Case Studies In Small Animal
Text from "Small Animal Cardiovascular Medicine"
Dogs with mild to moderate myocardial failure usually show no clinical signs. Syncope is occasionally observed, more commonly in boxers and Doberman pinschers. Most of the dogs and cats diagnosed with DCM have severe myocardial failure and are in heart failure at the time of presentation. Most of these dogs have had a short history of problems. Many are presented for acute clinical signs, prompting the owner to suspect trauma or toxins as the cause. Respiratory signs secondary to pulmonary edema predominate and include tachypnea, dyspnea, and a soft cough. Dogs with fulminate pulmonary edema are severely dyspneic, have respiratory rates that usually exceed 70 breaths/minute, and may cough up pink-tinged pulmonary edema fluid from their airways. Some dogs may also exhibit signs of right heart failure (i.e., ascites). A few dogs will have pleural effusion, most likely due to a combination of left and right heart failure. Weight loss may also be present and can be profound. Other dogs present with no evidence of weight loss. Some dogs also present with evidence of poor perfusion including cold extremities, cold ears, and weakness. When the hypoperfusion is profound, total body hypothermia (rectal temperature < 100 EC) may also be present. Dogs with DCM that become dehydrated more commonly have clinical signs referable to poor perfusion.
Some dogs with DCM present with a history of syncopal episodes or episodes of weakness. These signs are more common in Doberman pinschers and boxers where ventricular arrhythmias are common. These episodes are most commonly due to short periods of severe ventricular tachyarrhythmias and are probably aborted instances of sudden death. Approximately 20% of Doberman pinschers will die suddenly from their disease. Syncope is a clinical sign in about 35% of boxers with myocardial disease. Whereas Doberman pinschers that present because of syncope usually have evidence of myocardial failure, many boxers have apparently normal ventricular function on echocardiography and normal thoracic radiographs. Boxers with ventricular arrhythmias are at risk for sudden death whether or not myocardial function is depressed.
Dogs with early DCM that are not in heart failure are usually normal on physical examination. An arrhythmia, most commonly ventricular premature depolarizations, may be identified. Dogs that present with severe DCM that are in heart failure have many abnormal findings on physical examination. The most obvious signs are those of left and, sometimes, right congestive heart failure. Pulmonary edema produces tachypnea and dyspnea. A soft cough may be present in the examination room or may be elicited by tracheal palpation. If the rear quarters are elevated, blood-tinged fluid may run out of the mouth or nose in dogs with fulminate pulmonary edema. Auscultation of the lungs most commonly reveals increased bronchovesicular sounds due to the hyperpnea (increased air moving through the airways). Some dogs have soft crackles and some will have more coarse crackles. These are more commonly ausculted in dogs with severe edema. In dogs with right heart failure, ascites is usually present. Hepatomegaly and sometimes splenomegaly may be palpated. Jugular vein distension may be present.
Auscultation of the heart often reveals a soft systolic heart murmur, a gallop sound, or an arrhythmia. The murmur is most commonly due to mild mitral regurgitation and is usually grade 3 or softer. The gallop sound is usually a third heart sound. This sound is heard best in dogs that are in sinus rhythm and is impossible to distinguish from the other heart sounds in dogs in atrial fibrillation. The gallop sound is often subtle and to hear it one must listen carefully and know what one is listening for. In some dogs the sound is very loud and on occasion can be felt by placing one's fingers over the left apex beat.
Arrhythmias are common in dogs with DCM. Atrial fibrillation is very common in dogs with symptomatic DCM and especially common in giant breeds with DCM. The heart rate is rapid in these dogs when they are in heart failure. This is due to high circulating catecholamine concentrations enhancing the conduction patterns of the AV node. The heart rate commonly exceeds 200 beats/minute. The fast rate, the variability of the rate, and the admixture of heart sounds often make it impossible to count the heart rate on auscultation. Ventricular arrhythmias are common in Doberman pinschers and boxers with DCM. These range from isolated premature beats to salvos of rapid ventricular tachycardia to sustained ventricular tachycardia. Occasionally ventricular arrhythmias will be mistaken for atrial fibrillation on auscultation. Femoral pulse quality can range from normal to severely decreased. Pulse deficits and alternating pulse strength are common in dogs with atrial fibrillation and ventricular arrhythmia.
The electrocardiogram is used primarily to identify the type of arrhythmia present in a patient with DCM. Although QRS and P wave abnormalities are commonly present, they are nonspecific and rarely contribute to the diagnosis. Abnormalities include increased R wave height in leads II and aVF, prolonged QRS complexes and P waves, QRS complex notching and slurring, and ST segment and T wave abnormalities.
