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
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.
How does that work?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.
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.
Signs observedCough 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.
Respiratory coughIt 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.
Other cluesA 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
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
What elseIn 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.
Radiographic evaluationMVD 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.