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Chronic Valvular Heart Disease in Dogs

John Bonagura United States

Valvular endocardiosis is a degenerative change of unknown cause affecting the subendocardial valve leaflets and chordae tendineae in the middle aged to elderly dog. Smaller breeds are predisposed. Also known as chronic myxomatous valvular heart disease, this disorder is the most important cause of heart disease in veterinary practice. Endocardiosis leads to progressive valvular incompetency with regurgitation of blood across the closed valve. The mitral apparatus is affected most often (virtually all cases), with the tricuspid valve (34%) and aortic valve (3%) less frequently involved. In some cases, the valves are redundant and the chordae tendineae elongated, leading to prolapse of the valve into the atrium. Gross lesions of advanced endocardiosis include nodular thickening and shortening at the free edge and base of the valve leaflets. Valves appear opaque and white and can be rolled and contracted at their free edge. The chordae become thickened near the valve attachment and may rupture. Secondary dilatation of the left atrium (LA) and left ventricle (LV) develop. The mitral valve annulus also can be dilated. Ventricular hypertrophy is of the eccentric type (dilated chamber), and microscopic coronary disease can lead to focal areas of ischemia and fibrosis. The right ventricle may be dilated from tricuspid regurgitation (TR) complicated by pulmonary hypertension.

Clinical Pathophysiology

The lesions of endocardiosis represent a slowly progressive process and do not cause detectable signs during the period of early structural change. In some dogs, the chordae or valvular tissue is redundant or lax and the valve will prolapse leading to a midsystolic click. Eventually, significant valvular distortion leads to detectable murmurs of valvular insufficiency and some dogs will develop heart failure. The entire process can take many years. Once the mitral valve is incompetent, blood regurgitates from the high pressure (ventricular) to the low pressure (atrial) chamber. The determinants of regurgitant volume and disease severity include: regurgitant orifice size, pressure differences between LV and LA, and time from onset of contraction to opening of the aortic valve. Severe mitral regurgitation (MR) causes LV volume overload, which can lead to left heart failure. MR also predisposes to cardiac arrhythmias, especially those originating in the dilated atrium. If the regurgitant volume increases gradually and atrial compliance increases correspondingly, the atrium distends to a large volume with a minimal change in atrial pressure and the condition is well tolerated. This explains why many dogs have severe cardiomegaly but minimal clinical signs. If the regurgitant volume is large or if the regurgitation develops suddenly (as with chordal rupture), the limits of atrial distensibility are exceeded and the mean LA pressure increases, leading to pulmonary edema. Progressive MR is associated with elevated pulmonary venous pressures, increased hydrostatic pressure in pulmonary capillaries, and eventually by pulmonary edema. These can be explained by the combined effects of 1) regurgitant volume; 2) reduced distensibility of the dilated LV; and 3) renal retention of sodium and water triggered by decreased cardiac output. Clinical consequences include tachypnea, hypoxemia, tiring, and coughing. Pulmonary hypertension (elevated PA pressures) often develops related to increased LA pressure and possibly from narrowing in small pulmonary arteries. These increase resistance to flow through the lungs. Primary lung disease also can be a factor in increasing lung resistance. The development of pulmonary hypertension places a load on the right ventricle and predisposes to more TR. Signs of right sided CHF can ensue, including exercise intolerance, ascites, and syncope. Some dogs progress from a syndrome of left heart failure to one of right heart failure.

Other complications of MR include bronchial compression, cardiac arrhythmias, ruptured chordae tendineae, and rupture of the LA. Left atrial dilation compresses the left mainstem bronchus between the aorta and the enlarging atrium. Bronchial irritation and exertional coughing and wheezing may occur even in the absence of lung edema. Atrial arrhythmias such as premature atrial complexes are triggered in the enlarged atria. Ventricular premature complexes may develop in the dilated LV, though sustained ventricular tachycardia is less common in mitral disease than in dogs with dilated cardiomyopathy. Ruptured chordae tendineae are commonly observed during echocardiographic examination of dogs with advanced MR. Depending on the location of the chordal rupture, the added hemodynamic burden may be tolerated, or severe CHF may supervene. Left atrial rupture, while uncommon, can occur across linear tears in the endocardium; hemorrhage into the pericardial space causes cardiac tamponade, hypotension, and possibly death.

Clinical Findings

Endocardiosis is most common in toy and small breeds (Poodle, Dachshund, Yorkshire Terrier, Cavalier King Charles Spaniel, Schnauzer, Cocker Spaniel) and the condition is an incidental finding in many aged dogs. Some breeds (such as the CKCS) are affected relatively early in life. Larger dogs often develop endocardiosis, and will on occasion, develop CHF consequent to valvular insufficiency; however, the lesions are usually less severe and dilated cardiomyopathy is a more important cause of CHF in these breeds. Some canine breeds, particularly the spaniels, German Shepherd, and Afghan Hound, are prone to both valvular degeneration and cardiomyopathy. The client’s complaints are attributable to cardiac disease or left-sided heart failure and include tiring, progressive cough or tachypnea, and syncope. Syncope is a particularly bothersome problem and may be related to insufficient forward flow, pulmonary hypertension, arrhythmias, or neurocardiogenic syncope (inappropriate bradycardia and vasodilation triggered by sympathetic surges or coughing).

