Congestive Heart Failure

Clinical heart failure in dogs and cats occurs when the heart is either unable to adequately deliver blood for the body’s metabolic demands or when it can do so only with elevated filling pressures. Dog heart failure is not a specific diagnosis, but a syndrome caused by one or more underlying processes. Poor myocardial contractility (systolic disfunction), as a primary cause, can initiate the cascade of neurohormonal and other responses that result in clinical failure. However, other causes of chronic cardiac stress or injury can underlie the development of circulatory congestion and secondarily lead to myocardial systolic (and/or diastolic) dysfunction.

Chronic heart failure in dogs and cats cannot be framed simply and only in terms of a ”bad pump” that needs positive inotropic stimulation and a diuretic, although this therapeutic approach may be transiently necessary in some cases of acute, decompensated myocardial failure. The pathophysiology of the failing heart is much more complex and involves a number of structural and functional changes within cardiac and vascular cells, as well as within the extracellular matrix. The syndrome of heart failure can be viewed in terms of progressive ventricular remodeling that develops secondary to a cardiac injury or stress such as valvular disease, genetic mutations, acute inflammation, ischemia, incresed systolic pressure load, and other uses.

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The causes of heart failure in dogs and cats are quite diverse, and it is useful to think of them in terms of general pathophysiologic groups. These groups are myocardial failure, pressure overload, volume overload, and reduced ventricular compliance (impaired filling). The major underlying abnormality for most cases of heart failure falls into one of these pathophysiologic groups, although other pathophysiologic abnormalities often are also present. In advanced failure, abnormalities of both systolic and diastolic function are common.

Myocardial failure is characterized by poor ventricular contractile function; valvular insufficiency may or may not be present. Diseases that cause a volume or flow overload to the heart usually involve a primary ”plumbing” problem (e.g. a leaky valve or abnormal systemic-to-pulmonary connection). Cardiac pump function is often maintained near normal for a prolonged time, but myocardial contractility does eventually deteriorate. Pressure overload results when the ventricle must generate higher than normal systolic pressure to eject blood. Concentric hypertrophy increases ventricular wall thickness and stiffness and predisposes to ischemia. Excessive pressure loads eventually cause myocardial contractility to decline.

Diseases that restrict ventricular filling cause abnormal diastolic function. Contractile ability is usually normal initially, but inadequate filling causes congestion behind one or both ventricles and may diminish cardiac output. Therapy for these cases centers on enhancing ventricular filling.

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New York Heart Association Functional Classification
I: Heart disease present but no eveidence of heart failure or exercise intolerance; cardiomegaly minimal to absent
II: Signs of heart disease with evidence of exercise intolerance; radiographic cardiomegaly present
III: Signs of heart failure with normal activity or at night (e.g. cough, orthopnea); radiographic signs of significant cardiomegaly and pulmonary edema or pleural/abdominal effusion
IV: Severe heart failure with clinical signs at rest or with minimal activity; marked radiographic signs of congestive heart failure (CHF) and cardiomegaly

Forrester’s Classification (Group)
I: Normal cardiac output and pulmonary venous pressures
II: Pulmonary congestion but normal cardiac output
III: Low cardiac output and peripheral hypoperfusion with no pulmonary congestion
IV: Low cardiac output with pulmonary congestion

Most current treatment strategies for heart failure are aimed at modifying either the results of neurohormonal activation (e.g. sodium and water retention) or the activation process itself (e.g. angiotensin-converting enzyme inhibition). In most cases, therapy centers on controlling edema and effusions, improving cardiac output, reducing cardiac workload, supporting myocardial function, and managing concurrent arrhytmias. The approach of these goals varies somewhat with different diseases, most notably those causing restrictions to ventricular filling.

The clinical severity of heart failure is sometimes described according to a modified New York Heart Association classification scheme. This system groups patients into four functional classes based on subjective evaluation of the clinical condition, without consideration of etiology or myocardial function. This classification can be helpful conceptually and for categorizing study patients. However, to best individualize therapy, it is important to determine the etiology as well as the severity of heart failure. Forrester’s classification is another method of grouping heart failure patients. Dogs with chronic mitral regurgitation often fall into group II; severe dilated cardiomyopathy is the most common diagnosis in group IV. Diseases that cause group III characteristics are rare in dogs and cats. Regardless of the clinical classification scheme, identification of the underlying disease and pathophysiology is important for guiding therapy.

