Treating heart failure (Proceedings)


Treating heart failure (Proceedings)

Oct 01, 2008

Chronic heart failure (CHF) traditional therapy (for CHF secondary to chronic degenerative valvular disease etc.) still provides only an average a 4-6 months survival time in dogs. Though current standard treatment regimens provide a good quality of life for many canine patients, complications can lead to early patient loss. Ongoing congestion or syncope can be concerns, sudden death due to arrhythmias, or client-elected euthanasia due to poor quality of life may also lead to loss.

Combination therapy is essential and must be customized to each patient. Different stages of heart failure, and differences in types of failure depending on breed, etiology, and concurrent illness make it necessary to fine tune therapy both on a per-patient basis, and within the patient, to adjust therapy based on response or non-response during the treatment timeline.

Mild to Moderate Heart Failure

Clinical signs of heart failure are evident at rest or with mild exercise and adversely affect the quality of life. Typical signs of heart failure include exercise intolerance, cough, an increased respiratory rate, dyspnea, and mild to moderate ascites. Home treatment is often indicated at this stage. For mitral valvular endocardiosis patients, diuretic therapy, ACE inhibitor therapy, and sodium-restricted diets are indicated. Digitalis therapy would also be indicated, especially if the ECG shows any atrial arrhythmias. For the dilated form of cardiomyopathy, treatment recommendations would include digitalis (especially with atrial fibrillation), pimobendan, diuretic therapy, ACE inhibitors, antiarrhythmic drugs for atrial and/or ventricular arrhythmias, sodium restriction, possible indications for carnitine and/or taurine supplementation (especially for Cocker Spaniels) and, on some occasion, beta-blockers.

Advanced Heart Failure

Clinical signs of advanced congestive heart failure are immediately obvious. These clinical signs could include respiratory distress (dyspnea), marked ascites, profound exercise intolerance, or hypoperfusion at rest. In most cases, hospitalization is mandatory. Treatment for advanced heart failure includes: oxygen therapy, aggressive diuretic therapy, topical nitroglycerin, ACE inhibitors, pimobendan, digitalis (especially if atrial arrhythmias are present) and, in very severe cases, dobutamine or sodium nitroprusside. If ascites is refractive to therapy, combining spironolactone with furosemide can sometimes be effective. The fluid will also have to be periodically tapped. Antiarrhythmic drug therapy is also sometimes indicated to control the heart rate in atrial fibrillation and will often include digoxin, diltiazem, and also a beta-blocker.

It is important in all cardiac failure cases to monitor renal status, electrolytes, hydration, respiratory rate, heart rate and body weight. If azotemia develops, reduce the dosage of the diuretic. If azotemia persists and the animal is also on an ACE inhibitor, reduce or discontinue the ACE inhibitor. Use digoxin with caution if azotemia develops.

To prevent cardiac failure, it is important to restrict exercise and sodium intake in patients with heart disease. Recent studies are now showing that prescribing an ACE inhibitor early in the course of heart disease in patients with dilated cardiomyopathy may slow the progression of heart disease and delay the onset of heart failure. ACE inhibitors should be considered in asymptomatic animals if they have dilated cardiomyopathy. Studies are still pending on the use of ACE inhibitors for preventative care.


Benazepril is an angiotensin converting enzyme inhibitor (ACEI), licensed in Canada in dogs (0.25 mg/kg SID) and in Europe for use in cats greater than 2.5 kg (0.5-1.0- mg/kg SID); indications are for chronic renal insufficiency (CRI), and in dogs for congestive heart failure (CHF). This drug shows great promise as an adjunctive therapy because there is also new evidence to suggest that this drug may play a role in treatment of hypertrophic cardiomyopathy in cats, though this is currently an off-label use.

In cats with CRI, in vivo effects include increased blood flow in the kidneys, with efferent arteriolar vasodilation, variable GFR, reduced protein loss in the urine, significantly increased appetite and weight gain, prolonged survival, mild reduction in blood pressure, reduced risk of hypokalemia, and improved quality of life. The extent of proteinuria in CRI cats has been shown to be a predictor of rate of progression of CRI, and so U-protein levels may potentially serve a screening function, and reducing proteinuria may slow progression of CRI.

The usual benazepril dose for cats for CRI is 0.5-1.0 mg/kg once daily PO and dosage adjustment in mild to moderate renal insufficiency is not necessary since 85% of metabolites are excreted through biliary pathways, and only 15% via the kidneys.