Mitral regurgitation is the most important heart disease in dogs (comprising approximately 75% of all heart disease) because it occurs most commonly and may lead to dyspnea, decreased exercise capacity, and death. It occur most commonly in smaller dogs, middle age to old, males, and chondrodysplastic dogs; and occurs commonly concomitantly with tricuspid regurgitation.

Mitral regurgitation refers to the leaking of blood from the left ventricle into the left atrium during the period of left ventricular systole. It is caused by incomplete closure of the mitral orifice by the leaflets of the mitral valve, most often because the leaflets are thickened and gnarled, but occasionally with left ventricular dilatation due to dilated cardiomyopathy because the mitral annulus is dilated and the normal leaflet cannot come together. It is characterized by left atrial and left ventricular enlargement (predominantly eccentric hypertrophy), and in later stages with pulmonary venous engorgement. Atrial fibrillation occurs commonly in later stages when the left atrium is most dilated. In later stages pulmonary edema and increased heart rate develop, leading to signs/symptoms of left-sided congestive heart failure and to exercise intolerance.

All animals with mitral regurgitation have a systolic murmur, usually heard loudest at the left apex, that is heard between--and often hides--the 1^st and 2^nd heart sounds. The intensity of the murmur does not correlate with the amount of blood regurgitating, although when the valve first begins to leak the murmur starts out very softly. When the ventricle dilates ands begins to fail, the force driving blood regurgitantly decreases and even though there may be more regurgitation it does so at a lower velocity and therefore with a softer murmur. When the left ventricle begins to dilate and 3^rd heart sound may develop, but this may be obfuscated by the murmur.

Because of left atrial enlargement proportion with the degree of regurgitation, the left mainstem bronchus is frequently displaced dorsad and compressed, leading to a hacking cough. This cough does not indicate heart failure, but is caused by heart disease.

With left atrial enlargement, P waves in the ECG may be prolonged and notched, and atrial premature beats may develop and evolve into atrial fibrillation. With atrial fibrillation the heart rate is rapid, irregular, irregularly-irregular, heart sounds and femoral pressure pulses are of variable intensities, and there are many more heart sounds than pressure pulses...a pulse deficit. The degree of left atrial enlargement often predicts the degree of left ventricular enlargement, since it is the pressure within the venous side of the lungs--including the left atrium which is responsible for filling the left ventricle. Thus with mid and late stages of mitral regurgitation, left ventricular enlargement may be identified by tall R waves in lead II, by radiography, or best by echocardiography. Finally when left-sided heart failure develops, pulmonary venous engorgement, dramatic left-sided cardiomegaly, pulmonary edema, and severe exercise intolerance are observed.

Treatment of mitral regurgitation should be directed at minimizing mitral regurgitation, improving forward blood flow, minimizing chronic stretch of myocardial fibers, improving lung function, regulating the ventricular rate, and preventing "down-regulation" high pressure baroreceptors and B1 receptors. I use specific identifiable observations to determine precisely when to give each of the therapeutic agents. The following is a table which may serve to lead a discussion:

In addition, and of great importance, patients should receive, probably with the onset of cardiomegaly, spironolactone to minimize histological changes in the heart, kidneys and blood vessels (e.g., remodeling). I believe that ACE inhibitors should be instituted very early in the course of mitral regurgitation for a number of theoretical reasons: reduction in regurgitation, minimize remodeling, retard valvular degeneration, protect renal physiology. Furthermore more although a potentially dangerous drug, patients should receive low dose carvedilol at the onset of heart failure-this to minimize "down-regulation" of B receptors and to scavenge free radicals of oxygen. Whereas spironolactone and ACE inhibitors are extremely safe, carvedilol possesses a significant risk unless begun at the lowest dose and increased, slowly over months; however data from human beings in heart failure indicates that ACE inhibitors, spironolactone and carvedilol are the only pharmacological agents which lengthen life, whereas digitalis reduces symptoms and allows patients to spend less time in the hospital.

Techniques have emerged to correct a diseased mitral valve using surgical interventions short of the expensive, difficult installation of an artificial valve. These include repairing the valve or merely placing a suture around the entire orifice. Although proven for treatment of mitral regurgitation in man, this method is in its infancy for dogs.