* This is the Veterinary Version. *
- Myxomatous AV Valve Degeneration
- Valvular Blood Cysts or Hematomas
- Other Causes of Myocardial Failure
- Infective Endocarditis
- Pericardial Disease
- Systemic and Pulmonary Hypertension
- Arterial Thromboembolism
- Resources In This Article
Specific Cardiac Diseases
Myxomatous degeneration is a process of the fibrous layer of an AV valve breaking down to cause mitral valve prolapse (hooding) and the spongiform layer proliferating to cause nodular thickening of the cardiac valve leaflets, most severely at their tips. Myxomatous degeneration commonly affects the mitral and tricuspid valves in dogs. Chordae tendineae are also affected by the degenerative process, making them prone to rupture. The exact cause is unknown, but in Cavalier King Charles Spaniels and Dachshunds it is an inherited trait. Myxomatous degenerative valve disease is the most common cardiac disease in dogs and accounts for ~75% of cardiovascular disease in this species; ~60% of affected dogs have only the mitral valve affected, 30% have lesions in both the tricuspid and mitral valves, and 10% have only tricuspid valve disease. In dogs, the disease is age- and breed-related, with older, small-breed dogs demonstrating a much higher incidence. Horses and cats are also affected by this disease (most commonly affecting the mitral valve leaflets); however, it is uncommon in these species. In horses, a degenerative valve disease can also affect the aortic valve cusps and consists of valvular nodules or fibrous bands at the free borders of the valve. This condition is most common in older horses. It causes aortic regurgitation, which is heard as a diastolic murmur on the left side. The murmur is often "musical," meaning it has one frequency caused by the valve structures vibrating at the frequency heard. The murmur may be high-pitched and sound truly musical, or it may be low-pitched and sound like a grunt or a dive bomber. The murmur is often loud, but the aortic regurgitation is usually mild. Clinical signs (eg, heart failure) are usually not seen, because severe aortic regurgitation is uncommon.
Insufficiency of an AV valve results in turbulent, systolic (ie, during ventricular contraction) flow through the affected valve from a ventricle into an atrium. This regurgitation results in an increase in volume within the atrium and thus to an increase in atrial chamber size. When regurgitation is severe, atrial pressure may also increase. If the mitral valve is affected, the increased left atrial pressure results in increased pulmonary capillary pressures and, if the increase is high enough (ie, >20 mmHg), in cardiogenic pulmonary edema (ie, left heart failure). If the tricuspid valve is affected, severe regurgitation can result in an increased systemic venous pressure and signs of right heart failure (most commonly ascites in dogs). The constant, high-velocity, regurgitant jet of blood through the affected mitral valve physically damages the endocardium of the left atrium, resulting grossly in jet lesions. In cases with severe regurgitation, the chronic increase in left atrial size and pressure can also result in left atrial rupture and acute cardiac tamponade, often resulting in death.
Pathophysiologically, the body compensates for valvular regurgitation primarily by renal sodium and water retention, causing an increase in blood volume and in venous return to the heart. This results in an enlargement in ventricular chamber size and a left ventricle capable of ejecting a larger total stroke volume with each beat. That way, even though some percentage of blood flow is going backward into the left atrium, a normal or near normal amount can be ejected forward into the aorta. Multiple mechanisms exist for sodium and water retention, but the renin-angiotensin-aldosterone system (RAAS, see Compensatory Mechanisms) is one of the most active and best studied. Renin release by the juxtaglomerular apparatus in the kidneys cleaves angiotensinogen into angiotensin I, and angiotensin-converting enzyme then cleaves angiotensin I into angiotensin II. One of the main effects of angiotensin II is to stimulate aldosterone release by the adrenal glands. Aldosterone stimulates the cells in the distal renal tubules to bring sodium back into the vascular space, and water follows the sodium. The increase in blood volume and venous return to the heart places chronic stretch on cardiac myocytes, resulting in sarcomere replication within the myocytes and growth of longer myocytes. This allows the affected ventricle to develop a larger chamber (ie, eccentric or volume overload hypertrophy). This is the primary compensatory mechanism for valvular regurgitation. It is highly efficient and allows the heart to compensate not only for a valvular leak for years but also for an extreme amount of regurgitation. For example, a small dog can completely compensate for regurgitation in which as much as 75% of the blood flow from the left ventricle goes into the left atrium, while only 25% goes forward into the aorta.
Activation of the RAAS and other compensatory mechanisms are commonly seen as dysfunctional and increases of various neurohormones as detrimental, because overt increases are often seen in dogs that are in heart failure when compensatory mechanisms are overwhelmed. However, these mechanisms are detrimental for only a few months at the end stage of the disease.
Only ~30% of dogs with mitral regurgitation ever develop left heart failure. In dogs, there are no clinical signs in the early and middle stages of the disease, although a systolic murmur (grade I–VI) is heard with maximal intensity at the left apex. The heart murmur intensity often does not correlate with disease severity, although most soft murmurs are heard in dogs with mild mitral regurgitation. Some dogs may also develop a systolic click before developing a heart murmur. A systolic click is heard as a three-heart-sound rhythm and may be mistaken for a gallop sound (rhythm). A three-heart-sound rhythm in a middle-aged to older small-breed dog is almost always a systolic click rather than a gallop sound. A gallop sound may be heard in a dog with severe mitral regurgitation but is usually difficult to auscult because of the loud heart murmur also present. When the mitral regurgitation becomes severe and overwhelming, left heart failure (pulmonary edema) becomes evident, producing increases in respiratory rate (tachypnea) and effort (dyspnea), and cough. Syncope may also occur. Although syncope is not a sign of heart failure, it may be present when heart failure is evident and may improve when heart failure is controlled. Sudden death is rare but may occur secondary to left atrial rupture or rupture of a primary mitral valve chord. Physical examination findings in animals that have developed left heart failure are primarily referable to the increased respiratory rate and effort. Some dogs may have respiratory crackles and wheezes; however, these are much more common and more obvious in dogs with chronic bronchitis, and many dogs with pulmonary edema have no demonstrable abnormal pulmonary sounds. If tricuspid valve degeneration is significant, signs of right heart failure may be noted (eg, ascites, jugular distention/pulses).
A CBC, serum chemistry profile, and urinalysis are usually within normal limits. Left atrial enlargement is the characteristic finding on thoracic radiographs of an animal with myxomatous degeneration of the mitral valve, and the size of the left atrium correlates directly with the severity of the regurgitation in small dogs. Other changes include enlargement of the left ventricle and pulmonary veins. As left heart failure develops, increased interstitial density to the pulmonary parenchyma occurs, and as severity increases, an alveolar pattern with air bronchograms (ie, severe pulmonary edema) appears. In dogs, these changes are classically seen in the caudodorsal lung fields and may be more prominent on the right side. In older dogs, it is common to have an increased interstitial density in the lungs and to have radiographs taken at or near end-expiration. This commonly creates the illusion of pulmonary edema and therefore the misdiagnosis of left heart failure. This can be avoided by remembering that for a dog to be in chronic left heart failure, the regurgitation must be severe and overwhelming so the left atrium is usually severely enlarged. The exception to this rule is in dogs with acute heart failure due to a ruptured chord and a left atrium that is not severely enlarged. If the respiratory rate in the examination room is normal (<30 breaths/min), the dog cannot be in left heart failure. If there is doubt regarding the diagnosis of pulmonary edema in a dog that is not in critical condition, it is usually best to send the dog home and have the owner count the dog's respiratory rate when it is sound asleep in a cool environment. If pulmonary edema is present, the sleeping respiratory rate (SRR) will always be increased. If the rate is increased, the dog should be administered furosemide at a dosage of at least 2 mg/kg, PO, bid. If the SRR then decreases, the diagnosis of left heart failure can be made. In cats, the radiographic pattern is more diverse and often is not caudodorsal. A heavy interstitial to alveolar pattern in the accessory lung lobe on a lateral view is one of the more common findings. Cats in left heart failure also commonly have pleural effusion.