Atrial fibrillation is present in 75-80% of giant breed dogs at the time of presentation. In Doberman pinschers and boxer dogs, ventricular tachyarrhythmias are common although atrial fibrillation is also often present. An exam room ECG usually only encompasses about 30 seconds of information and may not typify the ventricular arrhythmias that occur during the rest of the day. In one report of three boxer dogs, ventricular ectopy constituted more than 20% of the depolarizations during the morning hours and only 2% at night. This can be reversed, however, such that most of the premature depolarizations occur while the dog is sleeping. The office ECG may show single, unifocal ventricular premature depolarizations on one end of the extreme or can show sustained, fast ventricular tachycardia at the other end. We have observed dogs that had severe ventricular arrhythmias in an examination room have less than 100 single premature beats during a 24-hour recording. We have also seen dogs with a single premature ventricular complex during an ECG recording that had thousands of premature ventricular complexes on a 24-hour recording.
The ventricular premature complexes in boxers are often upright in leads II, III, and aVF and so most likely originate from the right ventricle. Cats often only have sinus tachycardia although atrial fibrillation, premature depolarizations, isorhythmic AV dissociation, and sinus bradycardia may also occur.
In Doberman pinschers with DCM, ventricular arrhythmias are a consistent finding on 24-hour ECG (Holter) recordings. Doberman pinschers with echocardiographic evidence of the disease almost always have more than 50 premature ventricular depolarizations on a Holter recording. The number of premature depolarizations and the complexity of the premature depolarizations increases as the disease progresses. Doberman pinschers with ventricular tachyarrhythmias are at increased risk of sudden death.
Dogs with severe myocardial failure due to DCM consistently have cardiomegaly on thoracic radiographs. Dogs with lesser stages of the disease may or may not have cardiomegaly. Cardiomegaly ranges from mild to severe and depends on the severity of the disease and, to some degree, on the breed involved. Giant breed dogs and American cocker spaniels usually have severe cardiomegaly present. Doberman pinschers may only have apparent mild to moderate cardiomegaly although on echocardiography their cardiac enlargement is often severe. The severe cardiomegaly may not be readily detected on thoracic radiographs in this breed, presumably because of their chest configuration and possibly because they do not have as much right heart enlargement as giant breeds. The same may be true for boxers.
Evidence of heart failure is commonly present on thoracic radiographs. Dogs in left heart failure have pulmonary edema that can range from mild to severe. Enlarged pulmonary veins (pulmonary congestion) may also be evident. Dogs with both left and right heart failure may have pleural effusion.
The echocardiographic changes with DCM are the same in dogs and cats. The primary abnormality is an increase in the left ventricular end-systolic diameter. This increase can range from mild to severe depending on the severity of the disease. A compensatory increase in the left ventricular end-diastolic diameter is usually also present when the disease is moderate to severe. It often is not present in a patient with mild myocardial failure (mild increase in the end-systolic diameter) and may, on occasion, not be present in a patient with severe myocardial failure. The increase in the end-systolic diameter decreases the shortening fraction. The compensatory increase in the end-diastolic diameter increases the shortening fraction. Consequently, even in DCM shortening fraction is not a very accurate estimate of myocardial function. However, in most patients with DCM the shortening fraction is decreased although in patients with mild disease the decrease may be subtle. For classification purposes, using shortening fraction is easier than using end-systolic diameter as a measure of left ventricular function because it does not change between different size dogs. Consequently, a shortening fractions between 20 and 25% is considered evidence of mild disease, between 15 and 20% is moderate disease, and <15% is considered severe disease.
Controversy exists as to the lower limit of normal for shortening fraction, especially in large breed dogs. Studies have been performed to determine normal values for shortening fraction and other echocardiographic variables in specific large breeds. Because DCM is prevalent in these populations, these studies probably have not established values for normal. Instead they have established values for a mixture of normal dogs and dogs with DCM. Consequently, shortening fractions as low as 13% have been reported as normal. This is almost assuredly incorrect. It is known that sarcomeres normally contract about 30% (end-diastolic length of 2.2 Fm to an end-systolic length of 1.5 Fm). With normal coupling of sarcomeres together, this should translate into a 30% change in circumference of the left ventricle from end-diastole to end-systole and so also a 30% change in chamber diameter. The aforementioned studies have based their assessment of normal on the fact that the investigators have seen no progression of disease within a 2-3 year period. Unfortunately, this measure of normalcy is probably incorrect, i.e. dogs with DCM can most likely stabilize for long periods. We have observed cats with taurine deficiency stabilize for several years which sets a precedence for this type of behavior. Studies that have correlated other characteristics of DCM in certain breeds, such as ventricular arrhythmias, with shortening fraction are probably more accurate in predicting which dogs are normal and which have DCM. In these studies, dogs with shortening fractions <25% have been identified as being abnormal.
Dogs with heart failure secondary to DCM always have severe disease and so have a shortening fraction <15%. If a patient that is in heart failure is shown to have a shortening fraction >15%, the diagnosis of DCM should be reconsidered. It may be possible that DCM can be present along with another disease, such as primary mitral regurgitation, such that the patient does have DCM and is in heart failure and has a shortening fraction >15%. However, in the authors experience this is very unusual. Secondary myocardial failure (i.e., an increase in end-systolic diameter) is common for a large dog with primary mitral regurgitation. These dogs usually have a shortening fraction in the 20-40% range when they present for heart failure. The increase in the end-systolic diameter in these cases is secondary to myocardial failure caused by the mitral regurgitation and so is not DCM (primary idiopathic myocardial failure).
