Feline cardiovascular diseases: parts 1, 2, 3 (Proceedings)


Cardiovascular (CV) diseases in cats include congenital malformations, acquired heart, and vascular disorders. Myocardial disorders or cardiomyopathies, the major cause of heart failure, thromboembolism, and persistent arrhythmias in cats, constitute the focus of this presentation.

Cardiovascular (CV) diseases in cats include congenital malformations, acquired heart, and vascular disorders. Myocardial disorders or cardiomyopathies, the major cause of heart failure, thromboembolism, and persistent arrhythmias in cats, constitute the focus of this presentation. The clinical signs, diagnostic evaluation, complications, and management strategies pertinent to these disorders overlap considerably. Accordingly, an overview of feline heart muscle diseases is presented followed by general recommendations for diagnostic testing. Next, some of the unique features of specific myocardial diseases are addressed. Finally, specific therapeutic approaches are presented for the syndromes of acute and chronic congestive heart failure; the prevention and management of arterial thromboembolism; and the control of heart rhythm disturbances.

Overview of feline CV diseases

Genetic and idiopathic myocardial diseases are often termed 'primary' cardiomyopathies. These include hypertrophic, dilated, restrictive, right ventricular, and unclassified cardiomyopathies, as well as myocarditis. Myocardial infarction is a poorly characterized disorder in cats that causes regional or global ventricular dysfunction. Of these conditions, hypertrophic cardiomyopathy (HCM) is most common.

Secondary myocardial diseases develop from defined disorders such as systemic hypertension, hyperthyroidism, taurine deficiency, and growth hormone excess (acromegaly). Echocardiographic findings do overlap between primary and secondary myocardial disorders, however, these conditions should be distinguished as patient management and long-term prognoses can differ.

Other causes of feline heart disease must be considered in the differential diagnosis of feline cardiomyopathies. Congenital malformations of the heart and great vessels are observed regularly in cats. Mitral valve malformation, ventricular septal defects, and atrial septal defects are encountered most often, but other lesions, including peritoneopericardial diaphragmatic hernia and patent ductus arteriosus must be considered. Although cardiac malformations usually are considered problems of kittens and young cats, these defects may go unrecognized until maturity.

Moderate to severe anemia is an under-recognized reason for cardiac enlargement. Cats with diabetes mellitus may exhibit myocardial heart disease, in some cases related to growth hormone excess. Additionally, severe respiratory diseases in cats can induce pulmonary hypertension and cor pulmonale, sometimes resulting in marked enlargement of the right heart. In contrast to other species, both degenerative valvular disease and infective endocarditis are very rare in cats. Pericardial effusions in cats are generally caused by congestive heart failure (CHF) and often resolve with effective treatment of the underlying condition. Moderate to severe anemia is an under-recognized reason for cardiac enlargement. Cats with diabetes mellitus may myocardial heart disease, in some cases related to growth hormone excess.

Cardiac rhythm disturbances requiring treatment seem less common in cats when compared to dogs. However, atrial and ventricular ectopic rhythms do develop in association with cardiomyopathies, cardiomegaly, myocardial fibrosis, myocarditis, ischemia, infarction, increased sympathetic activity, electrolyte disturbances, hyperthyroidism, and cardiac or systemic neoplasia. Some persistent rhythm disturbances, including atrial fibrillation, can be idiopathic in cats. Atrioventricular blocks are observed most often in older cats.

In terms of vascular disorders, idiopathic aortic dilatation, systemic hypertension, and arterial thromboembolism (ATE) are common diseases of mature cats. Idiopathic aortic dilatation (aortoannular ectasia) is a seemingly benign disorder often observed in middle-aged and older cats. Whether or not aortic stiffness is altered in this disease, or whether this vascular change contributes to systolic hypertension, has not been studied. This lesion is frequently associated with subaortic septal hypertrophy and a systolic murmur, clinical findings that can create confusion about the underlying cardiac diagnosis. Systemic hypertension is a common cause of LV hypertrophy as well as cardiac murmurs in cats; it rarely advances to CHF or aortic rupture. When blood pressure (BP) is severely elevated, retinal detachments and hemorrhages, renal injury, CNS depression, and hemorrhagic stroke are more common outcomes.

Understanding different types of feline cardiomyopathies

The morphologic and functional characteristics, as well as the underlying etiology and severity of a cardiomyopathy, determine the classification, specific clinical findings, prognosis, and management of a particular myocardial disorder. The general clinical approach to feline cardiomyopathies is summarized later, as principles of management. This section reviews characteristic features of specific cardiomyopathies.

Hypertrophic cardiomyopathy

Feline HCM is characterized by thickening of the left ventricular walls and papillary muscles unexplained by congenital disease, hypertension, or endocrinopathy. Considering the prominence of HCM in the feline population and prevalence in certain breeds, it is not surprising that genetic mutations have been identified in some affected cats (including a mutation of myosin binding protein C). Some limited genetic testing is available currently; but this is mainly of value to breeders. Male cats are predisposed to HCM in some studies; however, there is no reported evidence of a sex-linked mode of inheritance. Specific breeds at risk for HCM include the Maine coon, Persian, Ragdoll, Bengal, American and British short-hair cats, and Norwegian Forest cat.

The variable pattern of ventricular hypertrophy in this disease, ranging from concentric to focal (segmental) thickening, can be demonstrated at necropsy or by 2D echocardiography. The pattern of segmental or regional hypertrophy can influence the prognosis. For example, asymmetric free wall hypertrophy is often associated with significant LV dysfunction and progressive left atrial (LA) dilation. Conversely, focal subaortic, focal mid-septal, or isolated papillary muscle hypertrophy are often well-tolerated forms of HCM. However, these lesions progress in some cats and thus warrant follow-up. A specific variant of HCM in older cats is a subaortic septal thickening associated with a dilated aorta. Whether this is a genetic HCM, or a degenerative aortic dilation (aortoannular ectasia) in which altered flow stimulates focal hypertrophy is undetermined. In most cases, this form is benign.

The key histologic findings of HCM are hypertrophy of cardiomyocytes with fiber disarray and interstitial fibrosis. Intramural coronary arteries are narrowed with foci of myocardial infarctions or replacement fibrosis observed. Some cats with HCM progress to a form of RCM or a type of DCM termed "burned out HCM". In each of these conditions, extensive myocardial fibrosis is evident histologically.

Systolic ventricular function in most cats with HCM is normal to hyperdynamic, but there can be regional or focal reductions that may require advanced echo studies to identify. When HCM evolves to a "burned out" form, the entire ventricle may be dilated and hypokinetic. RCM with severe biatrial dilatation also can evolve as a late phase of HCM. Should atrial fibrillation develop, ventricular function is further impaired and this can precipitate severe CHF or ATE.

Dynamic and labile pressure gradients between the LV and aorta are found frequently and confer the title of "obstructive" to HCM. These gradients stem from the combinations of septal and papillary muscle hypertrophy and systolic anterior motion (SAM) of the mitral valve. The latter is likely related to abnormalities of the papillary muscles or the valve itself. The major differential diagnosis is a primary mitral valve malformation.

The presumptive cause of CHF in feline HCM is diastolic LV dysfunction, which means that elevated left atrial and venous pressures are required to fill the ventricle. These abnormalities (discussed in the previous section) can be documented by advanced Doppler studies and generally evolve gradually, often over years. However, sudden sympathetic stress or abrupt impairment of myocardial perfusion can lead to rapidly-developing or "flash" pulmonary edema in cats with HCM with a need for emergent treatment. In some cases, diastolic function seems to improve with elimination of the stress, allowing a reduction in therapy over time.