Echocardiography demonstrates thickened and irregular valve leaflets of normal to increased echogenicity. Chordae tendineae may be ruptured, causing the AV leaflets to flail (ie, leaflet tips to protrude) into the atrium during ventricular contraction. Mitral valve prolapse (hooding), in which the body of a leaflet (not the tip) protrudes into the left atrium in systole, may also be present. The size of the left atrium increases in direct correlation with the severity of the mitral regurgitation in small dogs. Left ventricular chamber enlargement (ie, eccentric or volume overload hypertrophy) also occurs in correlation to disease severity. In small dogs, left ventricular myocardial contractility or function is often normal as evidenced by a normal end-systolic diameter or volume. The increase in end-diastolic diameter coupled with the normal end-systolic diameter results in the left ventricular fractional shortening (ie, the amount of contraction [not contractility]) being increased. Myocardial contractility is decreased in some small dogs and many large dogs at the onset of heart failure and may become decreased in small dogs when being treated for heart failure.
Electrocardiographically, animals with mild to moderate degenerative valve disease have a normal sinus arrhythmia or normal sinus rhythm. When CHF develops, the increase in sympathetic tone often results in loss of sinus arrhythmia and usually in an increase in heart rate (ie, sinus tachycardia). Left atrial enlargement promotes the development of atrial arrhythmias such as atrial premature complexes and atrial fibrillation. Ventricular tachyarrhythmias are uncommon. There may be evidence of left atrial enlargement (P mitrale or widened P waves) and left ventricular enlargement (tall and widened R waves) on an ECG, but these changes are unreliable indicators of chamber enlargement.
Measurement of the plasma or serum concentration of NT-proBNP may be useful in dogs with mitral regurgitation. It is usually not increased in dogs with mild mitral regurgitation, may be increased in some dogs with moderate to severe mitral regurgitation, and is increased in most dogs with left heart failure secondary to mitral regurgitation. It would be most useful in dogs presented with severe tachypnea/dyspnea if a rapid assay (bedside test) were available. It might be useful for differentiating dogs with chronic lung disease from dogs in chronic left heart failure, but this can often be accomplished with less expense and greater accuracy by having the owner count the dog's SRR and doing a furosemide response test if the rate is increased. NT-proBNP often decreases after successful treatment of left heart failure but frequently does not decrease to a value within the normal range. Predicting which dogs with mitral regurgitation will go into heart failure is difficult. As populations, dogs with a larger left ventricular diastolic dimension, larger left atrial size, and a higher NT-proBNP are at greater risk of developing heart failure, but translating that to an individual dog is often fraught with error. The same is true for predicting cardiac death (ie, from heart failure or sudden death) from severe mitral regurgitation. Higher dosages of furosemide are required in dogs with more severe heart failure, so higher furosemide dosages predict decreased survival.
Studies in dogs with degenerative mitral valve disease that are not yet in heart failure have failed to convincingly demonstrate a reduction in time to onset of CHF with use of ACE inhibitors. Thus, treatment in small-breed dogs should be reserved for dogs with clinical signs of heart failure, ie, those demonstrating cardiogenic pulmonary edema on thoracic radiographs and resting/sleeping tachypnea in the absence of other severe pulmonary disease. Treatment of CHF includes administration of a diuretic (almost always furosemide) and an ACE inhibitor as adjunctive therapy. Cardiogenic pulmonary edema should not be treated with an ACE inhibitor alone. Pimobendan (0.25–0.3 mg/kg, bid) is also indicated in dogs in heart failure. Spironolactone might have chronic, long-term benefits in dogs with heart failure due to myxomatous mitral valve degeneration, but there is no convincing evidence of this in dogs with mitral regurgitation, and it should not be relied on to produce clinically relevant diuresis. Dogs refractory to administration of a maximal dosage of furosemide (4 mg/kg, tid) can be treated with several additional drugs or a change in strategy. The pimobendan dosage can be increased to tid, or the bid dosage can be doubled. Amlodipine and hydralazine decrease the amount of regurgitation and improve perfusion and can be very effective. A thiazide diuretic combined with furosemide is another effective means of treating dogs with refractory heart failure, but care must be taken to not produce clinically relevant dehydration and hypokalemia. Torsemide may be used to replace furosemide. Torsemide is more bioavailable (better absorbed) and has a longer and more consistent half-life. The starting dose is determined by multiplying the total daily dose of furosemide by 0.1 and dividing that dose bid. Care must be taken to have the owner closely monitor the SRR when this is done. If the SRR increases, the dose of torsemide must be increased promptly.
Surgical treatment of mitral regurgitation is routine in human medicine and most commonly consists of mitral valve repair. Successful mitral valve repair has also been accomplished in dogs, but the only currently truly successful program is in Japan. Replacement of the mitral valve with a prosthetic valve is almost uniformly unsuccessful.
Abnormal arrhythmias such as atrial fibrillation or other severe and sustained supraventricular arrhythmias, if present, should either be resolved or the rate controlled with digitalis glycosides and diltiazem or a β-blocker (eg, atenolol) to prevent tachycardia-induced myocardial failure. Optimal therapy should be planned for each stage of disease. In acute and severe CHF, oxygen and aggressive parenteral furosemide administration are warranted. Nitroprusside can also be beneficial.
Some affected dogs can live for >1 yr with appropriate therapy. However, survival time is highly variable, and no firm estimates should be provided. If a dog has been treated for left heart failure for >2 yr, the diagnosis should be reassessed.
Cardiomyopathy is defined as any disease involving primarily and predominantly the heart muscle. Most of the cardiomyopathies of animals are idiopathic diseases that are not the result of any systemic or other primary cardiac disease. In several instances, a mutational cause has been identified. In others, a genetic cause has been identified. In animals (primarily dogs and cats), they are classified as dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and restrictive or unclassified cardiomyopathy. If a disease process has been identified as the cause of myocardial dysfunction, these are more correctly identified as secondary myocardial diseases or with a descriptive term preceding the term cardiomyopathy (eg, taurine-responsive dilated cardiomyopathy).
This disease is characterized by the progressive loss of myocyte number and/or function and a decrease in cardiac contractility. Several forms of secondary DCM exist (eg, taurine deficiency in cats, doxorubicin- or parvovirus-induced in dogs). In some Doberman Pinschers (primarily those in the USA), the disease is caused by a mutation in the gene that encodes for pyruvate dehydrogenase kinase 4 (PDK4), an enzyme in mitochondria required for ATP production. A small percentage of Boxers with arrhythmogenic right ventricular cardiomyopathy (see below) develop DCM. These dogs have a mutation in the gene that encodes for striatin, a desmosomal protein. DCM has a protracted subclinical phase in dogs, with clinical signs evident for a relatively short time. During the subclinical phase, compensatory mechanisms, primarily volume overload or eccentric hypertrophy, maintain normal hemodynamics. As cardiac contractile function is progressively lost, cardiac output, and so renal blood flow, decreases and then is normalized again as renal sodium and water retention increase blood volume and venous return and the affected ventricle is stimulated to grow larger. The increased activation of the sympathetic nervous system and the RAAS, after years of initial benefit, cause deleterious effects during the late phases of the disease (see Compensatory Mechanisms). Excessive stimulation of the myocardium by the sympathetic nervous system may stimulate ventricular arrhythmias and myocyte death, while excessive activation of the RAAS causes vasoconstriction and continued retention of sodium and water in the presence of edema/effusion.