The physical examination findings vary. The heart rate is typically, but not always, regular and increased when CHF is evident. Pronounced sinus arrhythmia is more common in compensated valvular disease. An early auscultatory finding in some dogs is the midsystolic click, suggesting valve prolapse. MR is heralded by a systolic murmur loudest over the mitral area and left apex. Brief and soft systolic murmurs usually indicate early disease unless associated with peracute CHF, hypotension, or concurrent dilated cardiomyopathy. The murmur usually changes from a soft, decrescendo murmur to a loud, holosystolic murmur over a period of months to years. A precordial thrill may be palpable over the left apex (MR) or tricuspid valve area (indicating TR). The typical MR murmur radiates in the direction of the regurgitant jet (dorsally and craniad or caudad) and projects straight across to the right hemithorax once the murmur reaches an intensity of grade 3 or 4. This may be confusing as a concurrent murmur of TR may be detected over the right side of the thorax, especially in dogs with progressive pulmonary hypertension. The first heart sound may be loud, indicating preserved LV systolic function; the second sound may be tympanic, suggesting pulmonary hypertension. An apical ventricular gallop (third heart sound), indicating elevated LV diastolic pressure, is heard in some dogs with untreated CHF, but often resolves following successful therapy. Cardiac arrhythmias, especially atrial premature beats, may be detected by auscultation. As the heart enlarges, the point of the left apical impulse shifts caudoventrally indicating left ventricular enlargement. The arterial pulse is variable depending on forward stroke volume, cardiac rhythm, and degree of systemic arterial vasodilation, and will be impacted by medical therapy. Arterial blood pressure is usually normal but can be low in severe CHF. Some dogs have systemic hypertension related to intercurrent renal or Cushing’s disease. This is problematic as elevated systolic pressure increases the MR fraction. If pulmonary congestion develops from CHF, ventilation and bronchial sounds become abnormal, and inspiratory crackles and cyanosis often develop. Wheezes may represent “cardiac asthma” from bronchial cuffing or left mainstem bronchial compression. Pleural effusion as an isolated finding is rare in patients with normal sinus rhythm, but is not uncommon in dogs with atrial fibrillation (AF). If the right heart fails, jugular pulses become prominent, jugular venous pressure increases, and the liver enlarges. Ascites indicates advanced right-sided CHF.

Laboratory tests can confirm the diagnosis and allow the clinician to categorize the patient. Radiography demonstrates progressive cardiomegaly with left-sided enlargement predominating. As the disease progresses, generalized cardiomegaly, left mainstem bronchial compression, and pulmonary venous distension are observed. Left-sided CHF increases lung density (interstitial and alveolar infiltrates) in the perihilar lung zones. These infiltrates are characteristically dorsal and bilaterally symmetric; however, edema may be worse in the right caudal lobe. Pleural effusion and ascites are findings of advanced heart disease and biventricular failure. Echocardiographic findings include cardiomegaly, thickened AV valves, and increased global LV shortening fraction. Overall, left ventricular contractility appears normal to increased because cardiac muscle failure is a less prominent feature of this disease and the LV ejects a portion of the stroke volume backwards, into the low resistance LA. The shortening fraction helps to distinguish this condition from dilated cardiomyopathy because only the atypical case of primary valvular disease have reduced shortening fraction (usually in large breed dogs). Valvular prolapse caused by elongated or ruptured chorda tendineae is observed frequently. Doppler studies demonstrate MR and TR, and often, silent aortic regurgitation. High velocity TR (> 3 m/sec) indicates pulmonary hypertension. The electrocardiogram may reveal cardiomegaly; however, the ECG is normal in some dogs and this finding does not exclude a diagnosis of CHF due to endocardiosis. Atrial enlargement can cause widening (P-mitrale) or increased amplitude (P-pulmonale) of the P-waves. Left ventricular hypertrophy is suggested by increased voltages in the caudal limb leads (II, III, aVF), widening of the QRS complex, or ST segment slurring or coving. Heart rate and rhythm are usually normal until significant cardiomegaly develops. Arrhythmias are common as the disease advances. Sinus tachycardia, atrial premature beats, paroxysmal or sustained atrial or supraventricular tachycardia, AF, and ventricular premature complexes are encountered in individual cases. The clinical laboratory tests in endocardiosis are often reflections of hemodynamic changes or concurrent organ diseases. Extracardiac disorders such as Cushing's disease, renal failure, and the effects of drug therapy (e.g., diuretics, angiotensin converting enzyme inhibitors (ACEI) can modify serum biochemistries. Significant pulmonary edema can lead to arterial hypoxemia (decreased PaO2), hypocarbia, and respiratory alkalosis. Tissue hypoperfusion causes metabolic acidosis. About 25% of dogs with CHF from endocardiosis have mild to moderate increases in BUN, serum creatinine, or phosphorus. Diuretics, hypotensive drug therapy, and ACEI increases the magnitude of azotemia in some dogs. Reduced hepatic perfusion and hepatic congestion may increase serum ALT and AST; however, these elevations tend to be mild to moderate, and persistently elevated liver enzymes, especially when > 400 iu/L usually indicate a primary disorder of the liver. Hypochloremia, metabolic alkalosis, and hypokalemia are most often iatrogenic, caused by diuretic therapy. Mild to moderate decreases in serum chloride are ignored. Hyponatremia is a poor prognostic sign and indicates free-water retention from severe biventricular heart failure. This is most often observed in dogs with marked ascites receiving high-dose diuretic or combination diuretic therapy. The CBC is unremarkable in most cases.

