What is Hypertrophic Cardiomyopathy in Cats?

By Dr. Phil Good, DVM | Reviewed by Dr. Phil Good, DVM

Introduction

When pet owners begin learning about the complexities of feline cardiovascular health, understanding hypertrophic cardiomyopathy in cats is absolutely essential. Characterized fundamentally by an abnormal thickening of the heart’s walls, this condition stands as the most frequently diagnosed cardiac abnormality in feline medicine. The disease primarily affects the left ventricle, which is the main pumping chamber of the heart responsible for sending oxygen-rich blood throughout the body. As the muscular walls of the left ventricle thicken—a process known clinically as hypertrophy—the chamber itself becomes stiff and non-compliant. This stiffness prevents the heart from relaxing properly during the diastolic phase, drastically reducing the amount of blood the heart can hold and subsequently pump out to the rest of the body.^[1]

The abnormal thickening of the heart’s walls initiates a dangerous cascade of cardiovascular events. Because the heart cannot fill properly, the pressure within the left atrium (the chamber that feeds blood into the left ventricle) begins to rise. This increased pressure can eventually back up into the pulmonary veins and the lungs, leading to congestive heart failure. The structural changes also distort the internal architecture of the heart, often affecting the function of the mitral valve and leading to life-threatening complications such as turbulent blood flow, arrhythmias, and the formation of blood clots.^[2]

Understanding the intricacies of this condition is vital because feline hypertrophic cardiomyopathy is notoriously insidious. Many cats affected by the disease are entirely asymptomatic during the early and moderate stages of the illness. Felines are masters of masking pain and weakness, an evolutionary trait that protects them from predators but hinders early medical detection. Consequently, a cat may harbor significant cardiac remodeling for years before displaying any overt clinical signs. By the time an owner notices that their cat is breathing heavily or acting lethargic, the disease has often progressed to a critical, life-threatening stage.^[3]

The prevalence of this disease in the general feline population is surprisingly high, with some veterinary cardiology studies suggesting that up to 15% of all domestic cats may develop some form of myocardial thickening during their lifetime. While certain purebreds are highly predisposed, domestic shorthairs and mixed breeds are also frequently diagnosed. Addressing this disease requires a comprehensive understanding of its genetic roots, secondary triggers, diagnostic nuances, and long-term management protocols. Only through proactive screening and a deep understanding of feline physiology can veterinarians and pet owners work together to improve the quality of life and longevity of cats facing this daunting diagnosis.^[4]

Types of Hypertrophic Cardiomyopathy in Cats

In veterinary cardiology, it is crucial to differentiate between true, primary hypertrophic cardiomyopathy and secondary myocardial hypertrophy. While both conditions present with an abnormal thickening of the heart’s walls on an ultrasound, their underlying cellular causes, genetic foundations, and long-term treatment strategies are entirely different. This distinction dictates how a veterinary cardiologist will approach the patient’s care plan.

Familial (Primary) HCM: This is the true, idiopathic form of the disease and is the most commonly recognized primary heart disease in cats. Familial HCM is a genetic disease caused by specific mutations in the DNA that codes for the proteins within the heart muscle cells (sarcomeres). Specifically, mutations in the cardiac myosin binding protein C (MYBPC3) gene have been definitively identified in several feline breeds. The MYBPC3 protein is responsible for regulating the cross-bridge cycling of muscle contractions. When this protein is defective, the heart muscle cells must work harder to contract, leading to a compensatory, disorganized thickening of the muscle fibers.^[5]

Because familial HCM is encoded in the cat’s DNA, the condition is irreversible and progressive. Cats with familial HCM may appear perfectly normal at birth and throughout their juvenile years. The abnormal thickening of the heart’s walls typically begins to manifest when the cat is between one and five years of age, though it can present much later. Breeds heavily associated with familial HCM include the Maine Coon, Ragdoll, Sphynx, Persian, and British Shorthair. In Maine Coons, the specific genetic anomaly is known as the A31P mutation, while in Ragdolls, it is the R820W mutation. Because of the genetic nature of primary HCM, there is no underlying systemic disease to “cure”; the focus is entirely on managing the cardiac remodeling and preventing heart failure.^[6]