Most cats with HCM are asymptomatic and recognized when a heart murmur or gallop sound is discovered during a routine examination. As described previously, there are no unique clinical findings of HCM, and symptomatic cats can present with any combination signs. Similarly, other than the echocardiographic examination (or results of genetic testing), ECG, clinical laboratory, and ancillary studies do not sufficiently distinguish HCM from other forms of cardiomyopathy. Thus, a careful clinical workup including high quality cardiac ultrasound is required for definitive diagnosis. LV hypertrophy, including papillary muscle thickening, is the requirement for diagnosis. The presence of significant SAM is invariably associated with an eccentric jet of mitral regurgitation (MR), and may represent an indication for beta-adrenergic blockade. Intraventricular or midcavitary obstructions often develop between the ventricular septum and papillary muscles and can be identified by Doppler studies.

Early diastolic dysfunction for the clinician is heralded by an atrial (S4) gallop. Progressive disease leads to decreased LV compliance, high venous pressures, a loud ventricular (S3) or summation gallop, and CHF. Progressive atrial dilatation and dysfunction go hand and hand with progressive loss of ventricular function. Thus, atrial size as observed by echocardiography or thoracic radiography stands as one of the best indicators of disease severity and short-term prognosis.

The natural history of feline HCM can be benign or lethal; brief or protracted; and some cats remain asymptomatic for many years before succumbing (if ever) to the disease. As in human patients with HCM, the vast majority of affected cats do not develop overt clinical signs. Even severely affected cats may be asymptomatic when diagnosed. However, cats with diffuse or regionally severe disease are at high risk for complications, and some cats with mild disease will experience bouts of thromboembolism. When clinical signs do develop, these are explained by left-sided CHF, complications of ATE, outflow tract obstruction, or arrhythmias. The latter can cause syncope or sudden cardiac death. Therapy is discussed below.

Restrictive (unclassified) cardiomyopathy

Feline RCM represents a heterogeneous disorder, and some latitude is used in placing cats within this group as opposed to the "unclassified" category of feline cardiomyopathy. discussed below. The key pathologic feature of RCM is myocardial fibrosis of uncertain pathogenesis. Antecedent myocarditis may be a cause, but in some cats RCM clearly represents a late stage of HCM. Burmese cats may have a predisposition to this disorder.

Post-mortem lesions in cats with clinical features of RCM are dominated by fibrosis that may be patchy, multifocal, or diffuse. The LV cavity is generally normal to reduced in size with variable but generally unimpressive hypertrophy, sometimes interspersed with regions of thinning or overt infarction. The latter changes are most evident in the LV free wall or apex. Prominent endocardial or papillary muscle fibrosis may be evident with extreme endocardial fibrotic scarring in some cases. Large moderator bands may be observed (and are classified by some as a congenital malformation or a separate form of cardiomyopathy). A consistent feature of RCM is striking left atrial or biatrial dilation. Histologic lesions include endocardial thickening, endomyocardial fibrosis, myocardial interstitial fibrosis, myocyte hypertrophy, focal myocytolysis and necrosis and arteriosclerosis. Systemic thromboemboli are common and LA and ventricular mural thrombi may be observed.

The clinical pathophysiology of RCM is compatible with a combined diastolic and systolic dysfunction syndrome. Increases of venous and atrial pressures, combined with ventricular dysfunction, atrial stiffness, and renal sodium retention, lead to CHF. Most cats with RCM are presented with overt clinical signs caused by CHF or ATE. Murmurs may not be evident, but loud gallop sounds are the rule, often punctuated by heart rhythm disturbances. The ECG is typically abnormal with wide P-waves, ventricular conduction disturbances, and ectopic complexes common.

Echocardiography and Doppler studies generally demonstrate the following: mild systolic dysfunction; regional LV wall dysfunction; mild mitral or tricuspid valvular insufficiency; elevated LA pressures; and impaired LV distensibility with a "restrictive" filling pattern. Pulmonary edema, pleural effusion, jugular venous distention, and hepatic congestion are commonly identified through physical examination and diagnostic imaging. The ECG is often abnormal and atrial and ventricular rhythm disturbances may be observed. Stasis of blood in a dilated left atrium places affected cats at high risk for atrial thrombi and ATE.

Management of RCM is based on control of CHF and prevention or treatment of ATE as discussed below. In cats with atrial fibrillation, diltiazem may provide the best control of ventricular heart rate. In the odd case that is diagnosed prior to onset of CHF, empirical use of an ACE-inhibitor and anti-platelet drug seems warranted. Treatment of these disorders is considered at the end of these notes.

Dilated Cardiomyopathy

This disorder is uncommon today. Taurine deficiency can cause DCM in cats, and this is still observed in cats eating off-brand or some "natural" diets, but most cases are idiopathic or related to diffuse myocarditis. The main postmortem lesions of DCM are left-sided or four-chamber dilatation, generally with necropsy findings of CHF and with no demonstrable congenital, coronary, or valvular heart disease. Histological findings include myocyte loss, prominent interstitial fibrosis, and variable degrees of hypertrophy and myocytolysis or apoptosis. Some cases are characterized by diffuse myocarditis.

The clinical features of DCM in cats are indistinguishable from those of other cardiomyopathies. Heart sounds may be soft owing to impaired contractility or pleural effusion. The principle functional disturbance as shown by echocardiography is marked reduction of LV ejection and shortening fractions, often with mitral and tricuspid regurgitation caused by ventricular dilation and dysfunction. While some cats are detected in the asymptomatic phase, cardiogenic shock, left-sided CHF, or biventricular CHF are the most common presentations. These may be complicated by ATE. Prognosis is poor unless the condition is related to taurine deficiency. Oral taurine supplementation should be administered while awaiting results of a blood taurine test or at a minimum for 2 to 3 months following diagnosis. Management is discussed below.

Right ventricular cardiomyopathy

This condition, sometimes referred to as arrhythmogenic right ventricular cardiomyopathy, has been observed in cats, and the necropsy features have been described (Fox et al, 2000). The right ventricle is replaced by fat and fibrous tissue with the consequences of right-sided myocardial failure and right-sided dilatation with tricuspid regurgitation. Right Ventricular Cardiomyopathy is characterized in most cases by right sided CHF. Atrial standstill or atrial fibrillation may be apparent on the ECG. Ventricular ectopic rhythms are common as well. These cats generally present for clinical signs of pleural effusion, sometimes with concurrent ascites, owing to right-sided CHF. Chylothorax may be evident. Sudden death can occur. Early cases may demonstrate only atrial or ventricular arrhythmias. Diagnosis hinges on echocardiography and exclusion of other predominately right-sided diseases such as atrial septal defect and cor pulmonale. Treatment involves control of CHF and possibly antiarrhythmic therapy (see below).

Other Acquired Myocardial Diseases

A number of other cardiomyopathies are encountered in cats. Some of the key features of these are summarized below.

Unclassified cardiomyopathy

The term "Unclassified Cardiomyopathy" describes a myocardial disease of unknown etiology that does not readily fit into one of the above categorizations. Findings of RCM and UCM are often very similar, and undoubtedly, what one cardiologist might call RCM is classified as UCM by another. Myocardial infarctions and primary atrial diseases may also lead to this diagnosis. Assessment and management of the patient with unclassified cardiomyopathy can be "simplified" by describing completely the clinical, imaging, ECG, and biochemical findings evident in the patient and then directing treatments towards managing these abnormalities. Practically, most cases of unclassified cardiomyopathy present with CHF or ATE and are treated for these problems (see below).

