Suspicion of cardiomyopathy occurs in one of three contexts: 1) A physical finding, such as a heart murmur or a cardiac arrhythmia, or a radiographic finding, like cardiomegaly, is identified in the course of an examination that was not primarily directed at the heart (“incidental finding”); 2) The patient shows overt physical signs consistent with congestive heart failure, arterial embolism, or syncope; or 3) Sudden death, often without premonitory signs. In a university-based referral center setting, the presenting concern in cats that are subsequently found to have hypertrophic cardiomyopathy (HCM) is 33%, 46%, 17%, and 4% in cats with an incidentally detected heart murmur, signs of congestive heart failure, signs of aortic thromboembolism, and syncope, respectively. Most cats with restrictive cardiomyopathy (RCM) are brought to veterinary attention due to dyspnea (83% in one study). Anecdotally, many cats with RCM are presented due to aortic thromboembolism, as might be expected with hypercoagulability from blood stasis resulting from marked left atrial enlargement. It is uncommon for RCM to be identified incidentally in a cat with no overt clinical signs; for example, only 3% of cats with RCM had no clinical signs at the time of diagnosis in one study.
In a typical hospital caseload, an incidentally detected heart murmur is the most common initial finding that first raises the possibility of cardiovascular disease. Heart murmurs occur in 40% of all cats in a shelter/rehoming setting, with 70% of those murmurs being physiologic, based on an echocardiogram showing normal cardiac structure. Therefore, the newfound presence of a murmur must be treated as a clue, but not necessarily indicative of a cardiac disorder.
Clinically, cardiomyopathy is confirmed or excluded with echocardiography. If an echocardiogram is not immediately available, measurement of plasma NT-proBNP concentration can be considered as a screening test. A high quantitative (central lab submission) NT-proBNP result does not differentiate between cardiomyopathy types (a differentiation that is of unproven therapeutic importance in cats anyway), but a low or normal value is strongly suggestive of the absence of cardiomyopathy.
Similarly, cardiomegaly on radiographs is consistent with structural heart disease if it is very substantial: a vertebral heart score >9.3 is strongly suggestive of heart disease in dyspneic cats, whereas a vertebral heart score <8.0 makes it very unlikely that a cat’s dyspnea is caused by congestive heart failure. Finally, several electrocardiographic abnormalities have been assessed as possible markers for feline hypertrophic cardiomyopathy: ST segment changes, increased QRS width, and increased QT interval prolongation have all been associated with cardiomyopathy in small case series of cats. Echocardiography provides the morphologic diagnosis. Since physiologic murmurs occur commonly in cats, the echocardiogram first serves to identify whether any structural abnormalities of the heart are present at all. If abnormalities are noted, they are typically categorized as one of the following, according to changes observed in the ventricles:
- Left ventricular hypertrophy (LVH): Thickening of the interventricular septum, left ventricular free wall, or both, and occurring either diffusely or regionally. In the absence of systemic causes or artifactual impostors (see separate topic), the diagnosis of exclusion is HCM.
- RCM: Presence of moderate or marked atrial enlargement, a restrictive ventricular filling pattern on Doppler echo assessment, or both, possibly coexisting with shelf of myocardium and fibrous connective tissue coursing obliquely along the endocardial surface of the ventricle.
- Dilated cardiomyopathy: Enlargement of the left ventricular lumen, with thin walls showing reduced motion. The least common of the cardiomyopathies, and only seldom associated with touring deficiency nowadays.
- Unclassified cardiomyopathy (UCM): a term given to a heart with an appearance that captures elements of more than one of the three cardiomyopathies listed above. The existence of this category highlights the fact that the categorization template is an imperfect approach to feline cardiomyopathies, because some ventricles show features that represent a hybrid of categories, or features (such as marked atrial enlargement with left ventricular thickening that is present but very minor) that deviate from the typical morphology of one of these categories. In addition to assessing the ventricles to establish a morphologic diagnosis, stratification of severity is an important part of echocardiography. This hinges on the appearance of secondary effects. Examples include visible systolic dysfunction of ventricular walls, presence of turbulence on Doppler evaluation, and perhaps most important, degree of atrial enlargement. Left atrial size has been associated with all of the major complications of cardiomyopathies in cats: Left atrial enlargement increases the risk of congestive heart failure, of aortic thromboembolism, and of a shortened lifespan.
