Infective Endocarditis. Infection of the endocardium typically involves one of the cardiac valves, although mural endocarditis may occur. Most investigators believe that some sort of endothelial defect must be present for infective endocarditis to develop. When the endothelium is partially eroded and underlying collagen exposed, platelets adhere and produce a local thrombus. Blood-borne bacteria may become enmeshed in this thrombic lattice resulting in a localized infection. This infection, through its own enzymes and host mediators, causes a progressive destruction of the valve resulting in valvular insufficiency. The aortic valve is most commonly affected in dogs producing aortic insufficiency. The left ventricle cannot tolerate the constant back flow of from the insufficient valve, and soon fails. Infective endocarditis of the atrioventricular valves (tricuspid and mitral) also occurs but is better tolerated than aortic endocarditis. The mitral valve is most commonly affected in horses, while the tricuspid valve is most frequently involved in cattle. Infective endocarditis is rare in cats and there are no feline breed predilections. For dogs, German shepherds and other large breed dogs are typically affected. There is a significant predilection for males (72%) and the mean age is 5 years.
Infective endocarditis can produce a very wide spectrum of clinical signs, as bacteria released from the infected valve enter the circulation and colonize other organs. There may be neurologic, gastrointestinal, urologic, orthopedic, and cardiovascular clinical signs. A chronic, fluctuating fever is usually present. Shifting leg lameness may occur. Malaise and weight loss are present in almost all cases. If a right-sided valve is affected (tricuspid, pulmonic), then ascites and jugular pulsations may be present. A murmur will be present in most cases, the exact type depending on the valve involved. When there is aortic endocarditis, a soft diastolic murmur will be present, heard best over the left heart base, and arterial pulses will be bounding. Mitral endocarditis will result in a murmur very similar to that caused by degenerative valve disease, i.e. a prominent systolic murmur heart best over the left cardiac apex.

Bacteria most often isolated from affected small animals include Streptococcus, Staphylococcus, E. coli, and Klebsiella. Other bacterial species and fungi may be involved. A precipitating infection (dental disease, pyoderma, prostatitis) can be determined in approximately 60% of affected dogs. Streptococcus and Actinobacillus equuli are the most common isolates of horses. A complete blood count often shows a neutrophilic leukocytosis. An active infection may be associated with the presence of band neutrophils, and a chronic disease with a monocytosis (90% of cases in one series). Anemia of chronic disease is frequently present.
Abnormalities of the chemistry panel reflect organ involvement and may include elevations in liver enzymes and BUN/Cr. The urinalysis will demonstrate an active sediment if pyelonephritis is present. Blood cultures with sensitivity should be obtained in affected patients. It is preferable to draw 2-3 blood samples 1 to 2 hours apart. A strict aseptic technique is required. Radiography demonstrates cardiac chamber enlargement dependent upon the location of the involved valve. If the aortic or mitral valve is affected, there will be left atrial and left ventricular dilatation. Evidence of left-sided failure may be seen as an increase in the interstitial densities and an alveolar pattern. If the tricuspid or pulmonic valve is affected, right-sided chamber enlargement is expected.
Diskospondylitis is a common sequela of infective endocarditis in the dog and is characterized by irregular, lytic vertebral endplates.
Echocardiography is the ideal test to definitively diagnose infective endocarditis. The affected valve is easily detected as the involved area is very hyperechoic (bright) and thickened. Doppler echocardiography will confirm insufficiency of the valve. There will be chamber enlargement on the side of the affected valve. Electrocardiographically, the rhythm in most cases is normal sinus rhythm.
Occasional to frequent atrial premature and ventricular complexes may occur. Infrequently, other arrhythmias such as atrial fibrillation or third degree AV block are found. The height of the R-waves may be increased (suggestive of left ventricular enlargement) and the width of the P-wave increased (suggestive of left atrial enlargement).

Therapy must be directed at 1) controlling the congestive heart failure state, and 2) sterilizing the lesion and stopping metastatic infection. The heart failure may be extreme and intractable if the aortic valve is involved causing the prognosis to be grave in these cases. The prognosis is more more favorable when infection is limited to one of the atrioventricular valves. Controlling the heart failure state requires the use of diuretics (furosemide), vasodilators (enalapril), and digoxin if there is a rapid rate, supraventricular arrhythmias, or decreased contractility. Initially, parenteral antibiotics are indicated for a period of one to two weeks, followed by oral antibiotics for 6-8 weeks. The choice of antibiotics should be based on sensitivity studies once they are available. Prior to these results, bactericidal antibiotics should be used. The most common combinations are ampicillin and gentamicin or cephalothin and gentamicin (monitor renal function). Infective endocarditis is a disease from which most affected animals do not survive. Those that respond to therapy will likely require long-term cardiac medications (diuretics, vasodilators, digoxin) and frequent reevaluations.
Considering the poor clinical course of affected animals, prophylaxis becomes a vital measure. When animals with co-existing heart disease are to be subjected to procedures with a potential to cause bacteremia (eg dentistry), a broad-spectrum antibiotic should be administered. Current guidelines call for the administration of ampicillin or amoxicillin one hour before the procedure, and for 2-3 days following the procedure.