Secondary HCM (Phenotypic Hypertrophy): Secondary hypertrophic cardiomyopathy is a condition where the heart muscle thickens not because of a genetic defect in the muscle fibers, but as a physiological response to an underlying systemic stressor. When the heart is forced to pump against high resistance or is overstimulated by metabolic hormones, the left ventricle undergoes compensatory concentric hypertrophy to manage the increased workload. This is often referred to as a “phenocopy” because it mimics the appearance of primary HCM on an echocardiogram. The critical difference is that if the underlying systemic disease is successfully treated and resolved, the abnormal thickening of the heart’s walls in secondary HCM can frequently be reversed, or at least halted, restoring normal cardiac function.^[7]

Causes of Feline Hypertrophic Cardiomyopathy

While primary HCM is intrinsically linked to genetic anomalies, acting as an inherited disease that parent cats pass down through generations, secondary hypertrophy is triggered by a variety of environmental, metabolic, and physiological stressors. Understanding these triggers is essential for differential diagnosis. If a veterinarian diagnoses a cat with thickened heart walls, they must systematically rule out the following underlying causes before confirming a diagnosis of primary, idiopathic HCM.

Hypertension (High Blood Pressure)

Systemic hypertension is one of the leading causes of secondary left ventricular hypertrophy in older felines. When a cat has high blood pressure, the systemic vascular resistance in their arteries is significantly elevated. To push blood out of the heart and into this high-pressure arterial system, the left ventricle must generate an immense amount of force. According to Laplace’s Law of fluid dynamics, the heart muscle adapts to this increased wall stress by adding layers of muscle fibers, leading to concentric hypertrophy. Chronic hypertension in cats is rarely a primary condition; it is almost always secondary to another serious systemic illness, most notably chronic kidney disease. When the kidneys begin to fail, they activate the renin-angiotensin-aldosterone system (RAAS), a hormonal cascade that constricts blood vessels and causes the body to retain sodium and water, driving up blood pressure and putting immense strain on the heart.^[8]

Hyperthyroidism

A highly common endocrine disorder in senior felines is Hyperthyroidism, which occurs when benign tumors on the thyroid gland produce excessive amounts of thyroid hormones (T3 and T4). These circulating hormones have a direct, toxic effect on the myocardium. Thyroid hormones upregulate beta-adrenergic receptors in the heart, making the cardiac muscle hyper-responsive to adrenaline. This results in a chronically elevated heart rate (tachycardia) and an increased force of contraction. Furthermore, the overall increased metabolic rate demands higher oxygen delivery to the tissues, forcing the heart into a state of volume overload. The combination of tachycardia, increased contractility, and volume overload reliably leads to thyrotoxic cardiomyopathy, a condition that mirrors the abnormal thickening of the heart’s walls seen in genetic HCM. Fortunately, radioactive iodine therapy or surgical removal of the thyroid tumor can often reverse these cardiac changes.^[9]

Obesity

The veterinary community increasingly recognizes that Cats’ excessive body weight is linked to various health problems, particularly regarding cardiovascular efficiency. Feline obesity is not merely a state of excess fat storage; adipose tissue is biologically active and secretes inflammatory cytokines and hormones known as adipokines. This chronic, low-grade systemic inflammation damages the endothelial lining of blood vessels. Furthermore, a massive increase in body mass requires a corresponding expansion of the vascular bed, meaning the heart must pump a significantly larger volume of blood with every beat. This chronic volume and pressure overload forces the left ventricle to remodel and thicken over time. Weight management is therefore a critical component of cardiovascular disease prevention in felines.^[10]

Heart Valve Diseases

While degenerative mitral valve disease is much more common in dogs, it can and does occur in cats. The mitral valve separates the left atrium from the left ventricle. If this valve becomes malformed or degenerates with age, it fails to close properly during systole (the contraction phase). This allows a jet of blood to flow backward into the left atrium, a condition known as mitral regurgitation. Because a portion of the blood is moving backward, the left ventricle must stretch and eventually thicken to accommodate a larger volume of blood to maintain adequate forward cardiac output. This extra workload stimulates hypertrophy. Additionally, in many cats with primary HCM, the thickened septum bulges into the outflow tract, physically pushing the mitral valve open during contraction, causing a secondary valve malfunction known as systolic anterior motion (SAM) of the mitral valve.^[11]

