Prevalence

The prevalence of cardiac disease in the general feline population is not currently determined. Stalis and coworkers⁸³ found that myopathic heart disease was identified in approximately 9% of 1472 feline necropsies from 1986 to 1992 at the University of Pennsylvania. More recently, two small studies (approximately 200 cats in total) have examined the prevalence of cardiac disease in apparently healthy cats.^18,61 Côté and colleagues¹⁸ examined the prevalence of heart murmurs in apparently healthy cats and detected murmurs in 22 of 103 cats examined. Of these 22 cats, seven had echocardiographic evaluations, and six were considered to have evidence of myocardial hypertrophy (one was normal). Paige and coworkers⁶¹ examined 103 apparently healthy cats: 16 of 103 had murmurs, and five of these had evidence of myocardial hypertrophy. Additionally, 11 of 103 cats had evidence of myocardial hypertrophy but no murmurs.

On the basis of these small epidemiologic studies, approximately 20% of apparently healthy cats examined at random will have cardiac murmurs, and a similar percentage might have myocardial hypertrophy. Of these, half will have murmurs, and half will have occult disease. Similarly, 50% or more of the cats with murmurs will not have identifiable cardiac disease; dynamic physiological murmurs likely account for some of these. It is important to note that both studies examined small numbers of cats. Furthermore, no longitudinal evaluation was performed to determine if the myocardial hypertrophy was transient (e.g., secondary to dehydration, thyroid disease or as yet unidentified causes of transient hypertrophy) or persistent. Only the latter would be consistent with hypertrophic cardiomyopathy. Thus the prevalence of cardiac disease in the general feline population remains unknown. However, a large longitudinal study of cats presenting to shelters in London is currently under way and may better define the prevalence of feline myocardial diseases.

Relative prevalence of cardiac disease has been examined by Harpster³¹ at a single referral institution. Of 500 cats presenting to the cardiology department at Angell Memorial Animal Hospital from 1987 to 1989, 22% had hypertrophic cardiomyopathy, 15% had unclassified cardiomyopathy, 14% had mitral valve disease, 12% had dilated cardiomyopathy, 10% had thyrotoxic heart disease, and approximately 7% had congenital diseases. Systemic hypertension was identified in 1%. It should be obvious that these percentages do not represent true prevalence (or incidence) but rather describe the distribution of heart diseases in patients presenting for evaluation of heart disease. Additionally, substantial changes in feline nutrition (namely taurine supplementation) and early detection and management of hyperthyroidism have greatly reduced the percentage of cats presenting with either dilated cardiomyopathy or thyrotoxic heart disease.

Similarly, the prevalence of congenital cardiac diseases in cats is much less comprehensively reported than that of dogs. Frequency of congenital heart disease has not been examined in the last 30 years. Buchanan¹¹ estimated that atrioventricular valve malformations were the most common congenital defect in cats, followed by ventricular septal defect (VSD), endocardial fibroelastosis and patent ductus arteriosus (PDA).

Côté and Jaeger¹⁷ examined the incidence of structural heart disease in 106 cats presenting with ventricular arrhythmias. Almost all cats with ventricular tachyarrhythmias had echocardiographic evidence of structural heart disease (102 of 106). Prior studies by Fox and associates²⁶ and Fox and Harpster²⁵ suggested substantially lower incidence rates of ventricular tachyarrhythmias in cats with hypertrophic cardiomyopathy (HCM) (10% to 40%). However, both studies reported all arrhythmias in cats with HCM at much higher rates (25% to 70%).

Risk Factors

Certain risk factors are associated with some feline heart disease. HCM has specific breed predispositions, and at least one identified genetic cause in each of two breeds (Maine Coons and Ragdolls).^53,55 Sphynx, Norwegian Forest Cats, American Shorthairs, Scottish Folds, Persians, Siamese, Abyssinians, Himalayans, and Birmans are all breeds considered to be predisposed to cardiomyopathies.²³ Whether there are any gender differences in expression of genetic traits or in prevalence of congenital disorders is not well defined.