DCM is most prevalent in dogs and is especially prevalent in certain breeds. It most commonly affects large-breed dogs and far less commonly small-breed dogs (with a few exceptions such as American Cocker Spaniels, Springer Spaniels, and English Cocker Spaniels). Doberman Pinschers, Boxers, Great Danes, German Shepherds, Irish Wolfhounds, Scottish Deerhounds, Newfoundlands, Saint Bernards, and Labrador Retrievers, among other large-breed dogs, are particularly at risk. In Portuguese Water Dogs, a juvenile form of the disease is seen. The disease is typically seen in middle-aged to older dogs; males are either affected more frequently or more severely than females. The incidence in cats has decreased dramatically since the discovery in 1987 that taurine deficiency was responsible for most cases (taurine-responsive DCM). Since then, taurine has been added to all commercial cat foods. Most cases today are not taurine responsive and reflect primary (or idiopathic) disease, although the disease is seen occasionally in cats fed noncommercial diets (eg, vegetarian, baby food, home-cooked food).
Doberman Pinschers typically develop concurrent and progressive ventricular arrhythmias along with progressive systolic dysfunction. Syncope and sudden death occur in as many as 20% of Doberman Pinschers, and signs of left heart failure eventually develop. Most Doberman Pinschers demonstrate evidence of myocardial failure at the time syncopal episodes are noted. In other breeds, such as Great Danes and Newfoundlands, sudden death and collapse are far less likely. Signs of left heart failure, including tachypnea and dyspnea due to pulmonary edema, weakness, and exercise intolerance often predominate, but signs of right heart failure (ascites) may also be present. Pleural effusion may be present, most commonly in dogs with both left and right heart failure. Ascites was noted in 35% of Newfoundlands with DCM in one study. Cats with DCM typically present with severe respiratory signs due to pulmonary edema and/or pleural effusion, and clinical signs are often rapidly progressive and refractory to therapy.
A soft systolic heart murmur, best heard at the left cardiac apex, is often present. A gallop sound may also be present but is subtle and usually identified in dogs only by an experienced examiner. It is often more obvious in cats. The femoral pulse may be weak, and an arrhythmia with associated pulse deficits may be noted. The arrhythmia is most commonly ventricular ectopy (eg, premature ventricular contractions, ventricular tachycardia) in Doberman Pinschers and Boxers, and atrial fibrillation in giant-breed dogs. Ascites, tachypnea, dyspnea, or cough may also be noted, depending on the type of heart failure that develops.
Blood work may demonstrate prerenal azotemia (increased BUN, creatinine). Thoracic radiographs typically demonstrate moderate to marked cardiomegaly. However, this finding may be masked by chest conformation (eg, a deep chest in a Doberman Pinscher). If left heart failure is present, pulmonary edema is more commonly evident in a large dog than it is in a small dog with mitral regurgitation, and the left atrium is moderately to markedly enlarged. Echocardiography is the best test to definitively diagnose DCM. In dogs with severe DCM that are in heart failure, there is a dramatic decrease in left ventricular fractional shortening caused by an increase in left ventricular end-systolic diameter. Cardiac chambers, especially the left atrium and left ventricle, are dilated. Mitral insufficiency typically develops as progressive left ventricular chamber dilation results in separation of the valve leaflets. Abnormal ECG findings may include ventricular premature complexes and ventricular tachycardia (especially in Doberman Pinschers and Boxers), and atrial fibrillation (especially giant breeds). There may be electrocardiographic evidence of left atrial enlargement (P mitrale or widened P waves) and left ventricular enlargement (tall and wide R waves). The occurrence of ventricular premature complexes on a routine ECG in a presumed healthy Doberman Pinscher is highly suggestive of DCM.
The objectives of therapy are to lessen edema/effusion formation (eg, with diuretics), improve contractility (eg, with pimobendan), and reduce adverse effects of angiotensin II and other neurohormonal changes (eg, with an ACE inhibitor). Taurine-responsive myocardial failure occurs in some breeds, particularly American Cocker Spaniels, and anecdotally in a few Golden Retrievers, Dalmatians, Welsh Corgis, Tibetan Terriers, and other breeds. In many of these breeds, taurine deficiency can be diagnosed by low plasma or whole blood concentrations. Response to taurine supplementation (which may take 2–4 mo) can be dramatic and may obviate the need for other cardiac medications. Carnitine-responsive cardiomyopathy, although reported, is almost a nonentity. Coenzyme Q10 supplementation is an unproven and, many say, irrational approach to the disease. Administration of fish oil might reduce the severity of cardiac cachexia in animals with DCM.
CHF, which may be severe, should be treated as discussed elsewhere (see Heart Failure). As severe pulmonary edema resolves, furosemide can be administered orally, with oxygen continued until clinical signs are controlled. Pimobendan and an ACE inhibitor (eg, enalapril, benazepril) should be started. Pimobendan may be indicated in Doberman Pinschers with DCM before the onset of heart failure. Antiarrhythmic therapy is frequently indicated, especially for Doberman Pinschers with severe ventricular arrhythmias. Holter monitoring is the ideal method to evaluate both the severity of an arrhythmia and therapeutic efficacy. Mexiletine (5–10 mg/kg, tid) may be useful in animals with ventricular arrhythmias and concurrent heart failure, because negative inotropy is less than with sotalol (1–3 mg/kg, bid); however, sotalol can be used if therapy is initiated with a low dose carefully titrated upward and if pimobendan is used concurrently. Amiodarone may be a more effective drug than mexiletine to prevent sudden death in Doberman Pinschers, but its use is associated with a relatively high incidence of hepatotoxicity in this breed.
The prognosis is grave for cats with DCM (not taurine responsive), with a median survival time of 2 wk. Cats that are taurine responsive also have an initial high risk of death. However, cats that survive long enough for taurine to become effective (2–3 wk) have an excellent prognosis, because the disease is completely reversible. Dogs that are taurine responsive also have a fair to good prognosis once signs of CHF abate. The short-term prognosis for other dogs with DCM depends primarily on the severity of the heart failure on presentation. Longterm prognosis is poor, with survival time measured in months. The prognosis is poor in most Doberman Pinschers: in the past, ~25% died within 2 wk of presenting with heart failure, and 65% died within 8 wk. Pimobendan apparently prolongs survival, sometimes dramatically (months). The prognosis in other breeds is better but remains guarded; 75% die within 6 mo of diagnosis. As expected, dogs with severe heart failure, particularly left heart failure, have a worse prognosis than those with milder signs or signs of right heart failure at presentation.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is seen almost exclusively in Boxers and is also known as Boxer cardiomyopathy. It is also rarely seen in cats. ARVC is characterized by a fatty or fibrofatty infiltrate of the right ventricular myocardium. In Boxers, the most common manifestation of the disease is syncope caused by a very fast (>400 bpm) nonsustained ventricular tachycardia. It takes 6–8 sec of no blood flow to the brain to result in unconsciousness, so the tachycardia must last for that long for syncope to occur and then must stop spontaneously for sudden death not to occur. The diagnosis is based on the number of premature ventricular complexes (PVCs) on a Holter monitor (>100–300 PVCs in 24 hr is generally considered diagnostic of ARVC in this breed). The QRS complexes of the PVCs are most commonly upright in the leads where the QRS complex is usually upright, meaning they originate from the right ventricle. The heart looks normal on thoracic radiographs and an echocardiogram in most Boxers with ARVC, although some will develop a true DCM and go into heart failure. Boxers presented for syncope without DCM are treated with sotalol (1–3 mg/kg, PO, bid) or a combination of mexiletine (5–10 mg/kg, PO, tid) and atenolol (12.5–25 mg/dog, PO, bid). Dogs refractory to sotalol may have mexiletine added. In Boxers with ARVC that do not have DCM, the prognosis is often good, and many live for several years on antiarrhythmic therapy. The longterm prognosis for dogs with DCM that are in heart failure is poor. Most live only several months.
In cats, the disease usually manifests as right ventricular and atrial enlargement and right heart failure, usually along with some supraventricular and ventricular tachyarrhythmias. Dyspnea and tachypnea due to pleural effusion, ascites, and nonspecific clinical signs such as anorexia and lethargy are reported in affected cats. Treatment is similar to that of DCM. Longterm prognosis is generally poor.
