disease progression of mitral regurgitation.
While the relationship between the intensity of the murmur and severity of mitral regurgitation is inconsistent, severe mitral regurgitation almost always results in a loud murmur. Conversely, soft murmurs resulting from MVD are seldom of clinical consequence. The information provided by pulmonary auscultation is important but is seldom specific. Crackles, for example, result from the snapping open of collapsed small airways and may be heard in the presence of pulmonary edema. However, it should be recognized that the "dry" lungs of dogs with bronchitis or airway collapse can also produce crackles.
MVD results in enlargement of the cardiac silhouette that is roughly commensurate with the severity of mitral valve regurgitation. The cardiac silhouette is typically normal when mitral regurgitation is mild while moderate and severe mitral regurgitation result in enlargement of the left atrium and left ventricle. In the lateral radiographic projection, this is apparent as an increase in the dorsoventral cardiac dimension - the heart is "taller" than normal resulting in elevation of the caudal aspect of the trachea and potentially, compression of the left mainstem bronchus.
Straightening of the caudal border of the laterally projected cardiac silhouette is a reliable marker of left atrial dilation. In the ventrodorsal view, left atrial enlargement may be apparent as "splitting" of the mainstem bronchi or by a prominence of the cardiac silhouette at the 3 o'clock position.
Distention of the pulmonary veins provides indirect evidence of venous hypertension and though this finding is relatively inconsistent, it heralds the development of edema. When present, pulmonary edema often has a central or perihilar distribution. Interstitial edema causes blurring of vascular detail and often precedes the development of alveolar edema that is indicated by the presence of air bronchograms.
Radiography is the single most informative diagnostic test in most cases of MVD. However, thoracic radiographs must be obtained and interpreted with careful attention to the dog's body type, phase of respiration during the exposure and radiographic technique.
The individual chambers of the heart are poorly resolved by plain radiography. Despite this, the thoracic radiograph usually provides an estimate of left atrial size that is adequate for clinical purposes. This is fortunate because assessment of left atrial size is crucial in making the determination of the relative importance of cardiac disease to the clinical presentation of coughing dogs with murmurs of mitral regurgitation.
With very few exceptions, a diagnosis of heart disease or failure as a cause of cough is simply untenable in the absence of radiographic left atrial enlargement. MVD is a chronic disease and, therefore, enlargement of the left atrium and ventricle precedes the development of pulmonary edema.
Obviously, the left atrium must be enlarged before it can be incriminated as a cause of bronchial compression. In the absence of radiographic left atrial enlargement, cough is related to primary respiratory tract disease.
Echocardiography can be used to assess the degree of left atrial and ventricular dilation and can provide estimates of systolic myocardial function (contractility). Doppler studies can be used to document the presence of disturbed systolic flow within the left atrium and, therefore, provide noninvasive confirmation that the murmur is indeed caused by mitral valve regurgitation.
However, mitral regurgitation is by far the most likely cause of an acquired murmur in older small breed dogs and, most often, Doppler studies are simply confirmatory.