Nonsuppurative myocarditis occurs sporadically in cats. The cause is unknown and definitive diagnosis requires microscopic examination of the tissues. There is a tendency for cats with myocarditis to be young. Some are presented for ventricular arrhythmias, while others develop fulminant heart failure, ATE or RCM. Death during anesthesia is another common scenario. The clinical diagnosis is based on suspicion and exclusion of other diseases. Blood cTnI is generally elevated, but this is not a specific finding for myocarditis, and there is no "gold standard" short of myocardial histology to confirm the diagnosis. Myocarditis can also be associated with infectious diseases including toxoplasmosis, so this should be a consideration before anti-inflammatory therapies are considered. No therapies have been shown to be effective in treating myocarditis and patient management is generally supportive, related to identifiable clinical problems.

Hyperthyroid heart disease

Thyrotoxicosis causes cardiac hypertrophy related to a hypermetabolic state, peripheral vasodilation, and increased demands for cardiac output. Increased sympathetic nervous system activity and elevated thyroid hormone levels may stimulate myocardial hypertrophy. In chronic cases of hyperthyroidism, the LV becomes thickened, and concurrent systemic hypertension probably contributes to this in many cases. Echocardiography typically shows LV hypertrophy, often indistinguishable from idiopathic HCM. In advanced cases associated with fluid retention there may be bi-atrial dilatation with normal or even reduced LV ejection fraction. These cats are at risk for CHF which is often precipitated by the administration of sodium containing fluids.

Clinical findings in feline cardiomypathies

Risk Factors

There are clearly breed risks for development of HCM, as discussed further in the section on specific feline cardiomyopathies. Cats of any age can be affected with HCM, including cats less than one year of age. This means HCM, as well as congenital heart defects, should be considered in the differential diagnosis of structural heart disease in young cats. Myocarditis can affect feline patients of any age, especially immature cats. Older cats are more likely to manifest a form of restrictive cardiomyopathy (RCM) or some type of unclassified cardiomyopathy (UCM). This is also true of the secondary cardiomyopathies, considering the older population is prone to hyperthyroidism, systemic hypertension, and diabetes mellitus.

Stress, fever, moderate-to-severe anemia, thyrotoxicosis, anesthesia, surgical procedures, trauma, or fluid therapy may precipitate CHF or ATE in a previously s cat with cardiomyopathy. Prior therapy with long-acting corticosteroids is considered another risk factor for development of CHF; however, the underlying mechanisms for this association are unresolved.

Medical History

The history of most cats with HCM reveals no historical signs of heart disease. Conversely, heart failure and ATE are common initial signs associated with a diagnosis of RCM, UCM, and dilated cardiomyopathy (DCM). Depression or reduced activity is observed in some cats with CV disease. Diet is not believed to play an important role with the exception of now-rare cases of taurine deficiency DCM. This situation is most often observed in home-restricted cats fed non-commercial or "custom" diets.

Cats with secondary cardiomyopathies are often more affected by the underlying disorder than any CV complications. For example, cats with moderate to severe systemic hypertension often demonstrate clinical signs related to target organ injury and to metabolic derangements of renal failure. Constitutional and extracardiac signs also may be evident when heart disease is caused by hyperthyroidism or anemia.

With the onset of congestive heart failure (CHF), respiratory signs consequent to pulmonary edema or pleural effusion can become evident. Some cats with heart disease cough, but this is a less common sign when compared to dogs. Chronic coughing in a cat with cardiomegaly is more likely to represent bronchopulmonary (or heartworm) disease with cor pulmonale rather than left-sided CHF.

Urgent presentation to the veterinary hospital is likely following a bout of ATE owing to the acute onset of pain and paresis in the affected limbs. Syncope is another distressing sign that may prompt an emergency visit. In cats syncope is commonly mistaken for a seizure disorder. Syncope and sudden cardiac death can occur with cardiomyopathy, myocarditis, or primary heart rhythm disturbances. The differential diagnosis of syncope in cats includes ventricular tachycardia; intermittent complete AV block with asystole; severe LV outflow tract obstruction related to HCM or mitral dysplasia; and rhythm disturbance due to myocardial infarction. Sudden cardiac death can occur consequent to one of these rhythm disturbances. Some cats are reported to die "suddenly" when the actual cause was hypoxia or shock from unappreciated CHF. Cerebrovascular complications of ATE or systemic hypertension are probably under-recognized, and include altered mental status, syncope, postural changes, seizures, or stroke.

Physical Examination

The examination findings of feline cardiomyopathies vary widely. Many cats are seemingly healthy. Cardiac, vascular, and respiratory problems are most often identified in cats with symptomatic cardiomyopathies; however, clinical findings referable to other organ systems may be evident. Often heart disease is discovered serendipitously following cardiac auscultation or thoracic radiography. Identification of a murmur, gallop sound, arrhythmia, or cardiomegaly usually prompts further investigation. The clinician must be mindful that secondary cardiomyopathies develop from other diseases, including hypertension and that other organ systems may be affected. Thus, a thorough physical examination and an open mind are critical to accurate and efficient diagnosis.

Auscultation - Auscultation of cats with cardiomyopathy often reveals an extra diastolic sound or gallop. Gallops are indicators of impaired ventricular filling. The atrial (S4) gallop is generally a sign of mild to moderate diastolic dysfunction, representing a transient increase in atrial pressure compensating for impaired ventricular relaxation. Some older cats develop atrial gallops unassociated with cardiomyopathy, but perhaps indicating an "aging" ventricle. The ventricular (S3) or summation (S3 + S4) gallop is more ominous and generally indicates advanced diastolic heart failure with a noncompliant ventricle and elevated venous pressures. It is very difficult to distinguish atrial from ventricular gallops in cats owing to the rapid heart rates typical of this species. Sometimes gentle pressure on the nasal planum for about 5 seconds will induce a transient slowing of the heart, and this vagal maneuver may help an astute examiner better determine the timing of the extra sound.

To state it clearly: it is very difficult to distinguish functional (innocent) murmurs from murmurs due to cardiac disease. Both are very common in cats and these murmurs can sound very similar. The genesis of heart murmurs can be difficult to sort out, even when a consistent examination approach is undertaken. Heightened sympathetic tone, peripheral vasodilation, or altered blood viscosity, are important causes of physiological murmurs. These situations can develop in thyrotoxicosis, anemia, fever, volume depletion, following sedatives (ketamine), and during the fright of a veterinary hospital visit. One interesting source of functional murmurs often observed by colour Doppler echocardiography is hyperdynamic contraction of the right ventricle leading to obstruction to flow in the proximal right ventricular outflow tract.

Importantly, organic murmurs in cats (i.e., murmurs due to structural disease) are usually related to a form of cardiomyopathy or to a heart malformation, as opposed to degenerative valve disease. Another potential source for a systolic murmur is ejection of blood into a dilated aorta, a common finding in older cats. Systolic murmurs in cats often involve dynamic obstruction in the mid-ventricle from hypertrophied muscle or in the outflow tract obstruction stemming from mitral–septal contact. Hyperdynamic contraction due to heightened sympathetic tone can create turbulence in either the left or right ventricle and can develop in either a structurally-normal or hypertrophied chamber. Thus, murmurs that increase in intensity with sympathetic stimulation (as indicated by a higher heart rate) can be functional or organic.

