Matthew W. Miller, DVM, MS, DACVIM (Cardiology)
College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA
Endocardiosis is most common in toy and small breeds (Poodle, Dachshund, Yorkshire terrier, Cavalier King Charles Spaniel (the CKCS), 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 congestive heart failure (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).
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 angiotensin converting enzyme inhibitor (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 ACEI (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.
Therapy of Feline Cardiovascular Diseases
Treatment of asymptomatic HCM is controversial, yet this is the most common form of idiopathic cardiomyopathy. No data indicate a substantial benefit of any therapy - beta-blockers, diltiazem, ACE inhibitors, or aspirin - in asymptomatic cats with mild HCM and normal LA size. Beta-blockers (e.g., atenolol 6.25 mg to 12.5 mg PO, twice daily) are superior to diltiazem for slowing heart rate, reducing SAM, and decreasing intensity of murmurs in cats with HCM and moderate to severe LV outflow tract obstruction. Atenolol dose can be regulated based on a post-treatment heart rate target of 140 to 160/minute. Many cats take "split doses" of 12.5 mg in the AM and 6.25 mg in the PM. Other potential benefits of beta-blockers in cats with HCM have not been proven. Beta-blockers are contraindicated in hypotension, bradycardia, thromboembolism, and CHF of recent onset.
When HCM is characterized by moderate to severe LV hypertrophy without obstruction, and especially when there is also LA dilatation, either diltiazem, atenolol, or an ACE inhibitor could represent logical therapeutic considerations. Benazepril or enalapril (0.25 to 0.5 mg/kg PO daily) are prescribed in the author's practice when there is clearly demonstrable LA dilation (typically LA diameter > 18 mm by 2D echo). Effects of various ACE inhibitors on progression of ventricular hypertrophy or myocardial fibrosis in this disease await further study. Atenolol reduces demand ischemia, increases ventricular filling time, and is well tolerated. Some clinicians prefer diltiazem in cats with unobstructed HCM, as this drug is thought to improve LV relaxation. However, as with beta-blockers, diltiazem is not indicated in CHF of recent onset. There is also a higher adverse effect profile for diltiazem (anorexia, weight loss, skin lesions), and dosing is more difficult (usual dose: 30 to 60 mg daily of a long-acting release preparation such as compounded Cardizem-CD® or Dilacor). Combining atenolol and diltiazem can cause bradycardia and hypotension and is not recommended.
Treatment of acute heart failure in cats is challenging. Thoracocentesis is performed for moderate or large pleural effusions. The cat with cardiogenic shock (hypothermia, bradycardia, systolic ABP < 80 mm Hg) is treated with IV dobutamine infusion for 24 to 48 hours (regardless of cause). Most cats can be managed medically with a F-O-N-S regimen. Furosemide is administered (2–4 mg/kg IV or IM; repeated q48h or as a constant IV infusion) and once diuresis occurs, the dose is reduced. Oxygen (40–50%) is delivered by cage oxygenator. Sedation is given if necessary (butorphanol at 0.25 mg/kg mixed with acepromazine at 0.05 mg/kg subcutaneously; avoid acepromazine in hypothermia.). Nitroglycerin (2%) ointment is administered at ¼ inch, q12h for 24 to 48 hours.
Home therapy of chronic CHF in cats with cardiomyopathy centers on furosemide (1 to 2 mg/kg, PO once or twice daily), combined with an ACE inhibitor, such as enalapril or benazepril (0.25 to 0.5 mg/kg, PO once or twice daily). Spironolactone (6.25 mg, once daily) also can be given for empiric cardioprotection and potassium-sparing effects. Neither atenolol nor diltiazem should be administered to cats with recent onset CHF (such therapy was not beneficial in an unpublished multi-center study). After one month of stable medical therapy for CHF, cats with severe LVOT obstruction may tolerate cautious up-titration of atenolol to reduce obstruction. Alternatively, diltiazem may be added if deemed useful. Rutin (250 mg BID), is prescribed when there is chylothorax. The inodilator pimobendan may provide an additional treatment approach for some cats with chronic CHF, but digoxin is rarely used today. The overall efficacy of heart failure therapy can be gauged by monitoring respiratory rate and depth at home and by regular reexaminations. Consideration of the affected cat's activity level, appetite, and interaction with family members offers a reasonable gauge of quality of life. Objective measures of CHF control can be obtained by a careful physical and cardiovascular examination and from inspection of serial thoracic radiographs. Morphologic or functional progression of heart disease can be assessed by echocardiography if desired. Clinical re-evaluation should include a client interview; physical examination; ABP measurement; serum biochemical profile; thoracic radiographs (even one lateral view can provide objective evidence regarding fluid retention); and a focused, recheck echocardiogram. The timing of specific examinations depends on clinical circumstances and economic considerations, but initially should occur within the first 7 to 10 days from initial diagnosis of CHF, and continue every one to two weeks until the CHF is controlled and renal function stable. Thereafter, the interval may be extended to every one to three months, depending on the patient's progress. In general, progressive azotemia indicates the effects of diuretics plus an ACEI. If possible, the doses should be reduced. In some cats, the heart may stabilize and allow drug diuretic therapy to cease. In other cases, there is a clear need to simply tolerate azotemia to prevent pleural effusion or pulmonary edema.