Acquired cardiac diseases of the dog and cat (Proceedings)

Common acquired cardiac diseases of the dog include those that are caused by valvular defects, myocardial failure, infectious reasons, as a result of arrhythmias, and parasitism.

The most common cardiac disease in dogs is valvular insufficiency caused by abnormal aging of the valves of the heart. Approximately 30% of dogs at age 13 are clinically affected. On necropsy, 90% of dogs at 13 have evidence of valvular degeneration. The disease also can be referred to as chronic myxomatous valvular degeneration, mitral valve disease, chronic valve disease, and endocardiosis. Breeds affected include Poodles, Yorkshire Terriers, Chihuahuas, and other small dogs, but the most commonly affected is the Cavalier King Charles Spaniel (CKCS). CKCS are known to be affected severely, often at quite a young age. The mitral valve is most commonly affected with CVD, but lesions can be seen on the other cardiac valves, as well. Valve leaflets are thickened and nodular, and the chordae tendinae can be thickened and elongated. Chordae may also rupture, causing flail or prolapse of the valvular leaflet. The consequence of valvular degeneration is insufficiency. In the case of the mitral valve, chronic significant insufficiency causes an increase in left atrial pressure, and atrial enlargement results. When the left atrium enlarges to a certain point, blood backs up into the pulmonary veins, and pulmonary edema develops. As the disease progresses, myocardial failure may also result.

The most significant physical exam characteristic of valvular degeneration is a heart murmur. Because the most common valve affected is the mitral valve, the most common murmur is systolic and located at the left apex. A right-sided murmur may also be ausculted, and it may be from tricuspid regurgitation or radiation of the mitral murmur. If the aortic valve is affected, a diastolic murmur may be detected. Generally, the intensity of the murmur correlates with severity of disease, but this is not exclusively true. Pulmonary edema results in respiratory distress and/or coughing, and in severe cases, is detected by the presence of crackles in the lung fields. Mild to moderate edema cannot typically be ausculted, so clear lung sounds do not rule out the presence of fluid.

Radiographic changes vary also with severity of the valve disease. With severe disease, the most common signs are left atrial and auricular enlargement and left ventricular enlargement. As the disease progresses to left-sided congestive heart failure, pulmonary edema can be seen. Some dogs will also develop ascites and/or pleural effusion as a consequence of right-sided failure. Valvular insufficiency is seen on color Doppler evaluation of the valve. Other echocardiographic findings include thickened valves, cardiac chamber enlargement, and flail or prolapsing valve leaflets.

There is some debate about the use of ACE inhibitors prior to the development of CHF, but at the author's institution, it is believed that treatment of CVD is effective after signs of congestive heart failure have developed. Treatment consists of stabilizing the patient with diuretics, primarily injectable furosemide. Long-term treatment includes oral furosemide, ACE inhibitors such as enalapril or benazepril, and pimobendan, a positive inotrope and venodilator. Renal values must be monitored serially to follow changes in BUN, creatinine, and electrolytes. Though highly effective at treating CHF and improving quality of life, some cardiologists will reserve pimobendan until there are signs of refractory congestive heart failure, i.e. doses of furosemide greater than 2 mg/kg PO q 8 h, because it has been shown to deteriorate valve function in long-term use. Other diuretics such as spironolactone and hydrochlorothiazide can be used to help manage signs of fluid overload. When arrhythmias such as atrial fibrillation result from CVD, antiarrhythmics are indicated. The most common antiarrhythmic used in this case is digoxin. Digoxin slows the heart rate by slowing the electrical impulse through the atrioventricular node. It also has positive inotropic effects, so it is useful when concurrently treating congestive heart failure. Because the therapeutic range of the digoxin dose overlaps with the toxic dose, it must be prescribed and monitored carefully. Signs of digoxin toxicity range from mild—inappetance and diarrhea—to fatal arrhythmias. Digoxin blood levels must be done 7-14 days after starting it at six to eight hours post-pill until an appropriate range is reached, and then every 3-4 months. Other antiarrhythmics have negative inotropic effects, and should be used with caution when treating a patient in active CHF.

Surgical repair or replacement of the mitral valve, while standard in humans, has been attempted in dogs, but unfortunately, it is not widely available; it is highly cost-prohibitive; requires intensive open heart surgery with cardiac bypass; and results are discouraging.

The end result of valve disease is often euthanasia due to refractory congestive heart failure, but some patients die suddenly as a result of a fatal arrhythmia. Endocarditis has not been associated with CVD. Rarely, the left atrium may perforate, or rupture, as a result of a jet lesion. This allows blood to leak from the atrium into the pericardium. Many of these patients die as a result of both sudden blood loss and compression of the heart by the pericardial effusion. Pericardiocentesis may be attempted, but because the defect in the left atrial wall still exists, it is risky. CPR for a patient with left atrial perforation is contraindicated, as the compressions will force more blood from the heart into the pericardial space, and may actually rupture the pericardium.