Other Heart Diseases

It is important to contrast the abnormal thickening of the heart’s walls seen in HCM with other forms of feline cardiac disease. For instance, dilated cardiomyopathy (DCM) represents the exact opposite physiological change. In dilated cardiomyopathy, the heart muscle walls become pathologically thin, weak, and overstretched, resulting in a large, flabby heart that lacks the strength to pump blood effectively. Historically, DCM was rampant in cats due to diets deficient in the essential amino acid taurine. Today, thanks to commercial dietary standards, DCM is rare, leaving HCM as the predominant feline cardiac disease. However, in the absolute end-stages of untreated hypertrophic cardiomyopathy, the overworked, oxygen-starved heart muscle cells can die off and be replaced by scar tissue in a process called myocardial fibrosis. This can occasionally cause an HCM heart to “burn out” and enter a dilated phase, complicating the clinical picture and requiring a drastic shift in medical management.^[12]

How Do I Know If My Cat Has Hypertrophic Cardiomyopathy?

Detecting the clinical signs of hypertrophic cardiomyopathy can be exceptionally challenging for pet owners. Because the disease progresses gradually, cats often adapt to their declining cardiac function by simply reducing their activity levels. An owner might mistakenly attribute a cat’s increased sleeping habits or reluctance to jump onto high furniture to normal aging. However, as the disease reaches advanced stages and the heart can no longer compensate for the severe diastolic dysfunction, outward symptoms become apparent and require immediate emergency veterinary intervention.^[13]

Heart Murmurs and Gallop Rhythms: One of the earliest indicators of HCM is often discovered incidentally during an annual veterinary exam. When the veterinarian listens to the cat’s chest with a stethoscope, they may hear a heart murmur. In cats with HCM, murmurs are frequently caused by dynamic left ventricular outflow tract obstruction (LVOTO). The thickened heart muscle narrows the pathway blood must take to exit the heart. As blood is forced through this narrowed corridor, it moves at a high velocity and creates turbulence, producing a “whooshing” sound. Additionally, the veterinarian might hear a gallop rhythm (an extra heart sound, S3 or S4), which occurs when the atria contract forcefully to push blood into the abnormally stiff ventricle.

Respiratory Distress: As the left ventricle becomes too stiff to fill, blood pressure within the left atrium skyrockets. This pressure is transmitted backward into the pulmonary veins, causing fluid to leak out of the blood vessels and into the air sacs of the lungs (pulmonary edema) or into the chest cavity surrounding the lungs (pleural effusion). This marks the onset of congestive heart failure. A cat in heart failure will exhibit tachypnea (an abnormally fast breathing rate, usually greater than 30 breaths per minute while sleeping) or dyspnea (labored, open-mouth breathing). While coughing can be a symptom in some cats, it is surprisingly less common in feline heart failure compared to canine heart failure; cats are more likely to simply heave and pant.

Aortic Thromboembolism (FATE): Perhaps the most devastating and horrific symptom of feline HCM is the sudden onset of a saddle thrombus. Because the left atrium in an HCM cat becomes massively enlarged, blood pools and stagnates within the chamber. According to Virchow’s Triad, blood stasis leads to hypercoagulability, causing a clot (thrombus) to form inside the heart. If this clot dislodges, it travels down the aorta and typically becomes wedged at the iliac trifurcation—the point where the aorta splits to supply blood to the hind legs. This results in feline aortic thromboembolism (FATE). The cat will suddenly lose the ability to use its back legs, which will feel cold to the touch (poikilothermy), lack a palpable pulse, and appear pale or blue. The cat will often vocalize in excruciating pain. This is a profound medical emergency with a historically guarded prognosis.^[14]

Lethargy, Weakness, and Syncope: Because the heart is failing to deliver adequate oxygenated blood to the brain and muscles, cats with advanced HCM will exhibit profound weakness. They may suffer from anorexia and subsequent weight loss (cardiac cachexia). In cases where the thickened heart muscle disrupts the heart’s electrical conduction system, life-threatening arrhythmias such as ventricular tachycardia can occur. This sudden drop in blood pressure can cause syncope, a temporary loss of consciousness or fainting spell.