Taurine deficiency was identified as a major cause of dilated cardiomyopathy in cats in the mid 1980s.⁶⁴ Subsequent supplementation of commercial diets with taurine has led to the almost complete disappearance of taurine-deficient myocardial failure in cats. However, homemade diets can still occasionally lead to taurine deficiency, resulting in dilated cardiomyopathy.

Hyperthyroidism is a risk factor for cardiac disease in cats. However, the prevalence of thyrotoxic heart disease has likely decreased since hyperthyroidism was first recognized, as clinicians have become more adept at identifying cats with hyperthyroidism earlier in the disease course, often before the development of severe cardiac remodeling and high-output heart failure. Other risk factors, such as acromegaly, appear to be extremely uncommon, and descriptions of these are limited to small case series or case reports.

Murmurs

The physical examination of cats with heart disease is often only modestly revealing. Many cats with cardiac disease have no indicative clinical signs or physical examination findings. In one small study, only 5 of 16 of cats with cardiomyopathy had murmurs at initial examination; 11 had occult disease.⁶¹ This number increased to 11 of 16 cats when dynamic murmurs (not necessarily ausculted at the time of examination but provoked during echocardiographic evaluation) were examined. Conversely, many cats with a murmur have no identifiable heart disease. Paige and coworkers⁶¹ also identified murmurs in 16 of 103 healthy cats but found cardiac disease in only 5 of these; 11 had no evidence of structural disease.

Dynamic murmurs are common findings in cats with and without heart disease. Paige and coworkers⁶¹ identified dynamic murmurs in 28 of 103 apparently healthy cats. Dynamic murmurs change in intensity or appear only after provocation (e.g., fear, aggression). They are generally parasternal murmurs (either right or left) and can be extremely transient, lasting only a few beats in some cats. Rishniw and Thomas⁷¹ identified a dynamic right ventricular outflow tract obstruction in 50 cats between 1994 and 1996 that was only occasionally associated with structural heart disease. The most common diseases associated with this physiologic murmur were chronic kidney disease and nasal squamous cell carcinoma (SCC), but these cats were examined in California, where nasal SCC is highly prevalent. Cats younger than 4 years of age with dynamic right ventricular outflow tract obstruction most often had HCM.

Systolic anterior motion of the mitral valve and the associated dynamic left ventricular obstruction account for most of the remainder of identifiable dynamic murmurs in cats. This phenomenon is observed predominantly in cats with HCM but can occasionally be observed in cats without any identifiable structural heart disease. Midventricular obstructions have also been identified in cats with HCM or other feline cardiac diseases⁴⁹ and might account for some dynamic murmurs in cats. In one study only 36% of provocable murmurs had an identifiable etiology; thus many dynamic murmurs might not have an easily identifiable cause.⁶¹

Heart Sounds and Arrhythmias

The most commonly observed abnormal heart sound in feline heart disease (excluding murmurs) is the gallop sound. This can be intermittent or sustained and results from an increased intensity of the third or fourth heart sound (or a summation of the two). A true gallop sound is indicative of severe heart disease in cats, associated with marked diastolic dysfunction. However, because of the almost identical systolic and diastolic time intervals in cats, feline gallop sounds are auscultably indistinguishable from systolic clicks. Systolic clicks are uncommon, and, as in dogs, they are thought to be associated with mild mitral valve disease in older cats. They can be distinguished from gallop sounds only by high-fidelity phonocardiograms that have electrocardiographic timing, which demonstrate that the extra heart sound occurs in midsystole. Finally, ventricular extrasystoles (ventricular bigeminy) can sometimes produce a gallop sound if the ventricular extrasystolic beat occurs close to the sinus beat. In these cases the mitral valve opens and then closes during the extrasystole, but the aortic valve fails to open (causing only one heart sound from the extrasystole and two heart sounds from the preceding sinus beat). This can be identified by electrocardiography (ECG). Thus the presence of an additional heart sound in a cat warrants further diagnostic investigation.