The examiner will find that almost every murmur in a cat is systolic in timing. Diastolic murmurs are rare, generally due to severe aortic root dilation and aortic regurgitation or infective endocarditis. Continuous (or "long-systolic") murmurs may be identified cranially in cats with patent ductus arteriosus. In the author's experience, it is not helpful to designate valve areas for auscultation in cats; instead, most systolic murmurs are characterized by their location relative to the sternum and palpable cardiac impulse. As a gross generality, murmurs loudest at the apex (caudal heart border) are more likely to be caused by mitral regurgitation (MR) from cardiomyopathy or valve malformation. In contrast, murmurs more intense at the cranial right sternal edge are suggestive of a ventricular septal defect, functional murmur, or turbulent flow into the ascending aorta. Murmurs stemming from LV obstruction tend to be loud at either location. These observations are guidelines at best and have not been tested critically in blinded auscultation-echocardiographic studies. When murmurs are loud, the vibrations can transmit widely, adding ambiguity to the diagnosis.

Diagnostic screening examinations are useful in assessing the cause of a heart murmur; however, overall the precise sensitivity and specificity of these studies has been poorly characterized with the possible exception of the prohormone of N-terminal brain natriuretic peptide (NT-pBNP). An emerging literature suggests that the NT-pBNP may be a cost-effective screening tool for excluding important structural heart disease in many cats with heart murmurs. While some studies support the use of serum cardiac troponin-I (cTnI) as a screening test for cardiomyopathy, in the author's experience, too many results fall into a grey zone for this to be consistently helpful in the differential diagnosis of heart murmurs. If all screening examinations are conducted, the likelihood of identifying structural heart disease is high; however, the attendant veterinary costs are similarly great. For this reason, many veterinarians simply advocate obtaining an echocardiogram (with Doppler study) when assessing asymptomatic cats with a heart murmur. As a more practical alternative, the NT-pBNP may gain prominence for separating "normal" from abnormal murmurs, especially if "cut-offs" can be defined.

Auscultation of the heart should be coupled with examination of the respiratory system. Tachypnea or respiratory distress in a cat should prompt keen observation of the pattern of ventilation. Significant findings include the presence of loud airway noises (suggesting large airway obstruction), wheezes or rhonchi (suggesting bronchial disease), crackles (suggesting edema or parenchymal disease), or a pleural fluid line. Distressed cats may require oxygen and sedation along with urgent therapy for upper airway obstruction (intubation), asthma (inhaled or injected bronchodilators), pulmonary edema (diuretics), or pleural effusion (thoracocentesis) before proceeding to radiography or other evaluations.

Pulse Abnormalities – Pulse abnormalities may point to a CV disorder. The jugular venous pulse may be prominent or the veins grossly distended in cats with CHF, cardiac tamponade, cor pulmonale, or circulatory volume overload. The latter situation is commonly observed when a cat with anemia, renal failure, or thyrotoxicosis is administered substantial volumes of sodium-replete fluids. Hyperdynamic arterial pulses are typical of bradycardia (heart block), hyperthyroidism, and anemia. Irregular pulses should be considered abnormal in cats and prompt an ECG to identify premature complexes or periods of atrioventricular block.

Loss of a peripheral arterial pulse in a cat is highly supportive of arterial thromboembolism (ATE). Vascular signs of ATE typically stem from an underlying cardiomyopathy (or myocarditis), although thrombi also can develop with multisystemic disorders including pulmonary malignancies. A thromboembolism usually originates in the left auricle and travels to the terminal aorta. Smaller thrombi may cause myocardial infarction, thrombotic stroke, forelimb monoparesis, renal infarcts, or rarely mesenteric ischemia with severe colic. Diffuse intra-abdominal ischemia also can be caused by a massive aortic thrombosis. Signs related to embolism to a forelimb can be relatively brief in duration (hours). Terminal aortic embolism is generally more severe, and signs may persist for hours to weeks, though many cats recover limb function if given sufficient time and care (see later). The physical diagnosis of terminal aortic embolism is straightforward and characterized by vascular, musculoskeletal, and neurological deficits, and associated laboratory abnormalities. Limb edema is not an early sign of ATE, though it may be observed days after the event as a consequence of severe muscle injury (and predicts a poorer chance for full recovery).

Other Physical Findings – Additional clinical signs are possible in cats with cardiomyopathy. Examination of the ocular fundus should be undertaken in cats with cardiac signs, to screen for hypertensive retinopathy in particular and for retinal degeneration when a diagnosis of DCM has been made. The general examination should consider the cervical region (for thyroid masses); the kidneys (as a risk factor for hypertension or as targets for hypertensive injury or thromboembolic events); and the mucous membranes (for signs of anemia, hypoperfusion, or cyanosis). Hypothermia is often observed in cats with ATE, and when profound, is a poor prognostic factor. The triad of reduced body temperature, heart rate, and blood pressure is highly suggestive of cardiogenic shock, a condition that demands aggressive inotropic therapy (see below). Weight loss is compatible with systemic disease of any origin, but is especially common in hyperthyroidism and chronic kidney disease and in some cats with chronic CHF. Abdominal distension related to hepatomegaly and ascites can develop in cats with cardiomyopathy, but are relatively uncommon except in cats with atrial standstill, primary right-sided heart disease, or atrial fibrillation.

Diagnostic & laboratory studies in feline cardiomypathies

A number of diagnostic tests can be useful in the evaluation of the cat with signs of CV disease or cardiomyopathy. These include indirect arterial blood pressure (BP) measurement, the electrocardiogram (ECG), thoracic radiography, clinical laboratory tests, and echocardiography with Doppler studies.

Blood Pressure

Systemic arterial BP is usually normal in cats with cardiomyopathy unless the cause of myocardial disease is systemic hypertension. The cat with profound CHF or ATE may be hypotensive, with hypothermia and reduced peripheral perfusion. Cardiogenic shock is not specific for any particular form of feline cardiomyopathy, but often suggests an acute event such as a regional infarction or thromboembolism has supervened. Technical details of indirect BP recording are quite important.


The ECG is insensitive as a screening test for cardiomyopathy, and probably has a greater positive than negative predictive value for feline heart disease. In other words, a normal ECG does not exclude a diagnosis of heart disease. Criteria used to identify cardiomegaly patterns in cats are similar to those of dogs qualitatively, but differ in terms of absolute voltages. No specific ECG can discriminate the various forms of cardiomyopathy in cats. Diagnostic criteria used by the author are noted below.

Widened (≥0.4 sec) or tall (≥0.25 mV) P-waves predict the finding of atrial enlargement on echocardiography. In the author's experience, R-waves or S-waves exceeding 0.7 in any frontal plane lead, or a left axis deviation with voltages of >0.7 mV in leads I or aVL are suggestive of LV hypertrophy or left anterior fascicular block. When the any ventricular waveform is ≥ 1 mV, cardiomegaly should be diagnosed by ECG. Right axis deviation or hypertrophy patterns (S-waves in leads I, II, III) and intraventricular conduction disturbances are more common with restrictive, right ventricular, and unclassified cardiomyopathies. Congenital heart defects are also a cause of high voltage or altered electrical axis in cats.

Identification of a suspected heart rhythm disturbance is the principal indication for an ECG in a cat with suspected cardiomyopathy. Since sinus arrhythmia is uncommon in the cat undergoing veterinary examination, an irregular rhythm as well as a heart rate <160 or heart rate >240 should prompt an ECG examination. Persistent or recurrent arrhythmias are relatively uncommon in cats, but seem more common with RCM, myocarditis, and ARVC. Sometimes an arrhythmia will predate the eventual appearance of a structural cardiomyopathy. Hyperthyroidism can lead to premature atrial and ventricular complexes that may improve following antithyroid therapy. Complete atrioventricular block can be overlooked since the typical escape rhythm is relatively fast, often in the 120-130/minute rate. This rhythm is most common in older cats, probably from degeneration of conduction tissues and perhaps exacerbated by myocardial diseases causing left ventricular (LV) concentric hypertrophy.