The left ventricular wall (free wall and interventricular septum) thickness is normal or thinner than normal. Wall thinning usually does not occur until the end-stages of the disease. It probably represents slippage of myofilaments that occur secondary to a prolonged and/or marked increase in diastolic intraventricular pressure. Systolic wall thickening (thickening fraction) is decreased. Myocardial function is often reduced similarly throughout the left ventricle, i.e., myocardial contractility is decreased similarly in the free wall and septum. However, there can be regional heterogeneity of myocardial function. Most commonly the free wall moves and thickens less than the interventricular septum although sometimes the septum may be more affected. Occasionally more discrete regions of heterogeneity exist within the free wall and septum. In the latter type of case, obtaining an accurate estimate of left ventricular function is more difficult because the shortening fraction differs depending on the site of measurement.
The left ventricular and left atrial chambers are increased in size on a two-dimensional echocardiogram with severe DCM. Usually this increase in size is comparable to the increase in left ventricular size. This is compared to the patient with primary mitral regurgitation in which the increase in left atrial size is commonly greater than the increase in left ventricular size. The right heart may also be enlarged.
Mitral valve diastolic excursion during rapid ventricular filling is decreased in patients with moderate to severe DCM. This results in an increase in the separation between the mitral valve E point and the interventricular septum (EPSS). The decreased early diastolic excursion of the mitral valve is due to decreased blood flow and flow velocity through the mitral valve orifice. Increased chamber size may also contribute to the increase in EPSS. In severe DCM, forward stroke volume is commonly decreased. Hemodynamically, whatever is pumped into the aorta in systole is replaced through the mitral valve in diastole. If systolic forward flow is decreased, diastolic mitral flow must also be decreased. Hence, the decrease in mitral valve diastolic excursion. In moderate DCM, forward stroke volume may be normal. Flow velocity however is commonly decreased and mitral inflow velocity during early diastole may also be decreased resulting in a lesser mitral valve excursion.
Aortic motion may be reduced on an M-mode echocardiogram. Effects of arrhythmias on hemodynamics may also be noted.
Treatment of DCM is aimed at reducing the clinical signs due to heart failure, at improving survival time, and at delaying or abolishing sudden death. Success at achieving any of these goals is generally poor in most dogs with DCM. Taurine supplementation (250 mg q12 hours) cures DCM in cats. Taurine +/- L-carnitine supplementation improves ventricular function in most American cocker spaniels to the point that they can be removed from drug therapy and are clinically normal.
Chronic medical therapy for heart failure
Treatment of chronic heart failure is generally attempted using a combination of a diuretic, an ACE inhibitor, and a digitalis glycoside. The primary clinical signs in dogs with DCM are usually referable to pulmonary edema. Consequently, drug therapy aimed at reducing pulmonary edema usually results in the most clinical benefit. All three drug types mentioned have the potential of reducing edema formation. They differ markedly in their ability to achieve this endpoint, however. Diuretics reduce blood volume, ventricular diastolic volumes, and so ventricular diastolic pressures. Diuretics are by far the most efficacious of the three drug classes, with furosemide being very efficacious and the most commonly used diuretic.
ACE inhibitors produce venodilation and reduce renal sodium and water retention by decreasing aldosterone secretion. In so doing, they reduce ventricular diastolic volumes, and so ventricular diastolic pressures. They are also efficacious drugs in this disease and should be used routinely to treat DCM. Their efficacy is less than furosemide, however. The fact that moderate to severe pulmonary edema can usually be controlled with just furosemide and almost never controlled with just an ACE inhibitor is a primary reason for this judgment. Ace inhibitors also produce arteriolar dilation which helps increase cardiac output.
Digoxin increases myocardial contractility, increases cardiac output and renal blood flow, and so reduces renal sodium and water retention in some dogs and cats. Digoxin is efficacious at reducing pulmonary edema in some dogs and not in others. The authors estimate that 20-30% of dogs with DCM have a clinically significant response to digoxin. Digoxin also increases vagal tone which helps decrease heart rate. It may also have a diuretic effect.
In some dogs, clinical signs of low-output heart failure predominate. These dogs may be weak and usually have cold extremities and ears. Often these dogs are clinically dehydrated. The dehydration, coupled with the decreased myocardial contractility, is often the primary cause of the severe decrease in cardiac output in these patients. The dehydration is most commonly due to anorexia, with or without concomitant diuretic administration. If dehydration is severe, cautious intravenous fluid administration is warranted. Complete rehydration will commonly result in edema formation. Diuretic administration must be discontinued in this type of case. Prerenal azotemia is commonly present in these dogs. Consequently, drugs that are cleared by the kidneys, such as digoxin, should also be discontinued or the dose reduced drastically. Inotropic support with a sympathomimetic such as dobutamine may be beneficial.
©Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.