top of page

Take It to Heart The Ins and Outs of Hypertrophic Cardiomyopathy HCM in Cats

It should be noted Elysian Bengals and its authors are not veterinarians in any capacity. Our information is for education purposes only but should not replace trained professionals and is not responsible for how readers use this information.

As a Breeder Hypertrophic Cardiomyopathy or HCM is something to be quite aware of; not only to understand what HCM is, but also concerning the breeders you are working with, buying cats from, how to screen for it, what to look for in the final report, and how to publicly deal with a positive result. As a kitten buyer, it is equally as important to know what HCM is as well as how breeders should be handling its prevention and diagnosis to ensure you are supporting ethical breeders and getting the healthiest kitten you can.

Hypertrophic Cardiomyopathy, or HCM, is a common disease, not only in purebred cats, but also in those of mixed ancestry. It affects approximately 15% of the cat population (1), with higher risk in specific breeds, as well in male cats (at a 3:1 ratio) (2). There is also a higher population of mixed breed cats than purebred cats (3). The most common cat breeds afflicted by this disease includes (4): Bengal


Maine Coon

Sphynx (5)



British Shorthair (6)

The condition affects the heart causing an enlargement and thickening of the heart wall, specifically the left ventricle. The left ventricle is responsible for being the main pump system in the body (7, 8). This can greatly alter the function of the heart, causing abnormal heartbeats and improper uptake or lack of oxygen. Furthermore, as the main center for pumping blood, the function of the lungs can be affected and blood clots can develop. Blood clots are one of the most concerning symptoms. These blood clots can break off and travel along the arteries eventually settling and blocking the proper flow of blood in the body. This can be so severe that a blockage causes paralysis, most often in the hind limbs. This event can seem quick and effect the cat immediately. Finally congestive heart failure often results, eventually leading to death.

Many cats live with heart diseases without symptoms. Unfortunately, symptoms typically don’t appear until the condition is fairly far along. Common symptoms one can see include getting winded easily, lethargy, and having trouble breathing (including open mouth breathing). At this point fluid around the lungs has affected their normal function. Symptoms can be exacerbated by stress, surgery under anesthesia, even fluids or pharmaceutical drug treatments.

If caught early enough, and with treatment, many cats are able to live a full, quality life.

7% of cats with onset signs of HCM will typically develop heart failure by 1 year of age, 20% by 5 years, and 25% within 10 years (9). These statistics are regardless of the size of the left atrium.

Of these cats, once in heart failure, 50% pass away within 2 months. For those that suffer a blood clot, 70% pass within a week. In other studies 37% of cats survived to 11.5 months and 20% survived to 4 years (10, 11).

A cat can be born with HCM or develop it as an adult later on in life. While HCM isn’t 100% understood, it is, in part, a genetic condition.This disease is hereditary in origin, as certain proteins mutate causing the wall thickening. In the Sphynx (12), Ragdoll (13) and Maine Coon (14) breeds, several gene markers have been identified and can be tested for.

For the breeds that do have genetic markers, the understanding is that a cat with no copies of the gene will not develop HCM; those with one copy are at risk for developing HCM, and those with two copies will develop the disease. This type of genetic inheritance is known as autosomal dominant. Autosomal means that the gene is located on a chromosome that is not a sex chromosome. Dominant means that only a single gene is required to cause the disease, compared to recessive, where the cat would always need two copies of the gene to cause the disease.

While a species-appropriate raw diet is ultimately the best diet for our carnivore companions and supports a happy, healthy heart, thus far diet is not a contributor to the development of HCM (15).

Excessive growth hormone and parathyroid hormones are other genetic causes of the disease.

While there are a few genetic tests for some breeds, there seems to be many variants and genes for HCM, so while some of these genetic tests can help identify carriers or affected/future affected cats, they are not 100% encompassing. An echocardiogram, or ultrasound of the heart, is the best preventative way to monitor the heart over time. An echocardiogram, through ultrasound waves, creates an image of the heart. A cardiologist is able to not only measure the heart, but also view the blood flow and take note of how the valves are functioning. Over time they are able to monitor the heart’s growth, as well as listen for murmurs, which indicates a restriction of blood through the heart.