Arrhythmias occur frequently in cats with heart disease. In one retrospective study, 96% of cats with ventricular tachyarrhythmias had echocardiographic evidence of structural heart disease. Thus auscultation of extrasystoles warrants further investigation. It is, however, more difficult to define sustained tachyarrhythmias in cats presenting to clinicians for physical evaluation. Feline heart rates can easily reach 240 to 260 beats per minute (bpm) in stressful situations and can do so in a matter of seconds. Cats stressed by a hospital visit or because of other systemic disease can have sustained heart rates above 220 bpm.¹ The astute clinician should note heart rates from prior visits in regular patients to determine whether the rate is appropriate for that patient. Unexpectedly high heart rates, especially those that deviate from rates obtained at prior visits, might warrant further investigation.

Bradyarrhythmias are less commonly ausculted but occur especially in older cats. The author considers any heart rate persistently lower than 130 bpm in a cat during a clinical examination to be unexpectedly low, warranting further diagnostic testing. However, healthy young (mostly) male cats occasionally appear to have low resting heart rates.

Sinus arrhythmias are uncommon in cats in the hospital environment and have been associated mostly with extracardiac disease.⁶⁹ However, some healthy young cats can have a mild sinus arrhythmia as an incidental finding. Additionally, most cats exhibit brief periods of sinus arrhythmia during sleep.⁸⁶

Clinical Signs of Congestive Heart Failure

Cats are extremely adept at hiding signs of heart disease until they reach a critical stage. Often, clinical signs such as mild tachypnea and reduced activity are not apparent to the owner, and cats present to the clinician with profound dyspnea. Thoracic auscultation might reveal signs of congestive heart failure (CHF). A murmur or gallop sound coupled with dyspnea increases the index of suspicion for CHF. Muffled or absent breath sounds or dorsally displaced breath sounds (absent ventrally) are suggestive of pleural effusion. On the other hand, coughing and gagging, wheezing, or auscultable crackles are rarely associated with CHF but are almost always indicative of primary respiratory disease. Extremities may be somewhat cool because of vasoconstriction that occurs with CHF, but this is an unreliable sign of CHF.

Physical Examination Procedures of Limited Value in Diagnosis of Feline Heart Disease

Electrocardiography

ECG is largely limited to diagnosis of arrhythmias and conduction disturbances in cats. It is best reserved for those patients that have auscultable arrhythmias. Arrhythmias are relatively uncommon in cats, with the exception of sinus tachycardia. However, their frequency increases substantially with the presence of heart disease.

In eupneic cats the ECG is recorded in right lateral recumbency. However, sternal recumbency alters few electrocardiographic parameters of clinical interest.^29,32 Therefore assessment in sternal recumbency in fractious, dyspneic, or fragile patients is acceptable.

Continuous 24-hour ambulatory ECG (Holter) monitoring has historically been less successful in cats than dogs, largely because of the size of the recording systems. New digital Holter systems are small enough to be attached to the cat with adhesive bandaging. Holter monitoring can provide diagnostic information in cats with syncope.²² Additionally, small event recorders can be surgically implanted into syncopal patients to increase the probability of arrhythmia detection.^20,38 Holter monitors should not be used on cats with severe structural heart disease or CHF because the stress of monitoring can result in the death of the patient.

Radiography

Radiography has been used for diagnosis of feline heart disease since the early 1970s. More recently, it has been supplanted by echocardiography for diagnosis of heart disease, but it is still a valuable diagnostic test for identification of CHF or discrimination of causes of dyspnea in cats.

Identification of cardiomegaly from radiographs in cats is difficult. Enlargement patterns most amenable to radiographic evaluation are left atrial or biatrial enlargement and left ventricular volume overload. Mild enlargement (as defined echocardiographically) is generally not detectable radiographically; chambers must be at least moderately enlarged before they are radiographically detectable. Right-sided heart changes are both uncommon and difficult to identify in cats (and dogs). Similarly, left ventricular concentric hypertrophy, as occurs with HCM, is not radiographically identifiable; cats can have profoundly thickened left ventricular walls that are radiographically undetectable.

