Acquired Valvular Disease

6 Acquired Valvular Disease

5. What are the pathophysiologic consequences of MVD?

Distortion of the mitral valve leaflets prevents normal coaptation of the mitral valve leaflets; the consequence is mitral valve regurgitation. Lengthening and rupture of the mitral chordae tendineae predisposes to mitral valve prolapse, which can also contribute to mitral valve incompetence. Inadequate leaflet apposition allows a portion of the left ventricular stroke volume to be ejected backward into the left atrium. This regurgitant volume is augmented by the pulmonary venous return and then returns to the left ventricle during diastole. Incompetence of the mitral valve therefore imposes a volume overload on the left atrium and the left ventricle. Volume loading of the left heart is a stimulus for eccentric hypertrophy (hypertrophy accompanied by dilation).

Small volumes of mitral valve regurgitation (MR) are usually well tolerated, but two factors can potentially contribute to worsening of MR. Although the speed at which it does so is highly individual, MVD is generally progressive; ongoing alterations in valvular structure worsen mitral valve incompetence. Additionally, atrial/ventricular dilation itself distorts valvular anatomy and this further limits leaflet coaptation worsening MR. Systolic myocardial function of the left ventricle is not obviously affected by MR unless the valvular lesion is severe and longstanding. When substantial MR is present, the isovolumic phase of ventricular contraction does not take place because the ventricle can unload into the low-pressure reservoir provided by the left atrium. Therefore, myocardial oxygen demand is relatively low in the setting of MR; as a result, MR tends to be a lesion that is well tolerated at least in the sense that contractility can be preserved until late in the natural history of the disease. Longstanding, severe MR can, however, result in myocardial cell death, replacement fibrosis, and myocardial dysfunction that is known as cardiomyopathy of overload.

13. Small-breed dogs with MR are often presented for the evaluation of cough; however, it can be difficult to determine whether heart disease or respiratory disease is the more important clinical problem. What history and physical findings are helpful in making this determination?

In small-breed dogs with MVD, heart disease or heart failure can explain cough; in some cases, however, the murmur of MR is incidental to the clinical presentation and the cough results from primary respiratory tract disease, such as collapsing trachea or chronic bronchitis. Although primary respiratory tract disease can certainly coexist, one of the two often dominates the clinical presentation.

A history of months or years of cough that occurs in the absence of dyspnea tends to support a diagnosis of airway disease. When MVD is sufficiently severe that it causes clinical signs, it is generally progressive. Therefore, untreated animals in which cardiac disease contributes importantly to cough tend to have a relatively short history; the clinical course often progresses to include dyspnea.

The body condition of the animal can provide useful clues. Animals that cough from heart disease or heart failure are often thin. Although exceptions certainly occur, obesity is more commonly associated with primary respiratory disease. The vital signs may also be useful. Healthy dogs often have a respiratory-associated arrhythmia that is evident on auscultation. In accordance with phasic variations in autonomic traffic, heart rate increases during inspiration and decreases during expiration. This respiratory sinus arrhythmia results primarily from fluctuations in vagal tone. When cardiac performance is impaired by severe MR, vagal discharge is inhibited and sympathetic tone becomes dominant. Thus in many animals with clinical signs related to cardiac disease, tachycardia develops and there is loss of physiologic, respiratory arrhythmia; the clinical finding of respiratory sinus arrhythmia is virtually incompatible with a diagnosis of heart failure. In contrast, many animals that cough mainly from primary respiratory disease have preserved and sometimes accentuated sinus arrhythmia.

In geriatric small-breed dogs, the absence of a cardiac murmur is generally an assurance that coughing results from primary respiratory tract disease. Soft murmurs resulting from MVD are seldom of clinical consequence. In contrast, animals that have clinical signs related to MVD almost always have loud cardiac murmurs.

It should be emphasized that these are guidelines only and exceptions do occur. Diagnostic studies, most particularly radiography, provide information that can help to solve the dilemma. As a general rule, however, respiratory disease is likely to be responsible for a chronic cough in an overweight dog with a soft murmur and preserved sinus arrhythmia. In contrast, heart disease, or even heart failure, is more likely responsible for cough in a thin animal with a loud murmur and tachycardia.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Acquired Valvular Disease

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