Valvular Heart Disease: Little Dogs, Bigger and Bigger Hearts
World Small Animal Veterinary Association World Congress Proceedings, 2013
Matthew W. Miller, DVM, MS, DACVIM(Cardiology)
College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA

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 mid-systolic 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.

Clinical Diagnostic Tests

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 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 increase 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. NT-proBNP levels may prove to be very helpful adjunctive test for determining if patients have CHF or a respiratory etiology for clinical signs of respiratory compromise.

In dogs with suspected chronic valvular heart disease the primary differentials include dilated cardiomyopathy, congenital AV valve malformations, and bacterial endocarditis (uncommon in small dogs). The typical age, breed predisposition, and clinical presentation usually make the diagnosis of valvular endocardiosis straightforward. The echocardiogram can distinguish endocardiosis from congenital valve malformation or dilated cardiomyopathy but is not an essential study in typical cases. Active bacterial endocarditis should cause multisystemic problems (fever, polyarthritis, metastatic infection, proteinuria, elevated WBC). Primary respiratory diseases especially chronic bronchitis, heartworm disease and tracheal collapse can produce similar signs (cough, shortness of breath, tachypnea, wheezes, lung crackles).


Treatment of the asymptomatic dog with a murmur caused by endocardiosis is not currently recommended unless there is evidence of impending heart failure (dramatic 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 suggest a possible benefit but were by no means conclusive. When left sided CHF occurs and pulmonary edema is evident, therapy should be initiated. Initial treatment includes 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. 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 chronic therapy of CHF from endocardiosis involves: furosemide, an ACEI, dietary modifications, and pimobendan. Furosemide (2-4 mg/kg PO q8–24h) is administered to effect to prevent sodium retention, edema and ascites. An ACE inhibitor (enalapril, benazepril, ramipril, 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. Pimobendan in our clinic is prescribed in any patient that is furosemide dependent (has radiographic evidence of pulmonary edema), as well as moderate to advanced CHF. The initial dose of pimobendan is 0.25-0.3 mg/kg PO q12h. Common additions for refractory heart failure include hydrochlorothiazide (starting at 1–2 mg/kg q12-24 hours), and or a second vasodilator such as amlodipine (0.25–0.75 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.


Speaker Information
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Matthew W. Miller, DVM, MS, DACVIM (Cardiology)
College of Veterinary Medicine and Biomedical Sciences
Texas A&M University
College Station, TX, USA

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