Endocardiosis (or Degenerative Valve Disease) is an acquired disease characterized by degeneration and fibrosis of the cardiac valves. As endocardiosis progresses, the affected valve becomes increasingly insufficient. For mitral valve disease, the valve most commonly affected in dogs, insufficiency allows blood to jet back into the left atrium during ventricular contraction. Blood jetting back into the left ventricle increases the pressure within the left atrium which decreases venous flow from the lungs. This results in pulmonary venous congestion and ultimately pulmonary edema. In addition, as the left atrium dilates, there is a high likelihood that atrial arrhythmias (APCs, atrial fibrillation) will occur, further decreasing cardiac output. The constant jetting of blood from the high pressure left ventricle physically damages the endocardium of the left atrium, and may result in left atrial rupture in chronic cases.
The decrease in the amount of blood ejected by the left ventricle (cardiac output) forces several compensatory mechanisms into action. The body responds to decreases in cardiac output by increasing sympathetic tone and activating angiotensin converting enzyme (ACE). Chronic elevation of these compensatory mechanisms become deleterious rather beneficial. Chronic elevation of sympathetic tone causes sustained tachycardia which increases the oxygen demand of the heart and predisposes the animal to arrhythmias. ACE activation results in the formation of angiotensin II which causes sustained arteriolar and venous constriction and release of aldosterone. Vasoconstriction increases the cardiac afterload, hampering ventricular ejection of blood. Aldosterone release results in sodium and water retention and predisposes the animal to pulmonary edema.

Endocardiosis is the most common cardiac disease in veterinary medicine. This disorder most commonly affects the left atrioventricular (mitral) valve in dogs, cats, and horses. Approximately 60% of dogs older that 8 years are affected. This disease is uncommon in cats. Endocardiosis occurs primarily in small breed, older dogs, particularly in the miniature poodle, Shetland sheepdog, lhasa apso, dachshund, and cocker spaniel. The severity of clinical signs depends upon the degree and chronicity of the valvular disease. Early in the course of the disease, there are no clinical signs present, although a systolic murmur of low intensity (grade 1-2) can be heard at the left apex. As the disease progresses, exercise intolerance gradually increases, and respiratory rate increases, followed by coughing and labored breathing. In general, as this disease progresses, the intensity of the murmur increases (up to grade 6) and a precordial thrill develops. A complete blood count, serum chemistry profile, and urinalysis are usually within normal limits. Radiographically, left atrial enlargement is the hallmark finding. Other changes include left ventricular enlargement, and enlargement of the pulmonary veins. As heart failure develops, there is a progressive increase in interstitial densities, and ultimately the appearance of air bronchograms, indicative of an alveolar pattern and severe pulmonary edema. Echocardiography reveals a thickened, enlarged, and irregular valvular leaflet of normal echogenicity. Chordae tendineae may be ruptured, and the atrioventricular leaflets may prolapse into the atrium during ventricular contraction. Ventricular enlargement is common. Contractility in most cases appears normal to exaggerated as the left ventricle is able to eject a significant portion of blood into left atrium rather than the high pressure aorta. A decrease in fractional shortening (contractility) signals the presence of myocardial failure. Electrocardiographically, the rhythm in most cases is normal sinus rhythm or sinus tachycardia. When congestive heart failure occurs, sinus arrhythmia converts to a very regular sinus rhythm and the rate increases. Left atrial enlargement promotes the occurrence of atrial arrhythmias such as atrial premature complexes and atrial fibrillation. Cardiac hypoxia causes ventricular arrhythmias - VPCs are common when
congestive heart failure is present. There may be evidence of left atrial enlargement (P-mitrale or widened P waves) and left ventricular enlargement (tall and widened R waves) when the mitral valve is involved.
The essentials of treatment are 1) to slow the progression of clinical signs early with vasodilators, 2) control pulmonary edema with vasodilators and diuretics when it occurs, and 3) reduce the heart rate and increase contractility later in the course of the disease when vasodilators and diuretics begin to lose their effectiveness. It is most convenient to plan the optimal therapy for each stage of this disease:

Stage I: A soft (grade 1-2) systolic murmur is present, but there are no clinical signs of heart failure and the left atrium is not enlarged radiographically. No cardiac medications are indicated. The client should be instructed to avoid feeding any foods or snacks high in sodium.

Stage 2: A systolic murmur (grade 2-3) is present, there are no clinical signs, yet the left atrium is enlarged radiographically.
Vasodilator therapy will likely be beneficial at this early stage. Enalapril therapy at 0.4 to 0.5 mg/kg once daily is  recommended.
Owners should avoid excessive sodium - a senior diet would be ideal.

Stage 3: A systolic murmur (grade 3-4) is present and there is cough at night and following activity. There is left atrial enlargement radiographically. Continue enalapril therapy but increase to 0.4 to 0.5 mg/kg BID. Add furosemide at 1 mg/kg SID to BID and determine the lowest effective dose. A senior diet should be part of the therapy.

Stage 4: A loud (grade 4-6) systolic murmur is present. There are signs of heart disease throughout the day consisting of exercise intolerance and cough. There is moderate to marked left atrial enlargement radiographically. The heart rate has increased. Enalapril (0.5 mg/kg BID), furosemide (1-2 mg/kg SID to BID) and digoxin at 0.22 mg/m2 are indicated. A diet moderately restricted in sodium should be part of the therapy.

Affected dogs can live for years with clinical signs of degenerative valve disease and proper treatment. The use of ACE inhibitors, such as enalapril, has greatly increased our ability to control the signs of heart failure and to maximize survival.

Degenerative valve disease often affects the aortic valve in horses and consists of valvular nodules or fibrous bands at the free borders of the valve. This condition is most common in middle-aged and old horses and causes a prominent (grade II to VI) holodiastolic murmur heard best at left fourth intercostal space. This murmur often has a high-pitched or musical quality. In most cases, as opposed to the dog, clinical signs are uncommon as significant left ventricular volume overload and dilatation do not occur.
Echocardiography is used to confirm the diagnosis and allows visualization of the valvular nodules, fibrous band lesions, and valvular prolapse. Treatment is seldom necessary due to the slow progression of the disease and the horse’s ability to tolerate aortic regurgitation.

Valvular blood cysts or hematomas. These benign valvular lesions are present in up to 75% of calves less than 3 weeks old. They are most commonly located on the atrioventricular valves.