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It is typical to see dilatation of all cardiac chambers in dogs with dilated cardiomyopathy (DCM), although left atrial and ventricular enlargement may predominate. The ventricular wall thickness appears decreased compared with the lumen size. Papillary muscles often look flattened and atrophic; endocardial thickening may be noted. The atrioventricular (AV) valves generally have only mild to moderate, if any, degenerative changes. Histopathologic findings include scattered areas of myocardial necrosis, degeneration and fibrosis, especially in the left ventricle.

The presence of narrowed (attenuated) myocardial cells with a wavy appearance is reported to be a common finding. Such abnormal cells have also been noted in some Newfoundlands thought to be predisposed to DCM but without any clinical or echocardiographic evidence of the disease. Inflammatory cell infiltrates and myocardial hypertrophy are inconsistent features.

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Idiopathic DCM is most common in large and giant breeds of dogs, including Great Danes, Doberman Pinschers, Saint Bernards, Scottish Deerhounds, Irish Wolfhounds, Boxers, Newfoundlands, Afghan Hounds, and Dalmatians. Among smaller breeds, English and American Cocker Spaniels, English Bulldogs, and others are affected, but the disease is rare in dogs weighing less than 25 lbs.

The prevalence of DCM increases with age, although most dogs presenting with heart failure are 4 to 10 years old. Most reports indicate that more male than female dogs are affected. Others suggest no gender predilection in Boxers and Doberman Pinschers once dogs with occult disease are included in the analysis. The nature of the cardiomyopathy in Boxers and Dobermans appears to be somewhat different from that in other large and giant breeds.

Clinical signs mat develop rapidly, especially in sedentary dogs in which ordinarily early signs may not be noticed until the disease is advanced. Presenting complaints include any or all of the following: weakness, lethargy, tachypnea or dyspnea, exercise intolerance, cough (sometimes described as ”gagging”, anorexia, abdominal distention (ascites), and syncope.

Loss of muscle mass (cardiac cachexia), accentuated along the dorsal midline, may be severe. Conversely, subclinical DCM is now being recognized more frequently, especially through the use of echocardiography. Some giant-breed dogs with mild-to-moderate left ventricular dysfunction are relatively asymptomatic, even in the presence of atrial fibrillation.

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Radiography in dogs and cats

Generalized cardiomegaly is usually evident, although left-heart enlargement may predominate. Cardiomegaly may be severe enough to mimic the globoid cardiac silhouette typical of large pericardial effusions. In contrast, Doberman Pinschers and some Boxers appear to have mainly left atrial enlargement without marked cardiomegaly. The stage of disease, chest conformation, and hydration status influence these radiographic findings. Distended pulmonary veins and pulmonary interstitial or alveolar opacities, especially in the hilar and dorsocaudal regions, indicate the presence of left heart failure and pulmonary edema. Some dogs have asymmetric or widespread distribution of pulmonary edema infiltrates. Pleural effusial, distention of the caudal vena cava, hepatomegaly, and ascites usually accompany right-sided heart failure.

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Echocardiography in dogs and cats is the best means of assessing cardiac chamber dimensions and myocardial function and for differentiating pericardial effusion or chronic valvular insufficiency from DCM. Dilated cardiac chambers and poor systolic ventricular wall and septal motion are characteristic findings in DCM. All chambers are usually affected, but right atrial and ventricular dimensions may appear normal, especially in Dobermans and Boxers. Left ventricular systolic dimension is increased, and fractional shortening is decreased.

Other common features are a wide mitral valve E point-septal separation and reduced aortic root motion. Left ventricular free-wall and septal thickness are normal to decreased. Mild to moderate AV valve regurgitation may be seen with Doppler echocardiography. Dobutamine stress testing may provide insight as to the presence of early myocardial dysfunction in dogs thought to be at risk for DCM, but further research is needed to define the clinical applicability and optimal dosage for this more clearly.

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