Treatment of preclinical (“asymptomatic”) HCM has not been shown to be successful. For example, based on retrospective analysis, no significant difference in survival has been identified when cats with hypertrophic cardiomyopathy and extended treatment with atenolol are compared to similar cats who are not treated. Therefore, the cornerstone of treatment of feline cardiomyopathies is the management of its consequences. In this brief presentation, the discussion will be centered on treatment of congestive heart failure (CHF) in the cardiomyopathic cat.
Furosemide. Furosemide is a potent, rapidly acting, high-ceiling, loop diuretic. It is the drug of choice for treating cardiogenic pulmonary edema. In patients that are severely dyspneic, it should be administered intravenously with judicious physical restraint of the animal. Moderately to markedly dyspneic cats should receive 3–4 mg/kg IV; with tolerant patients, skilled technical personnel, or both, a blood sample for baseline kidney and electrolytes values and urine sample for urinalysis should be obtained in addition to lateral and dorsoventral thoracic radiographs prior to the administration of furosemide. The expected onset of action is 5 to 10 minutes in healthy cats, and within the first 30 minutes in cats with severe CHF based on experience; objective information to support or refute this is not known to exist in publication currently. Absence of improvement in respiratory rate and character, which should be monitored closely, justifies re-administration of a similar dose of furosemide within 30 to 45 minutes if necessary, as well as reassessment of the diagnosis of CHF if any uncertainty exists. A patient that responds well has the dosage tapered rapidly; typically, one or two doses are needed intravenously for initial mobilization of pulmonary edema, and subsequent doses of 1–3 mg/kg can be given intravenously every 6 to 8 hours for 24 to 36 hours afterward. This regimen is modified based on improvement in respiratory clinical parameters. The decision to administer furosemide orally after 24 to 36 hours of IV use is based on the ease of medication administration, the resolution of dyspnea, and the cat’s willingness to eat in the hospital. Occasionally, it is necessary to discharge an inappetent cat with oral furosemide to be administered at home, even though the cat has only been receiving intravenous furosemide up until that point. This leap of faith assumes that the cat’s willingness to eat and to receive medication will be improved in the home environment, and no more than 24 hours of inappetence or anorexia should be allowed to lapse before the cat is returned to the hospital if this approach was unsuccessful. Atypical dosage of furosemide given orally is 2 mg/kg every 12 hours, and this is modified based on several parameters, including sodium content of the diet, and ease of resolution of respiratory clinical signs with intravenous furosemide administration. Some cats with apparent diuretic resistance, as evidenced by intermittent recurrence of signs of CHF (and especially a cat with urine specific gravity >1.020 while receiving diuretics), may benefit from supplementation of oral furosemide with furosemide 1–2 mg/kg SC as needed (e.g., once weekly) at home; this presumes that part of the reason for diuretic resistance is malabsorption of the oral formulation of the drug.
Angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors (enalapril, benazepril, ramipril, etc.; typically, 0.25 mg/kg PO q 12–24 h) are adjunctive treatments given concurrently with furosemide once the patient’s hemodynamic and respiratory parameters have stabilized. There is no known benefit or clear roll for their being instituted during acute CHF. Although their use has been suggested in preclinical HCM, such an application has been unsuccessful.
Spironolactone (typical dosage: 1–2 mg/kg PO q 12h). This potassium-sparing diuretic is routinely used in conjunction with furosemide in dogs with CHF. The concept of sequential nephron blockade, together with potassium retention, and additional anti-aldosterone affects, are important assets, although its efficacy as a diuretic in monotherapy appears very weak. In cats, by extrapolation, it can be considered as part of a treatment protocol for CHF, especially when there is concurrent hypokalemia. Possible anti-fibrotic effects that could slow the process of HCM progression have been evaluated, and were not found to be present. A substantial concern regarding acute, severe adverse dermatologic effects of spironolactone in cats appears to be infrequent, and possibly limited to the Maine Coon cat breed.