Diagnosis of HCM in Cats

Diagnosing hypertrophic cardiomyopathy requires a multi-modal approach, combining physical examination findings with advanced diagnostic imaging and laboratory testing. Because a heart murmur alone does not definitively indicate HCM (as many cats have innocent, benign murmurs), veterinarians must utilize a suite of diagnostic tools to confirm the structural abnormalities of the heart.

Echocardiography (Ultrasound): The gold standard for diagnosing feline HCM is a comprehensive two-dimensional, M-mode, and Doppler echocardiogram performed by a board-certified veterinary cardiologist. An echocardiogram uses high-frequency sound waves to create a real-time, moving image of the heart’s interior structures. The cardiologist will measure the thickness of the left ventricular free wall and the interventricular septum during diastole (the relaxation phase). In a healthy cat, these walls measure less than 5 millimeters in thickness. A definitive diagnosis of HCM is generally made when the wall thickness equals or exceeds 6 millimeters in the absence of other systemic causes. Furthermore, color flow Doppler allows the cardiologist to visualize blood flow, pinpointing any mitral valve regurgitation or outflow tract obstruction. They will also meticulously measure the size of the left atrium; a severely enlarged left atrium is a primary risk factor for blood clot formation and imminent congestive heart failure.^[15]

Biomarker Blood Tests: Recent advancements in veterinary laboratory medicine have provided practitioners with powerful blood tests to assess cardiac health. The most prominent is the N-terminal pro-B-type natriuretic peptide (NT-proBNP) assay. When the walls of the heart are excessively stretched due to pressure and volume overload, the cardiac muscle cells secrete the BNP hormone into the bloodstream. A highly elevated NT-proBNP level strongly suggests significant structural heart disease and can help differentiate cardiac-related respiratory distress from primary respiratory illnesses like feline asthma. Another useful biomarker is cardiac troponin I (cTnI), which elevates when there is active damage or death of heart muscle cells, often indicating active myocardial ischemia or severe disease progression.^[16]

Radiography (X-rays): While an X-ray cannot measure the thickness of the heart’s walls, thoracic radiographs are absolutely vital for assessing the secondary consequences of HCM. A cat with severe hypertrophic cardiomyopathy will often present with a classic “valentine-shaped heart” on a ventrodorsal X-ray view. This unique shape is caused by the massive enlargement of the left atrium combined with the thickened left ventricle. More importantly, radiographs are essential for diagnosing congestive heart failure, allowing the veterinarian to visualize pulmonary infiltrates (fluid in the lungs) or the presence of pleural effusion, which obscures the cardiac silhouette entirely.

Electrocardiography (ECG): Because the abnormal thickening of the heart’s walls distorts the cellular pathways that conduct electrical impulses, cats with HCM are highly prone to arrhythmias. An ECG records the electrical activity of the heart and is critical for identifying conduction blocks, premature ventricular complexes (PVCs), and atrial fibrillation. Identifying these arrhythmias is vital because they require specific anti-arrhythmic medications to prevent sudden cardiac death.

Systemic Diagnostics: To ensure the hypertrophy is primary and not secondary, the veterinarian will run a complete blood count (CBC), a serum biochemistry panel (to assess kidney and liver function), a total T4 test (to rule out hyperthyroidism), and a comprehensive blood pressure evaluation to rule out systemic hypertension.

Treatment and Management of Hypertrophic Cardiomyopathy in Cats

The management of hypertrophic cardiomyopathy is guided by the American College of Veterinary Internal Medicine (ACVIM) consensus statement, which categorizes the disease into progressive stages. Stage A includes cats genetically predisposed but showing no structural changes. Stage B1 includes cats with mild hypertrophy but a normal-sized left atrium (low risk). Stage B2 includes cats with severe hypertrophy and a massively enlarged left atrium (high risk for clots). Stage C includes cats actively in, or having survived, congestive heart failure or a thromboembolic event. Stage D represents refractory heart failure that no longer responds to standard medical therapy. Treatment protocols are strictly tailored to the cat’s specific ACVIM stage.^[17]

Medications

Pharmacological intervention forms the cornerstone of managing clinical HCM. For cats in Stage B2 (high risk of clotting), antithrombotic therapy is paramount. Based on the landmark FAT CAT (Feline Arterial Thromboembolism: Clopidogrel vs. Aspirin Trial) study, the antiplatelet drug Clopidogrel (Plavix) is the medication of choice for preventing saddle thrombus, significantly outperforming aspirin. In some severe cases, anticoagulants like Rivaroxaban (Xarelto) are added to the regimen.