The differential diagnosis of chronic valvular heart disease in dogs includes dilated cardiomyopathy, congenital AV valve malformations, and bacterial endocarditis (a relatively rare condition in small dogs). The typical age, breed predisposition, and clinical presentation make the diagnosis of valvular endocardiosis straightforward in most cases. The echocardiogram can distinguish endocardiosis from congenital valve malformation or dilated cardiomyopathy; however, this is not an essential study in classic presentations. Active bacterial endocarditis should cause multisystemic problems (fever, polyarthritis, metastatic infection, proteinuria, elevated WBC). Primary respiratory diseases are confusing and can cause identical pulmonary signs (cough, shortness of breath, tachypnea, wheezes, lung crackles). Common rule outs are tracheal collapse (especially in toy breeds), primary bronchial collapse, chronic bronchitis, pulmonary alveolitis-fibrosis, heartworm disease, pneumonia, and pulmonary neoplasia. The clinician should remember that pulmonary crackles (rales) indicate small airway dysfunction, not necessarily “wet lungs.”


Currently, treatment of the asymptomatic dog with a murmur caused by endocardiosis is not recommended unless there is evidence of impending heart failure such as gross cardiomegaly and pulmonary venous distension. Scandinavian studies in the CKCS dog have failed to reveal any benefit in asymptomatic dogs; results from a North American study are pending. When left sided CHF occurs and pulmonary edema is evident, hospital therapy of CHF should be initiated. Initial treatment includes FON: Furosemide for diuresis (2-4 mg/kg, IV, IM or SQ q6-8h), oxygen if needed to raise the pO2, and nitroglycerine ointment (¼ to ½ inch q12h in small dogs) to dilate veins. If pulmonary edema is severe, and if systolic ABP is at least 90 mm Hg, an arterial vasodilator should be given to reduce the MR fraction. Either hydralazine (1–2 mg/kg PO q8-12h) or sodium nitroprusside (0.5 to 5 mg/kg/minute) can be administered to rapidly unload the LV and reduce MR fraction. An ACEI also lowers blood pressure, but in emergent conditions, the onset of action is slower than with direct vasodilators. Following successful diuresis, therapy is switched to oral medications.

Baseline home therapy of CHF from endocardiosis involves FADD: Furosemide, an ACEI, Dietary modifications, and Digoxin. Furosemide (2-4 mg/kg PO q8–24h) is administered to effect to prevent sodium retention, edema and ascites. An ACE inhibitor (enalapril, benazepril, ramapril, or quinapril) is begun initially at 0.5 mg/kg PO q24h with the intent to increase the dose to q12h as CHF worsens. A reasonable reduction of dietary sodium should be recommended. Digoxin is prescribed in moderate to advanced CHF or when there are frequent atrial arrhythmias or AF. The initial dose of digoxin is 0.005 mg/kg PO q12h. Contraindications to digoxin are moderate azotemia and complex ventricular ectopy. A serum digoxin is checked in seven days. If progressive left sided or intercurrent right-sided CHF develops, spironolactone is added (6.25 to 12.5 mg once daily). Additional treatments for advancing CHF include hydrochlorothiazide (starting at 1–2 mg/kg on Monday/Wednesday/Friday; beware: azotemia and hyponatremia), or a second vasodilator such as amlodipine (0.05–0.1 mg/kg PO q24h; beware of hypotension) to further reduce the MR fraction. Airway dilators (theophylline) and cough suppressants (hydrocodone, butorphanol) may be added for symptomatic relief if control of CHF does not alleviate the respiratory signs. The long-term prognosis following successful therapy varies, but most dogs live at least six to 12 months with good home therapy. Follow-up examinations should concentrate on quality of life issues (attitude, appetite), activity and exercise capacity, heart rhythm, respiratory signs, fluid retention, blood pressure, renal function, and serum biochemistries.

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