Hypertrophic cardiomyopathy (HCM) is characterized by primary concentric left ventricular hypertrophy (ie, thick walls) resulting from an inherent myocardial disorder rather than pressure overload (such as caused by aortic stenosis), hormonal stimulation (such as hyperthyroidism or acromegaly), infiltration of the myocardium (eg, lymphoma), or other noncardiac disease. It is primarily seen in domestic cats and rarely in small dogs. It has also been reported in cattle. Papillary muscle enlargement is a consistent feature of the disease in cats. In people, HCM is caused by mutations in a number of sarcomeric genes. Mutations in one sarcomeric gene, the cardiac myosin binding C gene, have been identified in Maine Coon and Ragdoll cats. These mutations are thought to result in the production of dysfunctional sarcomeres within myocytes. The myocardium then produces new sarcomeres to help the dysfunctional ones, resulting in hypertrophy that may be mild to severe. Severe hypertrophy is often accompanied by cellular necrosis and resultant replacement fibrosis (myocardial scarring).
Increased fibrosis coupled with severe wall thickening results in a stiffer than normal left ventricle in diastole, which increases diastolic pressure for any given diastolic volume. The increased pressure is transmitted backward into the left atrium in diastole, resulting in left atrial enlargement and, if severe enough, in left heart failure. Left heart failure manifests as pulmonary edema and pleural effusion in cats. Myocardial contractility is normal, but left ventricular end-systolic diameter is usually less than normal and may become zero (end-systolic cavity obliteration) due to the increased wall thickness resulting in a decrease in systolic wall stress (ie, afterload). Severe left atrial enlargement can develop, which causes blood flow to stagnate. This can lead to the formation of a left atrial thrombus and the potential for systemic thromboembolism.
A cranial displacement of the anterior mitral valve leaflet during ventricular systole, a phenomenon termed systolic anterior motion of the mitral valve, is a common finding in cats with HCM and is due to marked enlargement of the papillary muscles that drag the mitral valve leaflet into the left ventricular outflow tract in systole. This phenomenon produces two turbulent jets—one of dynamic subaortic stenosis and the other of mitral regurgitation. Systolic anterior motion is the most common cause of a heart murmur in a cat with HCM. Gross pathology includes increased cardiac weight (>20 g), increased left ventricular wall thickness, papillary muscle hypertrophy, and often left atrial enlargement. The myocardium often contracts after death (ie, undergoes rigor), so the postmortem diagnosis of HCM often cannot be made based on left ventricular wall thickness alone.
HCM is the most common primary heart disease diagnosed in cats, but it is rare in dogs. It is familial in many breeds of cats, including Persians, Sphynx, Norwegian Forest Cats, Bengals, Turkish Vans, and American and British Shorthairs. As in Maine Coons and Ragdolls, the mode of inheritance is thought to be autosomal dominant. The disease is seen in cats from 3 mo to 17 yr of age, although most cats are middle aged at presentation. It is not present at birth but develops over time. Penetrance is often <100%. Male and female cats are equally predisposed, but males tend to develop more severe disease at an earlier age. In Maine Coon and Ragdoll cats, cats that are homozygous for the mutation often develop HCM earlier (often before 1 yr of age) and often develop a more severe form of the disease.
Many affected cats have no clinical signs, especially those with mild to moderate disease. Cats that develop severe disease may also have no clinical signs but will usually go on to develop left heart failure, systemic thromboembolism, or sudden death. Cats in heart failure have signs of tachypnea and dyspnea secondary to pulmonary edema or pleural effusion. Owners frequently do not note tachypnea and so do not present the cat for examination until dyspnea, often marked, is present. Cats with systemic thromboembolism most commonly have an acute onset of hindlimb paresis/paralysis coupled with acute pain, pulselessness, and poikilothermia. Cough is uncommon in cats with heart failure.
Physical examination frequently demonstrates abnormal heart sounds, including a soft to prominent systolic cardiac murmur and/or a gallop sound. The murmur is often dynamic, increasing in intensity with excitement and decreasing as the cat relaxes. A murmur is not present in at least one-third of cats with HCM. Increased respiratory sounds may suggest pulmonary edema, and decreased respiratory sounds may indicate pleural effusion, but auscultation of the lungs is often normal. The femoral pulse may be normal or weak, or absent if distal aortic thromboembolism has developed. Radiographically, there may be pronounced left atrial enlargement, especially in a cat in left heart failure, and variable left ventricular enlargement. The cardiac silhouette can appear relatively normal even in the presence of moderate to severe left ventricular hypertrophy if the left atrium is not enlarged. Echocardiography allows confirmation of the diagnosis and assessment of additional therapy needed (eg, anticoagulants may be more beneficial in cats with severe left atrial enlargement). Left ventricular wall thickening (≥6 mm; generalized or regional), along with papillary muscle hypertrophy are noted. Systolic anterior motion of the mitral valve may be present. ECG abnormalities may include supraventricular premature complexes, ventricular premature complexes, and ventricular tachycardia. With severe atrial enlargement, atrial fibrillation may rarely develop. An electrical axis deviation may be present. However, many cats with HCM have a normal ECG. The plasma concentration of NT-proBNP is often increased in cats with severe disease and particularly in those in heart failure (see Cardiac Biomarkers).
Treatment is directed at controlling signs of CHF, improving diastolic function, and reducing the incidence of systemic thromboembolism. Furosemide (2–4 mg/kg, IV or IM, as needed) administration and oxygen are needed when acute CHF is present. For chronic heart failure, furosemide and an ACE inhibitor, eg, enalapril (0.5 mg/kg/day, PO), are indicated. For cats not in heart failure, no drug strategy has been shown to alter the natural history of the disease. Diltiazem (7.5 mg, PO, tid), a calcium channel blocker, may improve diastolic function, but its effects are generally negligible and its use has diminished. Use of β-blockers such as atenolol (6.25–12.5 mg, PO, 1–2 times/day) may also be considered, but proof of benefit is lacking. People with HCM have shown improvement in exercise-induced angina and dyspnea, and exercise intolerance when given β-blockers. Cats rarely exert themselves, so those indications do not apply. However, a β-blocker does reduce systolic anterior motion of the mitral valve and should be considered when this abnormality is severe (pressure gradient across the dynamic subaortic stenosis is >80 mmHg). ACE inhibitors have no apparent beneficial effect before the onset of heart failure.
Prevention of left atrial thrombus formation and systemic thromboembolism is often a goal. Clopidogrel (18.75 mg/day/cat) is the only drug shown to decrease the incidence of systemic thromboembolism in cats. Warfarin (0.2–0.5 mg/day, PO) is probably ineffective and produces bleeding in some cats. Aspirin (80 mg, PO, every third day) is also believed to be ineffective. Clopidogrel plus aspirin is a common therapeutic strategy in people. A low-molecular-weight heparin such as enoxaparin (1 mg/kg, bid) might be efficacious but is expensive and must be administered parenterally.
The prognosis for cats with HCM is highly variable. Many mildly affected cats have a good longterm prognosis. Cats in CHF have a poor prognosis, with a median survival time of 3 mo. However, as many as 20% of cats with CHF might survive for a more prolonged period.
A less common form of cardiomyopathy in cats is characterized by a relatively normal-appearing left ventricle with left atrial enlargement. Although it is logical to believe that these cats have diastolic dysfunction, many do not. Those that do have diastolic dysfunction have some form of restrictive cardiomyopathy. However, because that diagnosis cannot be made using standard two-dimensional echocardiography, it is better to term this type of disease unclassified cardiomyopathy unless diastolic dysfunction can be documented, usually by using tissue Doppler imaging echocardiography. Restrictive cardiomyopathy is characterized by a stiff, noncompliant left ventricle, usually due to increased collagen (ie, scar) formation in the left ventricle. The increased stiffness increases diastolic pressure for any given diastolic volume. As in hypertrophic cardiomyopathy, this results in an increase in left atrial size and left heart failure. In some cats that have obvious endomyocardial thickening or partial cavity obliteration, the diagnosis of restrictive cardiomyopathy can be readily made using two-dimensional echocardiography. A left atrial thrombus may be evident. Systolic function is usually preserved. Color flow Doppler echocardiography may demonstrate mitral regurgitation.