For cats in Stage C (congestive heart failure), aggressive diuresis is required. Furosemide (Lasix), a potent loop diuretic, is administered to pull excess fluid out of the lungs and chest cavity, allowing the cat to breathe. If the cat becomes resistant to Furosemide, a stronger diuretic like Torsemide may be utilized. Spironolactone, an aldosterone antagonist, is often added to provide mild diuresis and help prevent myocardial fibrosis.

Drugs that alter the heart’s contractility and rate are also frequently prescribed. Beta-blockers, such as Atenolol, are commonly used in cats that suffer from severe dynamic left ventricular outflow tract obstruction (LVOTO). By slowing the heart rate, Atenolol allows the stiff left ventricle more time to fill with blood during diastole and reduces the force of contraction, which mitigates the severity of the obstruction. Calcium channel blockers like Diltiazem were historically popular for improving cardiac relaxation but are now used less frequently. The use of Pimobendan (Vetmedin), an inodilator, is highly nuanced in feline HCM. While it improves atrial function and helps with heart failure, it increases the force of contraction, which can be detrimental if the cat has an active outflow tract obstruction. Its use must be carefully directed by a cardiologist.

Dietary Management

Nutritional support is a vital adjunct to pharmacological therapy. Cats in heart failure are prone to cardiac cachexia, a severe loss of lean muscle mass driven by systemic inflammation and a poor appetite. Diets must be highly palatable and calorically dense. Mild sodium restriction is recommended for cats in Stage C heart failure to prevent excessive fluid retention, but severe sodium restriction is avoided in early stages as it can prematurely activate the detrimental RAAS hormonal cascade. Supplementation with Omega-3 fatty acids (EPA and DHA) from marine fish oils is highly beneficial, as these compounds reduce inflammatory cytokines, improve appetite, and may exert mild anti-arrhythmic effects. Ensuring adequate levels of the amino acid taurine is also standard practice, even though primary HCM is not caused by a taurine deficiency.

Lifestyle Adjustments

Cats with thickened, compromised hearts possess very little cardiovascular reserve. Therefore, environmental management is crucial to prevent sudden decompensation. Owners must cultivate a low-stress environment, free from sudden loud noises, aggressive housemates, or high-anxiety situations. The sympathetic nervous system’s “fight or flight” response releases surges of adrenaline; in an HCM cat, this adrenaline spike can trigger lethal arrhythmias or acute heart failure. Moderate, self-limited activity is acceptable, but forced exertion or intense play sessions using laser pointers should be strictly avoided.

Regular Monitoring

The most important monitoring tool an owner can utilize at home is tracking the cat’s Sleeping Respiratory Rate (SRR). When the cat is deeply asleep, the owner should count the number of breaths taken in one minute. A healthy cat, or a well-managed HCM cat, should have an SRR of fewer than 30 breaths per minute. A consistent rise in the SRR (e.g., creeping up to 35 or 40 breaths per minute) is often the very first indicator that fluid is beginning to accumulate in the lungs, signaling impending heart failure days before the cat shows outward distress. Regular veterinary rechecks, including updated echocardiograms and renal function blood tests (since diuretics impact the kidneys), are mandatory every 3 to 6 months.

Surgical Intervention

While open-heart surgery is common in human cardiology, it is exceedingly rare and largely experimental in feline medicine. Surgical intervention for feline HCM is generally limited to emergency procedures addressing complications. If a cat presents with severe pleural effusion, the veterinarian will perform a thoracocentesis, using a needle to manually drain the fluid from the chest cavity to restore breathing. In the event of a saddle thrombus, surgical embolectomy (physically removing the clot from the artery) is theoretically possible but carries a massive mortality rate due to reperfusion injury—where toxic byproducts from the dying limb flood the bloodstream once circulation is restored. Therefore, medical management with pain control and antithrombotics remains the standard of care over surgical intervention.^[18]

Prevention of Hypertrophic Cardiomyopathy in Cats

Because familial hypertrophic cardiomyopathy is a disease rooted in the cat’s genetic code, it cannot be entirely prevented by lifestyle choices alone. However, proactive management, aggressive screening, and diligent veterinary care can prevent the rapid progression of the disease, mitigate life-threatening complications, and entirely prevent secondary forms of the disease. Consult your veterinarian before making any changes to your pet’s care, as early intervention requires a tailored, medical approach.