Thoracic Radiography

Thoracic radiography plays a pivotal role in the differential diagnosis of cough, tachypnea, or respiratory distress. Common diagnostic considerations in feline patients with increased lung density or abnormal thoracic auscultation include pulmonary edema, bronchial disease/asthma, infective bronchopneumonia, atypical pneumonia, pulmonary neoplasia, and in some locales, respiratory parasites. Pleural effusions can stem from CHF, thoracic neoplasia, idiopathic chylothorax, pyothorax, and trauma.

Although results of thoracic radiography can be normal in mild disease, cardiac elongation, apex shifting, and atrial enlargement are observed frequently in advanced cardiomyopathies. However, radiographs cannot distinguish the various forms of cardiomyopathy. Typically cats shift the apex towards the midline with enlargement of the left atrium and ventricle, but this is variable. As with the ECG, there are no specific findings distinguishing the various forms of myocardial disease. With development of CHF, the cardiac silhouette may be further enlarged by a small to moderate pericardial effusion related to untreated CHF.

The radiographic features of CHF include cardiomegaly with evidence of fluid accumulation in the lung, pleural space, or in both locations. Typical cases demonstrate bulging of the left auricle on the dorsoventral projection, along with elongation or widening of the entire silhouette. A prominent pulmonary vascular pattern (involving both lobar veins and arteries) is anticipated. Pulmonary edema may be manifested as an interstitial or alveolar pattern, and may be focal, patchy, or diffuse. There is a tendency in cats towards a more caudoventral distribution of cardiogenic edema as seen on the lateral projections. Pleural effusions are common in both acute CHF and in chronic cases of CHF in cats, and at times can be very large, obscuring the cardiac silhouette.

Routine Clinical Laboratory Tests

A number of blood and other laboratory tests may be useful for evaluating cats with CV disease. A serum biochemistry profile may demonstrate abnormalities related to heart failure, ATE, or an underlying systemic disease. Biomarkers, in particular NT-pBNP and cardiac troponin-I (cTnI), may be released from diseased ventricles, and these are the most commonly-used "biomarkers" in feline cardiomyopathy. Cytologic examination contributes to the differential diagnosis of pleural effusions. Some of the major points are summarized below.

Renal function is often impaired in cats treated for CHF with diuretics and angiotensin converting enzyme (ACE) inhibitors. The serum creatinine and urea nitrogen should be followed whenever dosages are adjusted. Severe azotemia can occur in the setting of suprarenal ATE. Cats with hypertensive heart disease related to chronic kidney disease will often demonstrate azotemia and often hypokalemia, along with an abnormal urinalysis.

The serum creatine kinase, AST, and ALT (of apparent skeletal muscle origin) are often elevated dramatically in ATE. The AST will be significantly higher than ALT when the elevations are related to striated muscle damage. These enzymes also may be helpful in recognizing ATE in a cat with severe but rapidly improving paresis of a forelimb.

Other blood tests are relevant to the cat with cardiomyopathy. Serum thyroxine should be measured in older cats (> 7 years of age) showing any cardiac signs to exclude hyperthyroidism as a potential cause. A complete blood count may demonstrate anemia or evidence of inflammation, conditions that may allow for a functional heart murmur. Heartworm antibody and antigen tests are relevant when a cat lives in, has traveled to, or has relocated from a heartworm-endemic area. Lastly, in cats with DCM, a whole-blood taurine concentration may indicate if the etiology is a dietary deficiency in this amino acid.

A cytologic and biochemical evaluation can be instructive in the differential diagnosis of pleural effusion. Analysis generally reveals a modified transudate in CHF, often with a predominant population of small lymphocytes and mesothelial cells. Chylothorax is another common finding in severe CHF of cats, and can be confirmed by measuring serum versus fluid triglyceride concentrations (the latter is higher). Cats with chylothorax can develop a prominent neutrophilic reaction mixed into a mononuclear cell population, which can be confused with pleuritis.


In the author's opinion, troponin determination (cTnI) is most valuable when applied to evaluation of the cat with one of the following conditions: 1) arrhythmia of unexplained cause; 2) DCM; 3) cardiogenic shock; 4) CHF that is acute in onset; or 5) when myocardial infarction is suspected. Markedly-elevated cTnI in these settings may suggest myocarditis or ischemic heart injury. Echocardiographic evidence of a regional or diffuse wall motion abnormality is also supportive of vascular-induced muscle injury. Sometimes these conditions improve dramatically following a period of medical stabilization, so a marked elevation in serum troponin may influence prognosis and treatment decisions in these cases. The cTnI also may be elevated in asymptomatic HCM; however, too often the results return as equivocal. The NT-pBNP seems to discriminate better between normal and asymptomatic (but affected) cats in this situation.

The NT-pBNP appears to provide the best balance between specificity and sensitivity in the recognition of cardiomyopathies. The proper handling and shipping of the blood sample is critical for obtaining the best results. Specific optimal "cut-offs" for distinguishing healthy cats without cardiomyopathy have been established by reference laboratories. The literature is somewhat misleading as methodologies and reference values may differ. A higher cut-off value, approximately 250 pmol/L in one study, has successfully distinguished cats with respiratory signs caused by CHF from those related to primary respiratory disease. As with any laboratory test, there will be exceptions and ambiguous results, so the clinician must exercise appropriate judgment and integrate all clinical data when interpreting the results of NT-pBNP.


Definitive diagnosis of cardiomyopathy relies on cardiac ultrasound. Two-dimensional (2D) imaging is most important, supported by M-mode and a variety of Doppler studies. Some specific distinguishing features of the important cardiomyopathies are noted in the next section. Some points pertinent to all feline myocardial diseases are summarized in this section.

The 2D study provides information about lesions and cardiac motion, as well as wall thicknesses, chamber sizes, and ventricular systolic function. Left ventricular diastolic wall thickness in most cats is <5.5 mm and most consider 6 mm or more to indicate LV hypertrophy. The "HCM phenotype" is most often related to idiopathic/genetic HCM; however, hyperthyroid heart disease and hypertensive heart disease can also lead to papillary muscle thickening and increased wall thickness. A false positive diagnosis may occur in the setting of diminished LV lumen size caused by diuresis or dehydration or when an inexperienced examiner measures the papillary muscles instead of the free wall. Wall thinning can be generalized in cats with DCM, or segmental in as often observed in regions of infarction. Fibrosis occasionally is evident as a hyperechoic or speckled appearance to the myocardium.

In terms of LV chamber dimensions, the diastolic value measured by the 2D or M-mode exams across the minor axis is generally less than 18 to 19 mm in mature cats, but some healthy larger-breed cats (Maine coon) may exceed this value by 2 or 3 mm. Left heart or generalized cardiac dilatation is most often observed in DCM or in congenital lesions such as mitral dysplasia, ventricular septal defect, or patent ductus arteriosus. However, states predisposing to volume expansion, such as moderate to severe anemia, advanced thyrotoxicosis, or chronic bradycardia can also dilate cardiac chambers. Often one of these underlying conditions is complicated by fluid therapy, and elevated venous pressures create four-chamber dilation. Isolated right heart enlargement is most often observed with (arrhythmogenic) right ventricular cardiomyopathy, atrial septal defect, pulmonic stenosis, or cor pulmonale.

Global LV systolic function is generally in the normal range, with shortening fraction typically 35 to 50%, in cats with most forms of cardiomyopathy; however, there are notable exceptions. Hyperdynamic LV systolic function is common in HCM and in thyrotoxicosis. Reduced global function is a requisite for diagnosis of DCM, and most affected cats have a shortening fraction of <25%. Cats with RCM, UCM, and "burned out" HCM often have reduced systolic function, either globally or regionally. Segmental LV systolic dysfunction is common, especially involving the free wall, and may represent ischemic damage to that myocardium.