Clinical signs of and treatment for heart failure are similar to those for HCM (see Hypertrophic Cardiomyopathy); however, prognosis seems to be worse, especially in cats with CHF. The cause of restrictive/unclassified cardiomyopathy is unknown.
Myocarditis is a focal or diffuse inflammation of the myocardium with myocyte degeneration and/or necrosis. Myocarditis is rare in companion animals, although there are numerous causes, including several viruses and bacteria. Canine parvovirus (see Canine Parvovirus), encephalomyocarditis virus (see Encephalomyocarditis Virus Infection), and equine infectious anemia virus (see Equine Infectious Anemia) can cause myocarditis. Myocardial degeneration is seen in lambs, calves, and foals with white muscle disease and in pigs with mulberry heart disease or hepatosis dietetica. Streptococcus spp are the most common cause of bacterial myocarditis in horses. Salmonella, Clostridium, equine influenza, Borrelia burgdorferi, and strongylosis are other recognized causes. Mineral deficiencies (eg, iron, selenium, copper) can also result in myocardial degeneration (not myocarditis). Deficiencies of vitamin E or selenium may cause myocardial necrosis. Cardiac toxins include ionophore antibiotics such as monensin and salinomycin, cantharidin (blister beetle toxicosis, see Cantharidin Poisoning), Cryptostegia grandiflora (rubber vine), and Eupatorium rugosum (white snakeroot). These diseases cause typical signs of CHF. In horses, signs of right heart failure are common and include ventral edema, ascites, venous congestion, and jugular pulsations. A heart murmur of mitral or tricuspid regurgitation is usually audible as well as an irregular rhythm. Atrial fibrillation is common, and ventricular or atrial premature complexes may also be seen. Echocardiography reveals chamber dilation and poor contraction with essentially normal valves. Neutrophilic leukocytosis and hyperfibrinogenemia are common. Cardiac isoenzymes (CK, troponin, and lactate dehydrogenase) are often increased.
Treatment should be aimed at improving cardiac contractility, relieving congestion, and reducing vasoconstriction. Pimobendan and digoxin are used most commonly to improve contractility. Furosemide is indicated to control signs of pulmonary edema. Corticosteroids are often used when cardiac isoenzymes are increased and a viral infection is deemed unlikely.
Trypanosoma cruzi, a flagellate protozoa, causes Chagas’ disease (see Chagas’ Disease). Acutely, ECG abnormalities such as first-, second-, or third-degree AV block; right bundle-branch block; sinus tachycardia; and depressed R wave amplitude are noted. There are usually no echocardiographic abnormalities during the acute phase; however, sudden death is a concern. An asymptomatic latent phase then develops for 27–120 days in dogs, followed by a chronic stage demonstrating systolic dysfunction indistinguishable from DCM. Treatment for the chronic phase is as for DCM but is typically ineffective at controlling signs of progressive myocardial failure. The disease is most commonly identified in southern states (eg, Texas) but may be spreading.
Lyme disease (see Lyme Borreliosis) is caused by the spirochete Borrelia burgdorferi; infection might result in myocardial disease. In people, it causes a usually reversible third-degree AV block. Animals developing myocardial disease secondary to Lyme infection may, at least in theory, have ECG abnormalities such as ventricular arrhythmias or conduction disturbances such as first-, second-, or transient third-degree AV block. However, a recent study failed to identify evidence of any tickborne organism in a group of dogs presented for third-degree AV block. Two dogs with severe ventricular tachyarrhythmias with a high antibody titer to Anaplasma phagocytophilum required prednisone and azathioprine to control the arrhythmias. There are no reports of DCM due to these organisms in dogs or cats.
In addition to the diseases listed below, histophilosis in cattle (see Histophilosis) can result in myocardial infarcts and abscesses.
A form of cardiomyopathy resulting in destruction of the atrial myocardium (that may also affect the ventricular myocardium) has been reported in dogs. Affected breeds include English Springer Spaniels, Old English Sheepdogs, Shih Tzus, German Shorthaired Pointers, and mixed-breed dogs. The disease has also been reported in some cats with concurrent cardiomyopathy. Initially, atrial myocardial destruction leading to atrial standstill and an AV nodal escape rhythm is noted. Mitral regurgitation that may be severe is often seen at this stage. Eventually, myocardial failure may ensue. Clinical signs are similar to those in animals with DCM, with right or left heart failure being noted. Pacemaker implantation may improve heart rate and cardiac output. Other treatment aims to relieve signs of CHF. This treatment typically is ultimately unrewarding, similar to treatment results in other animals with myocardial failure.
Doxorubicin is a common chemotherapeutic agent that causes well-recognized cardiotoxicity. Cardiotoxicity tends to be dose dependent, but rare patients show toxicity at far lower dosages than others. Abnormalities include isolated ventricular premature complexes (which develop in 80% of dogs administered 80 mg/m2/day for 2 days or 25 mg/m2/wk for 4–11 wk) and periods of ventricular tachycardia. Myocardial failure may also develop and has been documented in 100% of dogs experimentally administered 25 mg/m2/wk for 20 wk. (Sudden death and heart failure were noted in 65% of dogs after administration of ~17 wk of therapy.) The cardiotoxic effects are irreversible. Severe cardiotoxicity is rare with current chemotherapeutic protocols but depends on how aggressive the chemotherapeutic protocol is.
Endocardial fibroelastosis,a disease of unknown cause, is characterized by diffuse thickening of the left atrial, left ventricular, and/or mitral valve endocardium. It is a rare cause of myocardial failure in young dogs and cats. Affected animals are usually <6 mo old and present with clinical signs of left heart failure. Breeds reported include Labrador Retrievers, Great Danes, English Bulldogs, Springer Spaniels, Boxers, Pit Bulls, and Siamese and Burmese cats (in which the disease is believed to be inherited). Echocardiography demonstrates dilation of the left ventricular and atrial chambers, decreased left ventricular fractional shortening due to an increased left ventricular end-systolic diameter, and possibly diffuse endocardial thickening. Clinical signs, treatment, and prognosis are similar to those of DCM.
Duchenne cardiomyopathy is an inherited, X-linked neuromuscular disorder reported in dogs, particularly Golden Retrievers. A similar disease called X-linked muscular dystrophy has been reported in Irish Terriers, Samoyeds, and Rottweilers. These diseases may result in myocardial as well as neuromuscular disease. ECG abnormalities include deep and narrow Q waves, a shortened PR interval, sinus arrest, and ventricular tachyarrhythmias. Echocardiography may demonstrate focal hyperechoic lesions affecting primarily the left ventricular and papillary muscle myocardium. This usually develops by 6–7 mo of age, with the lesions decreasing in size throughout the next 2 yr. The lesions result from calcification and fibrosis. In animals that survive, myocardial failure may develop.
Infection of the endocardium typically involves one of the cardiac valves, although mural endocarditis may occur. Endothelial damage is a predisposing factor for infective endocarditis to develop, although in dogs it is most common for endocarditis to form on a normal valve. When the endothelium is partially eroded and underlying collagen exposed, platelets adhere and produce a microthrombus. Immune deficiency may also be a predisposing factor. Bloodborne bacteria may become enmeshed in this thrombic lattice, resulting in a localized infection that causes a progressive destruction of the valve and results in valvular insufficiency. Vegetative lesions are the most common finding on cardiac valves and can create valvular stenosis (eg, aortic stenosis) but more commonly produce valvular insufficiency. In dogs, horses, and cats, the aortic and mitral valves are most commonly affected. The tricuspid valve is rarely affected, and pulmonic valve infective endocarditis is exceedingly rare. In contrast, the tricuspid valve is the most commonly affected valve in cattle. Infective endocarditis is rare in cats, and there are no breed predilections. In dogs, middle-aged, large-breed dogs are predisposed; <10% of dogs diagnosed with infective endocarditis weigh <15 kg. Most affected dogs are >4 yr old, and males are more commonly affected than females. Dogs with subaortic stenosis are at greater risk of developing infective endocarditis.