Regular Vet Check-ups

Routine wellness examinations are the front line defense against the silent progression of HCM. During an annual or bi-annual exam, the veterinarian’s use of a stethoscope is critical for detecting new heart murmurs or gallop rhythms. For high-risk breeds, or senior cats predisposed to secondary diseases, veterinarians frequently recommend incorporating an NT-proBNP “snap” blood test into the annual bloodwork panel. This quick, bedside test can alert the practitioner to hidden myocardial stretching long before symptoms arise, prompting an early referral to a veterinary cardiologist for an echocardiogram.

Genetic Testing

The veterinary community has made massive strides in identifying the genetic markers responsible for HCM. Simple cheek swab DNA tests are now widely available for the MYBPC3 gene mutations found in Maine Coons and Ragdolls. Responsible breeders must utilize these genetic tests on all breeding stock. Cats carrying one copy of the mutation (heterozygous) or two copies (homozygous) should be immediately removed from breeding programs to prevent passing the defect to future generations. By strictly breeding only cats that test negative for the mutation, the prevalence of primary familial HCM can be systematically eradicated from susceptible pedigrees over time.

Maintain a Healthy Weight and Diet

Preventing secondary cardiac stress is entirely within the owner’s control. Feeding a high-quality, species-appropriate diet and strictly regulating portion sizes prevents feline obesity. Maintaining a lean body condition score significantly reduces the systemic vascular resistance and inflammatory burden placed upon the cardiovascular system. Regular, mild exercise through interactive toys helps maintain cardiovascular tone and prevents the metabolic syndrome that often precedes secondary heart remodeling.

Reduce Stress

Felines are highly sensitive to environmental stressors, and chronic anxiety leads to a persistent state of sympathetic nervous system activation. This constant drip of cortisol and adrenaline into the bloodstream elevates heart rate and blood pressure, exacerbating any underlying cardiac pathology. Providing a stable routine, utilizing synthetic feline facial pheromones (such as Feliway) in the home, ensuring ample vertical hiding spaces, and utilizing fear-free handling techniques during veterinary visits all contribute to lowering the cat’s overall cardiovascular stress burden.

Medication Management

For cats already diagnosed with early-stage HCM or secondary trigger diseases (like hyperthyroidism or hypertension), rigorous compliance with prescribed medication is the ultimate preventative measure against congestive heart failure. Administering daily anti-thyroid medications or blood pressure regulators prevents the left ventricle from undergoing secondary hypertrophy. If a cat is prescribed Clopidogrel to prevent blood clots, missing even a few doses can allow a fatal thrombus to form. Complete adherence to the veterinary treatment plan, coupled with diligent at-home respiratory monitoring, offers the best possible prognosis for cats living with this complex disease.

Frequently Asked Questions

References

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5. Meurs, K. M., et al. “A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy.” Human Molecular Genetics, 2005.
6. Meurs, K. M., et al. “A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy.” Genomics, 2007.
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13. Côté, E., et al. “ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats.” Journal of Veterinary Internal Medicine, 2020.
14. Smith, S. A., et al. “Arterial thromboembolism in cats: acute crisis in 127 cases.” Journal of Veterinary Internal Medicine, 2012.
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16. Fox, P. R., et al. “Utility of plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) to distinguish between congestive heart failure and non-cardiac causes of acute dyspnea in cats.” Journal of Veterinary Cardiology, 2014.
17. Hogan, D. F., et al. “Secondary prevention of cardiogenic arterial thromboembolism in the cat: The double-blind, randomized, positive-controlled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT).” Journal of Veterinary Cardiology, 2015.
18. Ohio State University Veterinary Medical Center. “Feline Hypertrophic Cardiomyopathy Guidelines and Treatments.” OSU Vet Extensions, 2021.