This screening is not a guarantee a cat will never develop HCM, it is simply a precautionary practice. Early detection means earlier treatment and a better chance at a higher quality of life.

Breeding cats should be screened every year to year and a half. Reputable breeders will not only do these screens but will also provide the results for each cat. Unless one suspects HCM in a juvenile cat, screenings should not begin until the cat is at least 1 year old. Up until this point the heart is still growing and results may be inaccurate. Breeders and owners should then continue screening every 1-1.5 years.

As mentioned prior, many cats live asymptomatically. When symptoms start to appear, it is often too late. This is why yearly screenings are absolutely essential. It is the only way we can detect early signs of HCM in the hopes to prevent, or catch and treat the condition, to give our cats the best possible chance at a normal and long life.

First, other diseases should be ruled out including hyperthyroidism, high blood pressure, acromegaly (growth hormone abnormalities), and dehydration. Once other diseases are ruled out, the following is evaluated via M-mode and 2-D Echocardiograms methods. 1. Determine Left Ventricle enlargement (hypertrophy)

2. Determine LVOT obstruction (Left Ventricle Outflow Tract) - this looks at the blood flow out of the ventricle into the arteries

3. Evaluate SAM (Systolic Anterior Motion) - an LVOT obstruction creates a narrow pathway

due to the enlarged ventricle and papillary muscles. These muscles help prevent leakages between the atrium and ventricles when blood is being pumped from the heart chambers into the arteries (16, 17). This event is typically what is identified as a heart murmur.

4. Evaluate the contractions and emptying of the left ventricle (systolic) and the refilling of the left ventricle (diastolic) after systole of blood and oxygenation.

5. The size of the Left Atrium should also be measured and evaluated. In addition to size measurement, the ratio between the left atrium and aorta is also used to evaluate the Left Atrium (18). Typical ratios measure at <1.6 mm but when larger than 1.8-2.0 mm it is determined this cat will most likely develop heart failure or arterial thromboembolism (a blood clot causing a blockage in an artery) (19, 20).

There are two reliable methods for HCM diagnosis, typically used in conjunction with each other. An M-mode echocardiogram, where the M stands for movement or motion, is a chart or diagram of how the heart and its structural parts function through its cardiac cycle.

Essentially, a beam from the Echo doppler is directed at the heart and produces several readings. One is A-mode. Each time the beam hits a structure in the heart a spike is produced. In B-mode, the signals are now dots where the higher the peak the greater the intensity (bigger the dot).

M-mode is the compilation of A- and B-mode, where a single ECHO beam hits the heart, over time in the cycle, to give a picture of the overall cardiac function producing a graph-like diagram.

On the other hand, a 2-D echocardiogram (21) creates an image of the heart which allows the veterinarians to take digital measurements. There are many measurements that are taken. The primary measurement is the thickness of the Septal or Free wall. Generally anything over 6 mm is considered hypertrophic (21, 22). Generally speaking any enlargement of the left ventricle wall is concerning, but anything greater than 15 mm is typically diagnosed as HCM (23).

Another diagnostic method is detecting N-terminal (NT)-pro hormone BNP (NT-proBNP) in the blood plasma. NT-proBNP is a pro hormone, or a precursor to a hormone, that travels through the blood waiting to be activated. When activated it jumpstarts protein synthesis and thus muscle growth in a short period of time.

Similar to genetic testing the test is not 100% accurate or reliable, therefore it is best used with other methods of diagnosing HCM. For example, in studies, half of the samples with subclinical HCM had no changes in NT-proBNP levels (24). A result of <150 pmol/L is considered normal where 150–200 pmol/L is considered abnormal (25)

Post mortem, the best diagnosis method is by the weight of the heart in addition to heart wall thickening. In general the heart of a healthy cat is around 20 g, approximately a heart to body weight ratio of 3-4 g/kg. A cat suffering from HCM is greater than 20 g and a heart to body weight ratio of approximately 6.3 g/kg (26).