Infected thrombi released from the infected aortic or mitral valves enter the systemic circulation and can embolize other organs and limbs; therefore, infective endocarditis can produce a wide spectrum of clinical signs, including primary cardiovascular effects or signs related to the nervous system, GI tract, urogenital system, or joints. A chronic, intermittent or continuous fever is usually present. Shifting leg lameness may be reported, and weight loss and lethargy are frequently present. Acute to subacute mitral or aortic valve regurgitation can result in left heart failure (ie, pulmonary edema) and clinical signs of tachypnea, dyspnea, and cough. If the tricuspid valve is affected, ascites and jugular pulsations may be present. Mastitis and decreased milk production can be noted in affected cattle. Hematuria and pyuria may also be noted. A cardiac murmur is present in most cases; the exact type depends on the valve involved. When the aortic valve is affected, a low-intensity diastolic heart murmur is present, with maximal intensity over the left cardiac base. A soft systolic heart murmur caused by increased stroke volume may also be noted. In this instance, the arterial pulse is bounding (ie, increased pulse pressure) due to diastolic run-off and increased stroke volume. Mitral valve endocarditis results in a heart murmur similar to that caused by degenerative valve disease—a low- to high-intensity systolic heart murmur heard best over the left cardiac apex.
Bacteria most often isolated from affected dogs and cats include Streptococcus, Staphylococcus, Klebsiella spp, and Escherichia coli, although a host of other bacterial species may be involved. Bartonella is also a recognized cause of aortic valve infective endocarditis in dogs. In people, 60%–80% of patients with infective endocarditis have a predisposing cardiac lesion that facilitates bacterial attachment. In dogs, however, infection appears to develop commonly in those with no evidence of valve abnormalities. Streptococcus and Actinobacillus spp are the most common isolates in horses, and Trueperella pyogenes is most commonly cultured from cattle.
A CBC often shows a neutrophilic leukocytosis. Active infection may be associated with the presence of band neutrophils, and chronic infection with a monocytosis (90% of cases in one series). Anemia of chronic disease is frequently present. Serum analysis abnormalities reflect organ involvement secondary to infective emboli and may include increases in liver enzymes, BUN, and creatinine. In animals that develop immune complex glomerulonephritis, significant urinary protein loss and hypoalbuminemia may develop. Blood cultures with antibiotic sensitivity should be obtained in affected animals. It is preferable to draw two or three blood samples, each 1–2 hr apart, in a 24-hr period. Strict aseptic technique is required. However, blood culture results are frequently negative (and are positive in other types of septicemia) and cannot be used alone to make the diagnosis of endocarditis.
Radiography may demonstrate cardiac chamber enlargement, depending on the location and degree of insufficiency of the involved valve. If the aortic or mitral valve is severely affected, there will be left atrial and left ventricular chamber dilation. Evidence of left heart failure may be seen as an increase in interstitial density or, in severe CHF, an alveolar pattern in the pulmonary parenchyma. If the tricuspid or pulmonic valve is affected, right-side chamber enlargement is expected. Echocardiography is the diagnostic test of choice, because blood cultures are positive in only 50%–90% of dogs. The affected valve is usually easily detected—the involved area is hyperechoic (bright), thickened, and often vegetative (ie, looks like a cauliflower). The vegetative lesion may oscillate. Erosive lesions may predominate in some animals. Doppler echocardiography will confirm insufficiency of the valve, and chamber enlargement on the side of the affected valve is expected when significant insufficiency is present. Electrocardiography may demonstrate atrial and ventricular premature complexes. Infrequently, other arrhythmias such as atrial fibrillation or conduction disturbances are found.
Therapy is directed at controlling clinical signs of CHF, resolving any significant arrhythmias, sterilizing the lesion, and eliminating the spread of infection. The heart failure may be severe and intractable if the aortic valve is significantly involved; the prognosis is grave in these cases. The prognosis is much more favorable when infection is mild and limited to one of the AV valves. Controlling heart failure requires the use of diuretics such as furosemide, an ACE inhibitor, and when myocardial failure is present, pimobendan. Initially in dogs, parenteral antibiotics are indicated for 1–2 wk (which may be cost prohibitive), followed by oral antibiotics for at least 6–8 wk. Initial broad-spectrum bactericidal antibiotics (a combination of ampicillin plus gentamicin or enrofloxacin, or cephalothin plus gentamicin) should be used and changed, if needed, based on antibiotic sensitivity studies. Renal function should be monitored when gentamicin is used, because it is nephrotoxic. The prognosis is poor in most dogs. Those that respond to therapy often require longterm medications for heart failure (eg, diuretics, vasodilators, pimobendan) and frequent reevaluations. In large animals, rifampin (5 mg/kg, PO, bid), together with another broad-spectrum antibiotic, has been demonstrated to improve short-term outlook. Aspirin (100 mg/kg/day in ruminants and 17 mg/kg every other day in horses) or heparin (30 U/kg, SC, bid in ruminants and horses) may prevent further thrombus and vegetative growth in large animals.
Antibiotic prophylaxis is indicated in dogs with subaortic stenosis when any type of procedure that can result in significant bacteremia is performed. Routine antibiotic prophylaxis for dental procedures is not warranted with other types of cardiac disease and especially not in dogs with myxomatous mitral valve degeneration, because there is no evidence these dogs are at increased risk of infective endocarditis.
Pericardial disease most commonly causes an accumulation of fluid within the pericardial sac (ie, pericardial effusion). This accumulation can be acute or chronic, but chronic is much more common in veterinary medicine. When the fluid accumulation is severe enough to markedly increase the intrapericardial pressure, cardiac tamponade occurs. Acute cardiac tamponade (eg, due to left atrial rupture or thoracic trauma) primarily results in decreased cardiac filling and an abrupt decrease in cardiac output. Chronic cardiac tamponade primarily increases the diastolic intraventricular pressures. This causes signs of CHF. Right-side diastolic—and so systemic venous and capillary pressure—only have to increase from a normal of 5 mmHg to 10–15 mmHg to produce signs of right heart failure, whereas left-side pressures must increase from a normal of <10 mmHg to >20 mmHg to produce left heart failure. Thus, signs of right heart failure predominate.
Pericardial effusion is a relatively common form of acquired cardiovascular diseases in dogs, is uncommon in cattle, and is rare in horses and cats. In dogs, cases involving middle-aged, predominantly male, large breeds are most frequent. Idiopathic pericarditis and cardiac neoplasia are the most common causes of pericardial effusion in dogs. Hemangiosarcoma and heart base tumors (chemodectoma, ectopic thyroid carcinoma) are the most frequently seen cardiac neoplasms. Mesothelioma is a less common form of pericardial neoplasia. Using echocardiography, hemangiosarcoma is most frequently identified on the right auricle, in the right AV groove, and in the right atrial chamber in dogs. Heart base tumors usually are identified between the aorta and main pulmonary artery. In cats, the most common cardiac neoplasia is lymphoma, but the most common cause of mild pericardial effusion is heart failure. Most cases of pericardial effusion in cats are not severe enough to cause cardiac tamponade. Less common causes of pericardial effusion in dogs are infections (eg, coccidioidomycosis), trauma, left atrial rupture, and CHF. Cattle most often develop pericardial effusion secondary to traumatic reticulopericarditis (see Traumatic Reticuloperitonitis) or cardiac neoplasia (lymphoma). Lymphoma in cattle can also result in valvular insufficiencies. In horses, septic pericarditis and idiopathic pericarditis are most commonly reported.