Both lateral and dorsoventral (DV) or ventrodorsal (VD) views are required for the diagnosis of feline heart disease because atrial enlargement is best appreciated in the DV/VD view. There is little difference between VD or DV views. Cats that are dyspneic or tachypneic are best imaged in sternal recumbency to reduce the stress of restraint, which can result in severe clinical deterioration. End-inspiratory films are preferred, although this is not essential in most cases. In the author’s experience of evaluating feline thoracic radiographs obtained by general practitioners, most cats provide films of sufficient quality for interpretation. Obese cats can be problematic because of their reluctance to take deep breaths; in such patients, interpretation of the pulmonary parenchyma can be problematic.

Most traditional rules of cardiac mensuration (measurement) are of little value in cats. Comparisons of the cardiac silhouette to the thoracic cavity or degree of cardiosternal contact have no value in assessing feline thoracic radiographs for cardiac disease. Sternal contact is prominent in many cats and increases with age in cats with normal hearts.^57,59 Similarly, aortic “redundancy” or “undulation,” wherein the ascending aorta forms a prominent silhouette on thoracic films, along with a more sternally positioned heart, is commonly observed in older cats and is an incidental finding.⁵⁷ One study suggested that this finding is associated with systemic hypertension.⁶⁰

Vertebral heart scale (VHS) has been developed for assessment of cardiac size in cats⁴⁶ and can help with identification of atrial enlargement or generalized cardiomegaly. A VHS greater than 8.1 is consistent with cardiomegaly in the cat (Figures 20-1 and 20-2). However, clinicians should recognize that the most common adult-onset feline disease (HCM) often does not cause radiographically detectable ventricular enlargement, so a normal VHS does not rule out the presence of significant heart disease in cats.

FIGURE 20-1 Measurement of vertebral heart scale on the dorsoventral radiographic view. A, A line is drawn along the long axis of the heart from right atrium to left ventricular apex. A second line is drawn perpendicular to the long axis, spanning the atria. B, These lines are then transferred to the cranial edge of the fourth thoracic vertebra, and the number of vertebrae spanned by the two lines is summed. In this example the vertebral heart scale is approximately 9 vertebrae.

FIGURE 20-2 Measurement of vertebral heart scale on the lateral radiographic view. The same method is used as for the dorsoventral view. In this example the vertebral heart scale measures 9 vertebrae. Note the marked interstitial–alveolar pattern in the caudal and accessory lung lobes, consistent with congestive heart failure (pulmonary edema).

Assessment of pulmonary vasculature is substantially less reliable in cats than in dogs. Venous or arterial enlargement is subject to considerable misinterpretation and rarely accurately reflects the pulmonary hemodynamic state. In some cats with CHF, the pulmonary vasculature on the lateral projection appears to be pronounced, but this is subjective and unreliable.

Diagnosis of CHF in cats is aided by thoracic radiographs. Clinicians should not make a diagnosis of CHF in the absence of supportive clinical signs (i.e., radiographs should not be the primary means by which the diagnosis is made). Ideally, marked cardiomegaly is apparent radiographically to support the hypothesis of severe heart disease underlying the pulmonary changes. However, in many cats severe pulmonary changes (pulmonary edema or pleural effusion) obscure the cardiac silhouette, making interpretation of cardiac size impossible. In contrast to dogs, pulmonary edema in cats has little radiographic consistency.⁵⁰ One study of 23 cats with CHF showed at least six distinct pulmonary parenchymal patterns indicative of pulmonary edema (Figures 20-3 and 20-4).⁷ Thus pulmonary edema cannot be excluded on the basis of a radiographic pattern that is different from that seen in most dogs. This can complicate the diagnosis of CHF in cats when the cardiac silhouette is not clearly visible.

FIGURE 20-3 Lateral radiograph showing congestive heart failure secondary to hypertrophic cardiomyopathy in a cat. Note the prominent caudal lobar vessels with perivascular interstitial pattern. The left atrium is markedly enlarged.

FIGURE 20-4 Dorsoventral radiograph showing congestive heart failure secondary to hypertrophic cardiomyopathy in a cat. Note the marked cardiomegaly and heavy interstitial pattern throughout the lung fields.