In cats with cardiomyopathy of any type, the left atrial size is a strong indicator of disease severity and the risk for ATE or CHF. In the author's practice, left atrial size is an important factor in recommending therapies for otherwise asymptomatic cats (see below). Dilation (measured across the center of the chamber by 2D long-axis imaging) is present when the atrial diameter is ≥16 mm. Moderate and severe left atrial dilation can be defined arbitrarily as ≥20 mm and ≥25 mm, respectively. Equally important are imaging studies of the auricle that define presence or absence of intramural thrombi or echogenic intra-atrial contrast or "smoke". Doppler studies of auricular filling and emptying may help to identify cats at higher risk for thromboembolism with lower values (especially <20 cm/s) indicating a higher chance for blood stagnation and thrombogenesis.

Doppler studies demonstrate the direction, velocity, and patterns of blood flow in the heart and great vessels. Colour flow, pulsed-wave, and continuous wave Doppler are complementary examinations useful for identifying turbulent flow, mitral regurgitation, and intraventricular, and midventricular or outflow tract obstructions. Early detection of cardiomyopathy may be possible with advanced tissue imaging methods, but diagnostic criteria require better definition.

The various patterns and values of ventricular filling, tissue movement, and pulmonary venous flow can be combined to estimate diastolic heart function and ventricular filling pressures. The latter are predictive of CHF in many cats. Mild diastolic dysfunction is characterized by abnormal myocardial relaxation that is compensated by vigorous atrial contraction. Doppler examination is characterized by diminished and delayed early ventricular filling (E-waves) and tissue movements (Ea) with prominent atrial contraction waves (E/A reversal). Other markers of delayed relaxation such as prolonged isovolumetric relaxation time become evident. As the ventricle becomes less compliant and mean atrial pressure increases, these abnormalities "pseudo"-normalize. Progressive ventricular disease is associated with decreased compliance and elevated filling pressures creating high velocity, abbreviated E-waves followed by tiny A-waves. Cardiologists frequently use these Doppler methods to identify the various stages of ventricular diastolic dysfunction and to predict impending CHF.

Management of acquired feline cardiovascular diseases

Most treatments for feline myocardial diseases have evolved empirically. There are no published trial data regarding optimal management of cats with asymptomatic HCM, CHF, ATE, or arrhythmias. The author's empiric choices and recommendations are described below.

Asymptomatic Hypertrophic Cardiomyopathy

The treatment of asymptomatic HCM is controversial. No data indicate a pivotal benefit of beta-blockers, diltiazem, ACE inhibitors, spironolactone, aspirin, or clopidogrel in asymptomatic cats with mild HCM and normal LA size. Neither ACE inhibition (with ramipril) nor inhibition of aldosterone (with spironolactone) altered hypertrophy or estimated volume of fibrosis in controlled studies (MacDonald, et al., 2006 and 2008). Clients should be advised of this information prior to writing prescriptions for long term treatment. While dynamic LV outflow obstruction is a risk factor for sudden death in people with the disease, it is unknown if this is the situation in cats. However, the author does recommend empirical therapy with atenolol in cats with moderate to severe HCM accompanied by LV outflow tract obstruction. Atenolol appears superior to diltiazem for slowing heart rate, reducing dynamic outflow obstruction, and decreasing intensity of murmurs. Beta-blockade also diminishes demand ischemia, prolongs ventricular and coronary filling times, and carries a lower side-effect profile (when compared to diltiazem). Dosing is adjusted based on heart rate, and many cats take "split doses", for example: 12.5 mg in the AM and 6.25 mg in the PM. The ultimate daily dosage (6.25 mg to 12.5 mg PO, twice daily) is determined by the examination room heart rate obtained during stable, chronic therapy with a target of 120 to 160/minute. Beta-blockers are contraindicated in hypotension, bradycardia, thromboembolism, and in CHF of recent onset.

When HCM is characterized by significant LV hypertrophy and moderate left atrial dilation (diameter of ≥20 mm on 2D imaging) experience indicates that the risks of CHF and ATE are greater. In these cats, empiric use of atenolol, or the calcium channel blocker diltiazem, along with an ACE-inhibitor, is suggested. Antiplatelet therapy is also recommended in this group (see the last section for details). Again, in the setting of LV outflow obstruction, atenolol is chosen. When there is no obstruction, some clinicians prefer diltiazem, as this drug may improve myocardial relaxation. Unfortunately, there is a higher adverse effect profile for sustained release diltiazem (including anorexia, weight loss, and skin lesions) than for atenolol. Dosing is also problematic for lack of a simple clinical target (since heart rate response is inconsistent). For this reason, the author infrequently uses this drug, while accepting that other cardiologists prescribe it regularly and there are no major end-point studies (of survival, CHF, or ATE) on which to base an objective treatment decision. The usual daily dosage of diltiazem is 30 mg of a slow-release preparation administered once or twice daily. Twice daily dosing is preferable, but also is associated with higher plasma levels and more potential for side effects. Combining atenolol and diltiazem can cause bradycardia and hypotension and is not recommended. Finally, in asymptomatic cats with moderate LA dilatation the author empirically prescribes enalapril or benazepril (between 0.25 to 0.5 mg/kg PO daily) owing to the higher risk of CHF. Management approaches for the symptomatic cat with CHF, ATE, or arrhythmias related to HCM are discussed in the last section.

Acute Congestive Heart Failure

Management of the cat with acute or severe CHF begins with gentle handling. Thoracocentesis is the treatment of choice for moderate to large pleural effusions. This is most safely done using a small butterfly catheter or needle, with the cat in sternal recumbency and receiving supplemental oxygen by face mask, after sedation. For bilateral pleural effusions it is safest to tap on the right side to avoid puncturing a bulging left auricle.

Cats with pulmonary edema from CHF are managed by the author using the F-O-N-S regimen. Furosemide is administered (2–4 mg/kg IV or IM; repeated in 2 to 4 hours if necessary). Once diuresis occurs and symptoms improve, the dose is reduced to 1-2 mg/kg IV, IM, or SQ q8 to 12h). For life-threatening, poorly-responsive lung edema, initial boluses can be followed by a constant IV infusion of furosemide of 4 to 6 mg/kg given over 24h. Oxygen (40 – 50%) is delivered by cage oxygenator in most cases. Nitroglycerin (2%) ointment is administered for venodilation (¼ inch cutaneously, q12h) for 24 hours with the hope of reducing ventricular preload. Sedation is considered (butorphanol – 0.25 mg/kg IM; this can be mixed with acepromazine – 0.05 mg/kg, provided rectal temperature >100 degrees F and blood pressure >100 mm Hg).

The cat with cardiogenic shock (hypothermia often with bradycardia, systolic BP <70 mm Hg) is treated with passive warming and IV dobutamine infusion for 24 to 48 hours (regardless of type of cardiomyopathy). Dosing is initiated at 2.5 micrograms/kg/minute and increased to a range of 5 to 10 micrograms/kg/min). The final infusion rate targets a rectal temperature of >100° , heart rate >180/minute, and systolic BP >90 mm Hg. The dose is reduced by 50% every 2-3 hours before discontinuing the drug. Furosemide or thoracocentesis are used to treat CHF as appropriate. An ACE-inhibitor is started once BP exceeds 90 mm Hg. Cardiogenic shock carries a very guarded prognosis, but survival exceeding one year occurs in some cats following this aggressive treatment plan along with diligent home care. Other cats succumb from unresponsive CHF.