The severity of clinical signs depends on the rate of pericardial fluid accumulation. In dogs, ascites is by far the most common clinical manifestation. Collapse and vomiting may be seen. The femoral pulse may be weak or decrease on inspiration and increase on expiration (pulses paradoxus). In horses, there is often a history of respiratory tract infection, fever, anorexia, and depression. Physical examination findings, in addition to abdominal distention, include generalized weakness, jugular venous distention, muffled heart sounds, and occasionally a pericardial friction rub. With slow development of pericardial fluid, the pericardial sac is able to stretch or enlarge, and clinical signs of right heart failure may not develop until severe pericardial effusion is present.
CBC, serum chemistry profile, and urinalysis results are usually normal. Mild anemia, neutrophilic leukocytosis, hyperfibrinogenemia, and hyperproteinemia may be seen in horses with septic pericarditis and effusion. In horses with suspected septic pericarditis, culture and sensitivity of the fluid should be performed. In septic pericarditis, there will be a large number of neutrophils, with some being degenerate. Protein content of the fluid will be high, and bacteria may be seen. Cytologic features of idiopathic pericardial effusion in horses are variable, with neutrophils, eosinophils, and macrophages present in variable numbers. Cytologic evaluation of the pericardial fluid usually does not provide a definitive cause for the pericardial effusion in dogs unless an infection is present, which is uncommon. Rarely a tumor (most commonly a hemangiosarcoma) will acutely bleed, producing an effusion with a PCV similar to that of blood.
Radiographs often show an increase in the size of the cardiac silhouette, which often takes on a rounded (globoid) appearance. However, this classic appearance is not always present. If the cause is a cardiac tumor, especially a heart base tumor, the cardiac silhouette may have a bulge at the top of the heart cranial to the carina or at the region of the cranial waist if no or only slight effusion is present. The caudal vena cava may be dilated if cardiac tamponade is present. Pleural effusion may also be present, more commonly if mesothelioma is the cause of the pericardial effusion. The ECG in most cases shows normal sinus rhythm to sinus tachycardia. Occasional atrial premature and ventricular complexes may occur. The height of the R wave is often decreased (<1 mV in dogs), and there may be a pattern of alternating variation in R wave amplitude, referred to as electrical alternans, when there is a large amount of effusion present. This results from the swinging motion of the heart within the fluid-filled pericardial sac. Echocardiography is the most sensitive and specific test for detection of pericardial effusion. A tumor can be visualized in most cases of neoplastic effusion. When cardiac tamponade is present, the walls of the right atrium and right ventricle may collapse in systole or diastole.
Animals with cardiac tamponade require mechanical drainage of the pericardial space (pericardiocentesis) using a catheter. Medical therapy is typically ineffective at reducing pericardial effusion. Diuretics are contraindicated in acute cardiac tamponade because they decrease blood volume and cause a further decrease in cardiac output. Pericardiocentesis in dogs and cats is done by placement of a catheter through the chest wall on the right side, just above the costochondral junction at the fourth to fifth intercostal space. Echocardiography can be used to guide catheter placement at the point where the pericardial sac is closest to the thoracic wall and most distended with fluid, but it is not necessary. Fenestrating the catheter helps prevent blockage. A syringe or extension set with stopcock and syringe (preferred) is attached to the catheter. The system must be closed to air at all times once the chest wall has been penetrated, to avoid creating a pneumothorax. The catheter is passed directly toward the heart while gently aspirating. When the pericardial sac is entered, fluid (usually quite bloody) flows freely into the syringe. The catheter should be carefully advanced over the needle into the pericardial sac. The fluid should be placed either in a glass tube or in a tube containing thrombin to cause clotting if blood from the heart is aspirated; if it does clot, the catheter should be removed from the cardiac chamber it is in. As much fluid as possible should be removed from the sac and a sample submitted for analysis. When performing pericardiocentesis in horses, the left fifth intercostal space should be used to avoid the atria, coronary arteries, and right ventricle. Pericardial lavage, with or without antibiotics, is often performed in horses after pericardiocentesis. Pericardiocentesis is relatively easy to perform in dogs, and serious complications are rare. However, confirming the presence of pericardial effusion by echocardiography is advisable before performing pericardiocentesis.
Parenteral fluids may be given immediately before and after pericardiocentesis. Corticosteroids have not been shown to be beneficial in idiopathic pericarditis (benign pericardial effusion) in dogs, although they have been used with success in horses. Most tumors that cause neoplastic effusion do not respond well to chemotherapy. A heart base tumor can be surgically debulked, but only by a highly skilled surgeon. Rarely, a hemangiosarcoma can be surgically removed if it is confined to the right auricle and no metastatic disease is present. Chemotherapy (eg, adriamycin) might be beneficial in some dogs with hemangiosarcoma, although survival times are generally measured in months.
When idiopathic pericarditis is suspected (ie, no mass visible by echocardiography), the owner should be instructed to carefully monitor the animal for any signs of recurrence. Should this occur, a repeat pericardiocentesis is indicated. A subtotal pericardectomy is generally recommended after the third pericardiocentesis. Heart base tumors only rarely metastasize in dogs, although they can grow to be quite large and may compromise function of surrounding structures. If recurrent pericardial effusion secondary to a heart base tumor is diagnosed, subtotal pericardectomy should be considered. A dog can survive as long as 2 yr after successful subtotal pericardectomy. The prognosis for right atrial hemangiosarcoma is poor to grave. Many dogs have metastasis or micrometastasis (most commonly to the lungs and not visible on radiographs) at the time of diagnosis.
Constrictive and constrictive/effusive pericarditis is rare and primarily seen in dogs. It is thought to be an end result of chronic idiopathic pericarditis. A dog with constrictive pericarditis usually presents with ascites, no murmur, normal heart sounds, normal cardiac silhouette on thoracic radiographs, a positive hepatojugular reflux test, and distended hepatic veins on ultrasound. Diagnosis can be difficult and may require cardiac catheterization. Treatment is surgical. With constrictive/effusive pericarditis, there is still a fluid layer between the pericardial sac and the surface of the heart, so surgical removal of the pericardium is relatively easy. With constrictive pericarditis, the pericardium and epicardium are fused into one fibrous layer that must be painstakingly removed surgically.
Systemic hypertension is an increase in systemic arterial blood pressure. There are two major types of systemic hypertension. Essential hypertension, which is idiopathic (primary) hypertension, is rare (essentially nonexistent) in dogs and cats but common in people. Secondary hypertension results from a specific underlying disease. In dogs, the most common cause of hypertension is renal disease/failure; in cats, the most common causes are renal disease/failure and hyperthyroidism. Hyperadrenocorticism, diabetes mellitus, and pheochromocytoma are other causes of systemic hypertension in dogs.
The diagnosis of systemic hypertension is made by measurement of systemic blood pressure. The most accurate assessment method is direct measurement via arterial puncture, which is impractical in most instances. The next most accurate method (although still often inaccurate) is indirect measurement using a Doppler probe to assess blood flow in an artery (typically the superficial palmar arterial branch of the radial artery) distal to pressure cuff placement (typically on the forelimb). Cuff width should be 30% of the circumference of the forelimb in cats and 40% of the forelimb circumference in dogs. Shaving the hair just proximal to the palmar metacarpal pad for application of the Doppler probe allows for more accurate results. The hindlimb can also be used, in which case the superficial plantar arterial branch of the caudal tibial artery is assessed. The disadvantage of Doppler blood pressure measurement is that only systolic blood pressure is reliably measured. Other methods to measure systemic blood pressure, such as the oscillometric method, are even less accurate than the Doppler method, especially in small dogs and cats. Although indirect blood pressure measurement is less accurate than direct assessment, it can detect acute trends in blood pressure during anesthesia. In conscious animals, normal values vary with patient stress; values higher than expected for a healthy animal often are caused by the stress of examination. With certain exceptions, systolic pressures >180 mmHg are likely to be truly increased in an animal that appears calm, and values >200 mmHg should be strongly considered evidence of systemic hypertension. Because of the inaccuracy of noninvasive blood pressure measurement and the influence that stress has on blood pressure, blood pressure measurements should be done only in dogs and cats that have a disease that causes hypertension or that have a clinical problem referable to systemic hypertension (eg, detached retina). Blood pressure measurement is not a screening tool in veterinary medicine as it is in human medicine, except in patient populations that have a disease that causes systemic hypertension (eg, dogs with renal failure should be screened for systemic hypertension). Even in an animal with a disease that causes hypertension that has an increased blood pressure measurement, documenting end-organ damage (eg, presence of hypertensive retinopathy) is recommended before instituting therapy.