Myocardial Failure

Idiopathic dilated cardiomyopathy is a primary disease of the myocardium. Myocardial failure caused by nutritional deficiency, endocrinopathies, toxins, or infectious agents cause secondary cardiomyopathy. Dogs most commonly affected by DCM include large breed adult dogs, especially a large percentage of Doberman Pinschers, Great Danes, Irish Wolfhounds, and Scottish Deerhounds. Cocker Spaniels are also affected, and Portugese Water Dogs experience juvenile DCM. It is estimated that approximately 50% of Dobermans are affected.

Patients with DCM can be separated into two general categories: those with occult, or hidden, disease; and those with overt clinical signs. Dogs with occult DCM typically show no clinical signs. They may have a soft murmur, but generally, they do not exhibit any signs associated with cardiac disease. However, approximately 40% of Dobermans with DCM die suddenly as the first sign that they were affected. It is not known how long the occult phase lasts—it could be months to years.

When clinical signs develop, DCM is then in the overt stage. Clinical signs include signs of congestive heart failure, either pulmonary edema as a result of left sided CHF, or ascites/pleural effusion from right CHF. Physical exam may reveal a soft murmur or gallop as well as arrhythmias. The most common arrhythmias are ventricular premature contractions (VPCs). They may occur as single beats, or as groups—bigeminy, trigeminy, paroxysmal or sustained ventricular tachycardia. Atrial fibrillation is also a common arrhythmia associated with advancement of this disease. Chest radiographs reflect an enlarged cardiac silhouette. The degree of severity of pulmonary edema is often alarming, especially when compared to the patient's respiratory status, but these dogs can quickly deteriorate clinically. On echocardiogram, the left ventricle loses its elliptical shape, and becomes eccentrically hypertrophied, or dilated. As the ventricle enlarges, it pulls the mitral valve apparatus out of shape. The result is functional mitral regurgitation in a centrally directed jet. Fractional shortening, a measurement of systolic function that determines the degree to which the ventricle contracts during systole, can be useful in evaluating systolic function.

Treatment of CHF due to systolic dysfunction is similar to CVD. Injectable furosemide is used to stablize the patient until it can be discharged on oral medications, including furosemide, ACE inhibitors, pimobendan, and digoxin. In an emergency setting, dobutamine can be used in a constant rate infusion to increase cardiac output. It must be used carefully, monitoring heart rate and blood pressure in the ICU.

Since some types of secondary DCM may be reversible, dogs that are not of the usual breeds presenting with systolic dysfunction should be evaluated. Taurine deficiency, hypothyroidism, doxorubicin toxicity, as well as parvovirus, can cause systolic dysfunction. L-carnitine may be supplemented with taurine, but cannot be implicated as a cause of myocardial disease. Similarly, co-enzyme Q10, while a popular cardiac supplement, is not a cause of myocardial disease.

Arrhythmic Diseases

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC), also known as Boxer Cardiomyopathy, is a myocardial disease common in Boxers and occasionally reported in English Bulldogs. It is characterized by fibro-fatty infiltrate of the right ventricular myocardium. This results in ventricular arrhythmias and sometimes dilation of the right ventricle or a DCM-like disease. Clinical presentation can range widely, including incidental finding of arrhythmias on physical examination, syncopal episodes, congestive heart failure, and not uncommonly, sudden death. Washington State University has identified a gene associated with ARVC and developed a genetic test, which may be useful in screening breeding dogs. However, there are likely more genes associated with the disease, as some patients that fit the clinical picture test negative for this gene.

Except for patients that present with arrhythmias or congestive heart failure, physical examination can be completely normal, as can thoracic radiographs and echocardiography. Holter monitoring to detect ventricular arrhythmias is vital to diagnosing these patients.

Treatment of ARVC depends upon the clinical picture. If ventricular tachycardia is present, antiarrhythmics such as Sotalol or Mexiletine can be prescribed. However, sudden death is still possible. Some research into the use of implantable cardiac defibrillators in dogs has been done, but because these devices are designed for humans, they have not been widely used. If CHF is present, standard therapy similar to that of DCM is indicated.

Infectious Endocarditis

Infectious endocarditis (IE) is a condition in which bacteria seeds the valves of the heart. Mitral valve disease is not a known risk factor for IE, but aortic stenosis is. The most common patient affected is a middle-aged, large breed male dog. Dental disease has often been implicated as a cause, but there is actually little evidence that it does cause IE. Vegetative lesions may be seen on the mitral or aortic valves. The patient shows signs of extreme illness due to septicemia, fever, and a new murmur. If the mitral valve is affected, the patient will have a systolic murmur. If the aorta is affected, there will be a diastolic murmur. The left side of the heart will overload, and some patients will develop congestive heart failure as a consequence.