Echocardiography

Echocardiography remains the most useful tool in identifying feline heart disease. Feline echocardiography requires substantial skill in both acquisition and interpretation of data. Additionally, many of the more common conditions require spectral and color Doppler analysis. Thus feline echocardiography remains largely a specialist diagnostic test. It is important to recognize these requirements when considering echocardiography for a patient because an incomplete or substandard echocardiographic evaluation can impoverish the client without providing a diagnosis.

Because of the cat’s high heart rate and small heart size, imaging is usually performed with a high-frequency transducer (7 to 10 MHz). Advances in processing capabilities of ultrasound machines over the last 20 years have allowed most measurements of chamber and wall dimensions to be made from two-dimensional images rather than M-mode images. This also allows the echocardiographer to measure dimensions in regions not measurable by M-mode echocardiography (e.g., anterior and posterior aspects of the left ventricular wall). Linear and area chamber dimensions can be obtained.

A detailed explanation of echocardiographic technique is beyond the scope of this chapter, and readers should consult cardiology or echocardiography textbooks for additional details.

Biomarkers

Most recently, biochemical indicators of heart disease have been developed and marketed. These include cardiac troponin I; atrial natriuretic peptide (ANP) and its prohormone, NT-proANP; and B-type natriuretic peptide (BNP) and its prohormone, NT-proBNP. These are proteins either secreted or released by cardiomyocytes in response to stretch or injury and can be measured in serum or plasma. In humans these biomarkers have allowed early, rapid identification of acute myocardial injury and stratification of patients for appropriate acute interventions or additional diagnostic testing.

Use of biomarkers in feline medicine has been restricted largely to identification of subclinical heart disease (i.e., as a screening test) and differentiation of causes of acute dyspnea (cardiogenic versus pneumogenic/other).

Definitions

Systemic hypertension is well documented in cats and can result in significant morbidity and potentially mortality. Clinically, systolic hypertension is identified most commonly, whereas diastolic hypertension has not been reported routinely. Systolic hypertension has been defined as a systolic blood pressure (BP) greater than 160 mm Hg. A grading scheme has been devised, with increasing levels of hypertension presumably associated with worse outcomes (Table 20-1).¹⁰

TABLE 20-1 Classification of Systolic Blood Pressure by Risk of Target Organ Damage in the Cat

Causes

Feline systemic hypertension is generally thought to be associated with underlying systemic diseases, such as renal disease and hyperthyroidism. Essential hypertension and geriatric hypertension (the most common causes of hypertension in humans) have not been recognized as distinct entities in domestic animals. These forms of hypertension are secondary to various, mostly genetic factors (compounded by environmental factors, such as obesity) in the former case and loss of vascular elastance in the latter case. Thus any feline patient diagnosed with systemic hypertension should have an underlying etiology identified. Renal disease is the most common cause of systemic hypertension in cats, resulting in hyperreninemic hypertension. However, measurement of plasma renin activity is not routinely available to document a renal etiology. Because renal disease in cats most commonly manifests initially as a loss of urine-concentrating ability, the majority of older cats with hypertension would be expected to have suboptimal urine-concentrating ability.

Clinical Signs

Systemic hypertension has been described as a “silent killer” in humans because clinical signs of disease are often inapparent while end-organ damage is occurring. Similarly, in feline patients, few clinical signs are apparent, and they may be subtle and nonspecific, such as anorexia and lethargy. Renal disease can be extremely mild and not clinically apparent. The most common clinical presentation with severe systemic hypertension is acute retinopathy (retinal separation or hemorrhage) (see Figure 29-59).⁵² Ocular signs may also include dilated pupils and hyphema. Experimentally, acute severe hypertension has resulted in hemorrhagic encephalopathy (“stroke”), but this is not commonly identified in cats with spontaneous disease. Neurologic signs may include head tilt, ataxia, disorientation, and seizures. Cardiac murmurs have been associated with hypertension; however, there is no physiologic reason for systemic hypertension to produce turbulence that would result in a murmur. Thus it is likely that this association is coincidental rather than causal. Several authors have reported cardiac changes in cats with hypertension, including concentric left ventricular hypertrophy and redundancy of the ascending aorta.^12,14,34,60 These changes are generally mild but can be confused with a diagnosis of HCM.