Dogs and cats with severe systemic hypertension often have no clinical signs. Acute blindness is the most common clinical sign. Retinal lesions (eg, retinal hemorrhage, retinal detachment, arterial tortuosity, focal or diffuse retinal edema) were found in 80% of hypertensive cats in one study. Blood tests may demonstrate abnormalities consistent with the cause of hypertension (eg, increased T4 levels in hyperthyroid cats, increased BUN and creatinine in animals with renal failure). Treatment should be initiated in animals with consistently measurable hypertension that are documented to have an underlying cause such as renal disease/failure and evidence of end-organ damage. Systemic hypertension in cats and dogs appears to be due to constriction of systemic arterioles, because only potent systemic arteriolar dilators are reasonably effective to decrease systemic blood pressure to a clinically significant degree. The treatment for cats is amlodipine (0.625–1.25 mg/day, PO). Other drugs, such as enalapril, diltiazem, β-blockers (eg, atenolol), and diuretics (eg, furosemide) are generally ineffective. In dogs, amlodipine (0.2–1 mg/kg/day) and hydralazine (1–3 mg/kg, bid) are the only consistently effective drugs. Some clinicians have had success with prazosin (1–4 mg [total dose], PO, 1–2 times/day) in dogs. Phenoxybenzamine (0.25–2 mg/kg, PO, bid) is expensive but can also be effective in dogs. It is most often used in dogs with a pheochromocytoma but can also be effective in dogs with systemic hypertension due to other causes.
Pulmonary hypertension is increased blood pressure in the pulmonary arterial circulation. Possible causes include increased pulmonary blood flow (eg, ventricular septal defect, patent ductus arteriosus), increased pulmonary vascular resistance due to decreased overall cross-sectional area of the pulmonary vascular bed (such as caused by pulmonary arterial wall hypertrophy, pulmonary thromboembolism, and pulmonary vasoconstriction), or both. Primary pulmonary hypertension is rare in any species other than people. In cattle, the most common cause is hypoxia-induced pulmonary vasoconstriction caused by high altitude (see Bovine High-Mountain Disease). Chronic ingestion of locoweed (Oxytropis and Astragalus spp) or chronic pulmonary disease caused by bronchopneumonia or lungworm infestation can also result in pulmonary hypertension severe enough to result in right heart failure. In horses, pulmonary hypertension may occur secondary to left heart failure. In dogs, pulmonary hypertension most commonly occurs secondary to heartworm disease, pulmonary thromboembolism, severe hypoxemia due to primary pulmonary disease, and left heart failure.
Clinical signs are typically those of right heart failure (ascites, exercise intolerance) and episodic collapse or syncope, usually after exercise or excitement. Physical examination findings may include evidence of ascites in dogs and ventral edema in cattle and horses along with jugular vein distention and pulsation. Definitive diagnosis requires direct measurement of pulmonary arterial pressure (rarely performed), or estimation of pulmonary pressures by Doppler echocardiography (via measuring the velocity of a tricuspid or pulmonary regurgitant jet). Echocardiography may demonstrate flattening of the interventricular septum in systole, right ventricular chamber dilatation and/or free wall thickening, and right atrial enlargement. Treatment is typically unrewarding, and the prognosis is often poor, depending on the cause. In heartworm disease, successful clearance of adult worms from the pulmonary arterial vasculature often results in a reduction in pulmonary artery pressure and resolution of right heart failure. Dogs with a right-to-left shunting PDA can live for several years despite severe pulmonary hypertension if their polycythemia is adequately controlled. Sildenafil (1–3 mg/kg, bid-tid), a phosphodiesterase V inhibitor, is probably the most effective drug to lower pulmonary artery pressure and improve clinical signs in dogs with pulmonary hypertension, but it is expensive. It is primarily warranted in dogs with clinical signs due to pulmonary hypertension, most commonly syncope and right heart failure. In these patient populations, sildenafil often will reduce or stop syncope and allow easier control of ascites. Exercise tolerance may be improved. There is limited experience with tadalafil (1 mg/kg, PO, 1–2 times/day) but, in theory, it should have the same effects. Pimobendan reduces pulmonary artery pressure in dogs with pulmonary hypertension secondary to left heart failure. The best chance for a successful longterm outcome is when the underlying disease can be identified and treated, but this is rare.
Overt intravascular thrombus formation is rare with heart failure in most species other than domestic cats and people. Cats frequently form a thrombus in a severely enlarged left atrium, most commonly in the left auricle. This thrombus then commonly breaks loose and flows into the systemic circulation. Although this occurs most commonly in a cat with a large left atrium due to cardiomyopathy, it can also occur without left atrial enlargement, sometimes even happening in an otherwise healthy cat. In a cat with severe left atrial enlargement, it is assumed that the primary reason the thrombus develops is because of blood flow stasis. Red cells aggregate when blood flow decreases below a critical velocity. When the left atrium enlarges, blood flow velocity decreases (assuming no mitral regurgitation). The area of lowest velocity is the left auricle. In some cats, red cell aggregation can be visualized as so-called spontaneous contrast or "smoke" within the left atrium. In a few cats, both a thrombus and spontaneous contrast can be noted. However, in most cats, the thrombus has already become an embolus by the time an echocardiogram is done.
The site the thromboembolus lodges once it has broken loose from its site of attachment in the left atrium depends on the size of the thrombus and blood flow patterns. A very small thrombus can gain entrance to a coronary artery and cause myocardial infarction. A mid-sized thrombus can exit into a branch coming off the aorta, such as the brachiocephalic trunk (and then most commonly to the right subclavian) or an intestinal branch. Most of these thrombi, however, are large and so cannot exit off any branch of the aorta and end up at the terminal aorta. Here, they occlude aortic flow and release vasoactive amines that shut down collateral circulation. Consequently, they cause acute cessation of blood flow to the hindlimbs. This results in pulselessness (no femoral pulse), pallor (pale or purple foot pads), poikilothermia (decreased rectal temperature and cold hindlimbs), and initially extreme pain. The gastrocnemius muscles are often very firm. The cat can often move the legs above the stifles, and the tail is commonly unaffected. In some cats, only one hindlimb is affected.
Diagnosis is most commonly based on clinical signs, physical examination findings, and Doppler blood flow readings of the hindlimbs. Ultrasound can also be used to identify the thromboembolus. Misdiagnosis of neurologic abnormalities as an arterial thromboembolus in cats is common. In some cats, the clot will lyse on its own over time (1–72 hours). However, some of these cats have residual problems (eg, dry gangrene). Numerous treatments, including surgery, thrombolytic agents, and rheolytic thrombectomy, have been tried but are largely unsuccessful when compared with waiting for the thromboembolus to lyse on its own. Euthanasia is common. Clopidogrel (18.75 mg/day/cat) has been shown to be effective at preventing recurrence of these events in cats and so is assumed to be effective at preventing first occurrence also; however, it is, by no means, 100% effective. Aspirin is believed to be ineffective.
* This is the Veterinary Version. *