Chronic Therapy of CHF

The home therapy of chronic CHF provided by cat owners centers on administration of furosemide (usual dosage: 1 to 2 mg/kg, PO once or twice daily), combined with an ACE-inhibitor such as enalapril or benazepril (usual dosage: 0.25 to 0.5 mg/kg, PO once or twice daily). Occasionally furosemide is given subcutaneously on a regular schedule (1 mg/kg SQ once to three times weekly in place of an oral dose) for poorly responsive pulmonary edema or pleural effusion. Spironolactone (6.25 to 12.5 mg, once daily) can be given for possible cardioprotection and potassium sparring effects (beware: anorexia, skin lesions). Neither atenolol nor diltiazem should be administered to cats with recent onset CHF (such therapy was not beneficial in an unpublished multi-center study reported by Fox).

When CHF develops in a cat with HCM receiving chronic atenolol or diltiazem therapy, the daily dosage is reduced by ~50%, but is not stopped unless the cat exhibits cardiogenic shock. In cats with well-defined dynamic LV tract outflow obstruction, cautious up-titration of atenolol may be initiated to reduce the gradient once the cat is completely stable. Alternatively, diltiazem may be added if it is deemed useful for ventricular diastolic function.

Additional treatments may improve CHF in some cats. The extralabel use of the inodilator pimobendan (~0.25 mg/kg PO q12h or 1.25 mg per cat PO q12h) provides an additional treatment approach for cats with chronic CHF. In the author's opinion, pimobendan should be prescribed immediately for cats with CHF due to DCM, RCM, UCM, or right ventricular cardiomyopathy. In contrast, pimobendan is not recommended for the cat with well-defined HCM until CHF becomes progressive or unresponsive to furosemide and an ACE-inhibitor. Today, digoxin is rarely used in cats. Rutin (250 mg q12h) is prescribed when there is chylothorax associated with CHF. Famotidine (2.5 to 5 mg once or twice daily for one to two weeks) represents an empirical treatment for cats with partial anorexia associated with CHF; this drug also can be prescribed long-term.

The overall efficacy of heart failure therapy and quality of life can be gauged using practical means. The client interview should ascertain activity level, resting respiratory rate and depth, appetite, and interaction with the family/housemates/environment. Objective measures of CHF control and adverse drug effects can be obtained through a physical examination, measurement of blood pressure, evaluation of serum chemistries, inspection of thoracic radiographs, and perhaps by echocardiography. The timing of specific examinations depends on clinical circumstances and economic considerations, but initially should occur within the first 7 to 10 days from the first diagnosis of CHF, and continue every one to two weeks until the CHF is controlled and renal function and blood pressure are stable. Thereafter, the interval is extended to every one to three months, depending on the patient's progress. In general, progressive azotemia indicates the effects of diuretics plus an ACE-inhibitor, and when possible, the dosages should be reduced, so long as cat is free of edema or effusions. In some cats with HCM, the heart stabilizes, allowing diuretic therapy to cease. In other cases, there is a clear need to tolerate azotemia to prevent discomforting pleural effusion or pulmonary edema. Life-long therapy is anticipated for most cats with CHF.

Management of Arterial Thromboembolism

Clinical signs of ATE have been discussed previously. The diagnosis is generally straightforward and is supported by markedly elevated serum muscle enzymes. The medial management of an acute thromboembolic event demands high quality critical and nursing care. The client should be advised about the 1) need for intensive therapy (typically 2 to 3 days in the hospital); 2) the risk of ATE recurrence (high); 3) the need for future daily home medical care; 4) the likely presence of underlying cardiomyopathy; 5) the attendant costs of managing the condition; and 6) the potential for sudden death during hospitalization (or thereafter).

Experience and published retrospective reports suggest a 40 to 50% chance for functional limb recovery if treatment is administered. In a retrospective study (Smith et al., 2003) the median survival time was 223 days for cats not presenting in CHF (median survival for those cats was 77 days). It is emphasized that there are no prospective trials of therapy. Retrospective data probably represent less than optimal outcomes since care is not standardized in these observational studies and many cats are euthanatized at admission.

If the client decides to proceed, the first treatment is analgesia with a mu agonist for the first 24–48 hours following an event. While there are no comparative studies of pain control in this condition, fentanyl is most commonly used in our practice and provides good to excellent analgesia. Transdermal therapy is too slow in onset for management of this severe pain and IV administration is needed. Although fentanyl has been administered intravenously to healthy cats at a "slow bolus dose" of between 5 to 10 micrograms/kg, it is suggested to initiate therapy with a lower dose of 3 microgram/kg (very slow IV bolus) and follow that with an intravenous maintenance infusion of 1 to 5 micrograms per kg per hour (not per minute). Morphine (0.1 to 0.2 mg/kg IM or SQ q6h) or buprenorphine (0.005 to 0.01 mg/kg, IM or SQ, q6h) represent other options. Buprenorphine can also provide some analgesia when administered at 0.01 to 0.02 mg/kg (10 to 20 micrograms/kg) on the buccal (oral) mucosa, and it may be useful to dispense one or two doses to client for immediate administration should an ATE occur at home. In the absence of hypothermia or hypotension, acepromazine (0.025 mg/kg subcutaneously) will sedate the cat further. Pain in most cats is markedly diminished by 48 hours, allowing for less aggressive analgesia.

Heparin is administered in the setting of acute ATE to prevent further thrombosis (300 units/kg IV, then 150 to 250 U/kg subcutaneously q8h for 48–72 hours). Some clinicians administer one aspirin dose (~40) when a cat presents within 3 hours of the embolic event.

Passive warming is undertaken, but the limbs should not be burned. Some cats are profoundly hypothermic, and these cats have a poorer prognosis. This finding may indicate shock accompanied by severe metabolic acidosis. Hypotension in the absence of CHF should be treated with fluid therapy initially; when associated with CHF dobutamine at low infusion rates (2.5 micrograms/kg/minute) is preferred. Cats on opiates may pant in a heated environment, creating a situation that can be confused with CHF. This sign will abate once the external environmental temperature is lowered. If true fever occurs following an ATE, IV cefazolin or oral amoxicillin-clavalenic acid are usually effective. The patient should be monitored for potentially fatal hyperkalemia from potassium leaked from necrotic muscles during the first 48 to 72 hours of treatment. Most cats that do improve are better within 72 hours of admission and can be released for home care. There is often asymmetry noted between the limbs. With revascularization, tail function returns and limb function is reinstated from proximal to distal. Reassessment every two to three days is recommended following release until the status of ishcemic tissues is determined.

Home care includes: 1) protecting the limbs; 2) daily inspection for subcutaneous or muscle edema (a poor prognostic sign); 3) cleaning urine-soaked hair and bedding; 4) providing a soft bed; 5) encouragement to eat; and 6) a low stress area for convalescence. Physical therapy of the limbs characterized by passive flexion of the limbs is encouraged. Additional consideration should be given to a soft bandage of a contracted limb (another adverse outcome) to place it in a functional position. If constipation becomes a problem, a small amount of soluble fiber (1/4 teaspoon of guar gum) or some canned pumpkin may be added to food to soften the stool.