Pimobendan (typical dosage: 1.25 mg/cat PO q 12 h). This inodilator drug, which is used widely in dogs, has markedly different pharmacokinetic properties in cats, and has not been investigated with any prospective trials. Nevertheless, it is the only drug for cats with HCM and CHF that has been shown in a controlled (retrospective) study to be associated with significantly longer survival. Given both this limitation and this apparent benefit, pimobendan is recommended off-label for cats with HCM and CHF, if such a diagnosis is confirmed unambiguously with clinical, radiographic, and echocardiographic evidence, especially if there is evidence of decreased left ventricular systolic function.
Additional Management Strategies: Acute CHF
Oxygen supplementation. In the acute setting, oxygen supplementation can be beneficial, provided its delivery is not detrimental to the cat. Specifically, an oxygen cage can be excessively hot, distressing to a cat (loud blasts of noise from oxygen flow valves), or can limit personnel’s ability to work with and monitor the patient properly. Intranasal delivery is not typically practical in cats, but an Elizabethan collar covered by a transparent plastic membrane may be an effective alternative to oxygen cages. The oxygen flow setting should achieve an inspired orambient oxygen concentration of 40%.
Stress reduction. Excessive restraint can be catastrophically detrimental to a cat with CHF. One important source of this stress to be avoided is physical restraint when thoracic radiographs are being taken. A solution to minimize this problem is to take only a dorsoventral radiograph, with the patient in sternal recumbency. This position mimics the cat’s natural posture when dyspneic; it appears less distressing to a cat compared to lateral recumbency, and certainly is much less likely to trigger a respiratory crisis than is dorsal recumbency. Another important opportunity for avoiding stress is to provide a hiding place for cat in its cage. A cardboard box or soft, washable, dome-covered bed are excellent options.
Thoracocentesis. Physical withdrawal of free fluid from the pleural space can be accomplished safely and promptly. The ideal volume to be withdrawn is not known; it should be sufficient to relieve clinical signs, but excessive removal, especially if a chylous effusion and secondary fibrosing pleuritis are present. This consequence can cause trapped lung, and has been associated with bronchopleural fistula and intractable pneumothorax in a small but clinically significant number of cases. Thoracocentesis can be repeated chronically as needed, and no precise limit has been defined regarding a maximum number of times this procedure can be performed on a particular patient.
Additional Management Strategies: Chronic CHF
Dietary sodium restriction. The function of diuretics is to reduce circulating blood volume. Doing so favors movement of fluid from the extravascular space back into the vascular space, which is the fundamental principle behind elimination of edema. All the diuretics used clinically for this purpose in cardiology accomplish this effect by inhibiting renal sodium resorption. Therefore, it is logical that a reduction in sodium intake can lead to resolution of edema, and maintenance of an edema-free state, with less diuretic. A nutritionally balanced diet fed in calorically appropriate amounts must above all continue to be eaten willingly by the cat. Diets that are sodium-restricted but not palatable are detrimental if the patient refuses to eat well. Ideally, a patient that develops acute CHF continues to be fed its regular diet until CHF signs are well-controlled. Then, if the patient is tolerant to it, a balanced low-sodium diet can be introduced gradually (over a week or so), with the proportion of the regular diet decreasing day by day as the proportion of low-sodium diet is increased.
Acute ingestions of sodium (e.g., canned tuna, commercial cat treat, etc.) must then be avoided since a salt-avid state exists and such excesses can quickly trigger recurrent pulmonary edema or pleural effusion. Ultimately, a low-sodium diet that is eaten willingly by the patient means a lower dosage of diuretic can be administered while the patient remains free of edema and effusions. The degree to which such a dosage reduction is possible depends on many factors, some of which can be assessed (e.g., severity of underlying heart disease, sodium content of food) and others not (e.g., efficacy of pulmonary lymphatic drainage).