Diagnosis

The diagnosis of systemic hypertension in cats is problematic for several reasons. First, the equipment currently available for noninvasive blood pressure (NIBP) measurement is neither accurate nor precise. Despite multiple studies claiming to validate NIBP systems, most have not compared to a true gold standard (direct, invasive telemetric instantaneous BP monitoring). Additionally, many of these studies have examined systems in anesthetized cats rather than conscious animals. Recently, a study comparing oscillometric systems with direct measurements in anesthetized cats found that no system was sufficiently accurate or precise to be useful.² Recommendations for measuring NIBP in cats have been made by multiple investigators who suggest that four measurements should be made, with the first measurement discarded and the remaining three measurements averaged. However, this method does not guarantee either accuracy or precision of the measurement.

Several NIBP systems are currently marketed and used for measuring systolic blood pressure (SBP) in cats: traditional oscillometric systems; Doppler systems; and, most recently, high-definition oscillometric (HDO) systems. Anecdotal perceptions among clinicians suggested that Doppler-based methodology was more accurate than oscillometric methodology, but unpublished studies comparing both systems in the same animals against invasive measurements have failed to support this perception; both methodologies are equally inaccurate.^18b No studies exist detailing performance of HDO systems in cats. However, studies in dogs suggest that these systems would perform no better than standard oscillometric and Doppler systems.⁸⁷

Complicating the accurate measurement of SBP is the lability of feline BP. The author has observed conscious cats, gently restrained and accustomed to handling, with SBP measurements that vary by as much as 100 mm Hg in the space of a few seconds with little change in heart rate or perceived stress level. Many clinicians attempt to measure SBP at the patient’s home to reduce the impact of stress, but no studies have demonstrated that this strategy results in more accurate measurement. One study examining the effect of conditioning on SBP in dogs showed that repeated measurements over several weeks resulted in a significant gradual reduction in measured BP as the “white-coat” effect subsided in these patients.⁷³ A similar pattern might be anticipated in cats. A study in cats demonstrated a significant white-coat effect in cats that would result in substantially higher SBP measurements than those obtained at rest.⁶

Sustained SBP above 200 mm Hg generally results in end-organ damage. This can often be appreciated in retinal vascular pathology because retinal blood vessels are exquisitely susceptible to hypertensive injury. Vascular engorgement and tortuosity or retinal hemorrhage should be searched for if repeated SBP measurements exceed 200 mm Hg. If the retinas appear normal, the diagnosis of systemic hypertension should be questioned. However, repeated measurements above 220 mm Hg are likely indicative of true hypertension. Similarly, evidence of severe hypertension in patients with acute retinopathy increases the probability of an accurate diagnosis.

Clinicians should adopt several steps in the diagnosis of feline systemic hypertension:

FIGURE 20-5 Use of headphones with Doppler blood pressure units minimizes noise that might be stressful to the patient.

FIGURE 20-6 The width of the blood pressure cuff should be 30% to 40% of the circumference of the leg.

One study recently evaluated the use of NT-proBNP in hypertensive cats with chronic kidney disease (CKD).⁴⁴ These authors found elevated NT-proBNP concentrations in hypertensive cats with CKD and occasionally in normotensive cats with severe CKD. Thus NT-proBNP might help identify hypertension in cats with CKD in the absence of cardiac disease. Additional larger studies would be necessary to confirm this initial observation.

Treatment

Treatment of systemic hypertension generally involves administration of arteriodilators (Table 20-2). The most common drug used for management of feline hypertension is amlodipine. This is usually administered at 0.625 mg per cat, every 12 to 24 hours, by mouth. The medication can be administered transdermally, but reductions in SBP are less predictable and of lesser magnitude than with oral administration.³³ Reductions in SBP of 20 to 50 mm Hg can be anticipated with oral amlodipine therapy.

TABLE 20-2 Drugs Used in the Treatment of Feline Hypertension

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