Prevention of Thromboembolism

Number of approaches have been advocated for prevention of ATE in cats. These include: 1) aspirin monotherapy (dosed between 5 mg to 81 mg q72h); 2) warfarin (Coumadin® 0.5 mg PO daily); 3) low molecular weight heparins including enoxaparin (Lovenox®, 1 mg/kg) and dalteparin (Fragmin®, 100 IU/kg) injected subcutaneously once or twice daily; or 4) clopidogrel (Plavix®, 75 mg tablets, ¼ tablet – or 18.75 mg – PO once daily). Aside from an ongoing clinical trial evaluating clopidogrel versus aspirin, and a number of retrospective reports indicating apparently-safe dosages of these drugs and effects on in vitro coagulation tests, there are no prospective trial data demonstrating efficacy for any prevention of ATE in cats with cardiomyopathy.

In terms of specific recommendations, the author does not routinely prescribe antithrombotic therapy in asymptomatic cats with a normal or minimally dilated left atrium and auricular emptying velocities >20 to 30 cm/s. Clopidogrel (¼ of a 75 mg tablet) is prescribed for the cat with a moderate (≥20 mm) to severely dilated left atrium, or when auricular emptying velocities are <20 cm/s. Adult-regimen 81 mg aspirin dosed at one tablet PO q72h is an alternative to clopidogrel, but is often ineffective. In cats at high risk for ATE (LA dilation ≥25 mm, echogenic smoke in LA, auricular emptying velocities <20 cm/s, or a history of prior ATE) more aggressive therapy is recommended. The author typically prescribes clopidogrel (¼ of a 75 mg tablet once daily) along with low dose daily aspirin (compounded or "crumbled" to a dose of 5 to 10 mg). The risk of gastric ulceration must be appreciated with these treatments and managed if anorexia, vomiting, or anemia becomes evident. An alternative for cats at high risk of ATE is once or twice-daily administration of a low molecular weight heparin preparation, generally enoxaparin. There is some controversy about the efficacy of this treatment and best manner of monitoring therapy of these heparins in cats. Clinical trials in cats with spontaneous disease are needed to settle the issues. Practically, since the drugs are prohibitively expensive for most clients and require one or two daily injections, the treatment holds a low acceptability to clients. Some clinicians use low molecular weight heparin as a bridge therapy for a few weeks following recovery of aortic ATE. Warfarin therapy is difficult to control in cats and rarely prescribed.

Cardiac Arrhythmias

Heart rhythm disturbances can complicate cardiomyopathies in some cats. Isolated atrial or ventricular premature complexes are not treated. Ventricular tachycardia is managed in hospital with lidocaine (0.5 – 1 mg/kg IV); esmolol (500 micrograms/kg over 5 minutes, followed by 50 to 100 micrograms/kg/min); atenolol (6.25 mg to 12.5 mg PO q12h); or sotalol (1-2 mg/kg PO q12h). Sustained, regular supraventricular tachycardia also may respond to beta blockade, or to IV diltiazem (0.1 mg/kg IV, repeated to a cumulative dosage of 0.5 mg/kg with BP monitoring). The negative inotropic effects of beta-blockers and of diltiazem may limit usage, especially in cats with LV dysfunction of CHF.

Diltiazem is an effective blocker of AV nodal conduction and represents an excellent choice for heart rate control in cats with atrial fibrillation or sustained SVT. Atrial fibrillation is most often – though not always – associated with significant left or right atrial dilatation in cats. Atenolol represents an alternative therapy for heart rate control. Digoxin is rarely used by the author as an antiarrhythmic drug in cats.

Circulatory Volume Overload

Fluid therapy with lactated Ringer's solution, Plasmalyte®, or saline solution in cats with common medical conditions can lead to CV complications that can mimic or precipitate CHF. Conditions likely to lead to volume retention include moderate to severe anemia (PCV <20%), thyrotoxicosis, some forms of chronic renal disease, and possibly glucocorticoid administration. Often these cats receive appropriate crystalloid therapy for their medical disease at one to two times "maintenance" requirements but develop respiratory problems related to volume overload of the circulation. Most of these cats have evidence of cardiac dysfunction on examination.

Clinical examination and diagnostic imaging are useful for diagnosis. Most cats develop tachypnea, jugular venous engorgement, and radiographic evidence of pleural effusion or pulmonary infiltration. Echocardiography typically shows dilated atria (moderate), a prominent right ventricle, and variable changes in the LV related that will be modified by any underlying disease (such as HCM, hypertensive heart disease, or thyrotoxic heart disease). Prompt recognition, diuresis, reduction of fluid administration, and treatment of the underlying disorder will generally resolve the situation.

Hyperthyroid Heart Disease

Management of hyperthyroid heart disease is centered on controlling the endocrine disorder. In cats with compensated heart disease as judged by radiography or echocardiography, no specific heart treatment is required. For severe sinus tachycardia (>280 per minute) or for ectopic atrial or ventricular rhythms, atenolol (6.25 mg PO q12h) can be administered, but this may not be needed if anti-thyroid medications are given. In cats that cannot receive radioactive iodine treatment and cannot tolerate anti-thyroid medications (due to hepatic or renal complications), long-term therapy with atenolol is recommended to mitigate the sympathomimetic effects of hyperthyroidism on the CV system. When volume overload or CHF have developed, beta-blockers should be avoided and management with anti-thyroid medication, low-dose furosemide (5 to 6.25 mg PO once or twice daily) and an ACE-inhibitor with or without additional antihypertensive therapy (amlodipine) is suggested.

Since many cats with this condition are also hypertensive, BP control is important. Hypertension in these cats can be multifactorial: from high cardiac output; aortic stiffness in cats related to aortoannular ectasia; or concurrent renal disease. Atenolol monotherapy is generally insufficient to control hypertension in cats with hyperthyroidism. Furthermore, the clinician should not assume that hypertension will resolve following successful treatment of the endocrine disorder with drugs such as methimazole. When moderate to severe hypertension is evident, treatment with amlodipine (0.625 to 1.25 mg, PO, once or twice daily) is suggested. Atenolol is a reasonable adjunctive therapy in these cats if more control is needed. Benazepril or enalapril may also represent appropriate co-therapy if there is concurrent renal disease. Ventricular changes may improve with effective long-term control of the hyperthyroid state.

Systemic hypertension

The heart, along with the brain, eyes, kidneys, and small arterioles, are the "target organs" for elevated systemic arterial blood pressure (BP). Most healthy cats have systolic BP measurements of <150 to 160 mm Hg in the hospital setting. Persistent elevation of BP, particularly values exceeding 160 to 170 mm Hg in the presence of target organ injury, is highly suggestive of hypertensive disease. While systemic hypertension does stimulate LV hypertrophy, neither CHF nor ATE is a common complication. More often clinical signs of hypertension are referable to the eyes (retinal hemorrhages, detachments), brain (depression, stroke), or kidneys (progressive azotemia). Dissection of the aorta is a rare complication. The cardiac condition most often resembles mild HCM, with a gallop or murmur along detected during examination. Mild cardiac enlargement is often evident by radiography and LV wall hypertrophy may be demonstrated by echocardiography.

The diagnosis of systemic hypertension is usually straightforward, provided attention is paid to technical details. Treatment of underlying disorders including renal, adrenal, or thyroid diseases, is a critical aspect of treating hypertension. LV hypertrophy may regress in part following successful control of blood pressure. The most effective treatment for systemic hypertension in cats is the calcium channel antagonist amlodipine (0.625 to 1.25 mg PO, once or twice daily). Co-therapy with an ACE-inhibitor is often considered when there is intercurrent renal disease. It is stressed that monotherapy with an ACE-inhibitor such as benazapril is inadequate to treat moderate to severe systemic hypertension in cats. If triple therapy is needed for severe hypertension, either a beta-blocker or an alpha-blocker such as prazosin (compounded to a dose of 0.05 to 0.1 mg/kg PO q12h) can be added.

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