Diagnosis of IE is accomplished by detected the presence of a vegetative lesion and performing blood cultures. The protocol for blood cultures is generally to draw at least three samples from two different sites an hour apart. Isolating the bacteria responsible will allow the clinician to treat with the appropriate antibiotic. Rarely, a fungal etiology such as Blastomycosis may be found as a cause of IE.

Treatment of IE is generally supportive. Injectable antibiotics are used when indicated, but the valve will be permanently damaged. Because of this, the prognosis with IE is generally poor.

Tachycardia-induced cardiomyopathy is a rare cause of congestive heart failure in dogs. Long term arrhythmias, most often supraventricular tachycardia, causes myocardial failure. Controlling the arrhythmia gives the patient the best chance of recovery. Medications are somewhat effective, but catheter ablation of the arrhythmic focus is the best treatment. Unfortunately, this is only offered at one location in the US, and it must be performed on patients greater than 10 kg body weight. In addition to antiarrhythmic medications, standard treatment of CHF is recommended where indicated.

Heartworm disease can also cause severe heart disease, especially with severe infestation. Heartworms live in the pulmonary arteries, but with increasing numbers of worms, they may inhabit the main pulmonary artery, as well as the right atrium and ventricle. If the worms migrate as far as the right heart, blood flow is restricted, and the tricuspid valve cannot close properly. This is called caval syndrome. As a consequence of this, there is often a loud murmur on the right thorax, and red blood cells are damaged, causing hemoglobinemia and hemoglobinuria. At this point, adulticide treatment is quite dangerous. The treatment of choice is surgical extraction of the worms as soon as possible.

Feline Cardiac Disease

In cats, cardiac disease occurs most often as a result of primary myocardial illness. The most common of these is hypertrophic cardiomyopathy (HCM). Breeds commonly affected include Maine Coon, Ragdolls, and Rexes. HCM is found in cats of almost all age, from as young as six months to over ten. HCM is likely caused by many different genes, but it has been linked to a specific gene in Maine Coons. In HCM, the walls of the heart become concentrically hypertrophied, or thickened to the point that the left ventricle has difficulty filling with blood. In the obstructive form of HCM, HOCM, the mitral valve apparatus is pulled into the LVOT, and a murmur results from mitral regurgitation and increased velocity of blood passing through the LVOT. Therefore, on physical exam, a murmur is not always detected, though a gallop heart sound may be. Left ventricular hypertrophy may also result from hyperthyroidism, Cushing's disease, acromegaly, and hypertension. For this reason, these conditions should also be a part of screening when left ventricular hypertrophy is found.

The incidence of dilated cardiomyopathy in cats has greatly reduced since discovering taurine deficiency as an etiology. Now, as taurine deficiency has been prevented by including it as an essential amino acid in cat diets, it is rarely seen, as is primary DCM in cats. Similar to DCM in dogs, the ventricular walls are eccentrically hypertrophied, or dilated, and contract poorly. DCM generally affects middle aged to older cats.

In restrictive cardiomyopathy, the walls of the left ventricle become stiffened and do not fill normally in diastole. Unclassified cardiomyopathy includes those types of cardiac disease in cats that essentially cannot be classified into HCM, DCM, or RCM.

The sequelae of feline cardiac disease are generally uniform across all diseases. Congestive heart failure may manifest as pulmonary edema and/or pleural effusion, regardless of which side of the heart is affected. If the cat has pleural effusion, removal of the fluid via thoracocentesis may be necessary, as medications will not have the same effect on effusion as edema. Generally, the prognosis for cats with CHF is approximately one year, but occasionally a cat may long outlive this prognosis and survive several years after their first diagnosis of CHF. Some cats will present with arterial thromboembolism (ATE), a painful condition where a thrombus, or clot, lodges in a peripheral artery. Many cat owners opt for euthanasia at this point, but about 50% of patients with a rectal temperature greater than 98.9 F will survive to discharge. The use of low dose aspirin (5 mg PO q 72 h) or clopidigrel (Plavix) may prevent ATE, though studies have not proven this benefit. Sudden death may also occur as the first clinical sign.

A rare cause of congestive heart failure in cats is associated with corticosteroid administration. Cats are reported to be remarkably resistant to the normal side-effects of steroids, but the development of congestive heart failure without the presence of heart disease and after steroid administration has been reported. These cats typically present in respiratory distress within a week of receiving steroids. They are often hypothermic, hypotensive, and bradycardic. While the first few days may be very difficult for these cats, if they survive to discharge and do not have underlying heart disease, they may go on to survive long-term.