It is highly recommended a board-certified cardiologist or radiologist perform an echocardiogram of the heart. These veterinarians have additional training specifically in cardiology and the circulatory system. After a one year internship, veterinarians then participate in a 3-5 year residency to do additional training. Finally, they must pass a plethora of exams. “The American College of Veterinary Internal Medicine Specialty of Cardiology (ACVIM Cardiology) is the recognized governing body for the specialty, and is responsible for establishing training requirements, evaluating and accrediting training programs, and examining and certifying veterinary cardiologists”(27).

You will want to look for this prefix after your veterinarian's name. If this prefix is not that, simply ask to gather further insight into their training and experience.

A general veterinarian or veterinary technician who simply listens to the heart with a stethoscope will not suffice in diagnosing or seeing early signs of HCM. While it is true a stethoscope can detect a heart murmur, which will prompt further investigation, in many cases there are cats with HCM or other heart conditions that do NOT have a heart murmur (21). In addition a heart murmur can also be caused by many other things.

It is especially essential that a trained professional is evaluating your cat’s heart in moderate or lesser cases because of the bigger challenge of diagnosis. Severe HCM is “easy” to diagnose. Now that all being said, especially since COVID HCM and heart screenings of cats especially those that are for maintenance versus affected cats has dwindled. While a board certified cardiologist is absolutely the best option, a small animal internal medicine specialist or a radiologist is also acceptable. A small animal internal medicine specialist for example has a 1 year internship followed by a 3 year residency after veterinary school where as a radiologist has 4 years of additional school says Corrie Barker DVM, DACVIM (SAIM) at Woodlands Veterinary Referral, a small animal internal medicine specialist with a special interested in cardiology who worked with Dr. Gil Jacobs, a board certified cardiologist for over a decade. Dr. Barker agrees that in an ideal world, a board certified cardiologist should be the one performing the echocardiogram but screening by an internal specialist or radiologist is better than no screening at all (28).

Almost every Veterinary College or University typically has a cardiology department but you also may find a referral veterinarian or specialist who owns their own practice or travels to various practices to screen cats. Below are several links to lists of board certified cardiologists

Cost of screening will depend on your location. Screening has been as low as $150 or as high as upwards of $500 or more per cat. You will also find discounts if you can get a clinic together or participate in one. When clinics are put together, typically groups of breeders and owners can get lower prices and deals on screenings. Many times these will be in the $150-$250 range but will typically require at least 10 cats to get these discounts.

First let’s take a look at some important terms, abbreviations, and statements you may find on the report like the one above typically used by bengal breeders.


Diastolic - blood pressure term relating to the force of heart on the arteries between heart beats. Normal 70 to 90 mm Hg (29, 30)

Systolic - blood pressure term relating to the force of the heart on the arteries during a heart beat. Normal 120 to 140 mm Hg (29, 30)

Heart Murmur - an abnormal sound typically when the heart is beating, but it can occur while the heart is at rest as well. Heart murmurs are typically graded from 1-6 and can be caused by something minor like the stress of a veterinary visit or severe like in heart disease. The number denotes the loudness of the murmur.

M-Mode - a one dimensional view of the heart

2-D Mode - a 2 dimensional view of the heart

Equivocal - diagnosis for cats with questionable readings. These cats may have a normal left atrium, no signs of SAM but large papillary muscles and a questionable left ventricle. These cats should be re-evaluated in 6 months (21, 31).


IVSd - Interventricular Septum thickness at end of-diastole

LVIDd - Left Ventricular Internatal Dimension at end-diastole

LVFWd - Left Ventricular Free Wall diameter during diastole

IVSs - Interventricular Septum Thickness at end-systole

LVIDs - Left Ventricular Internal Dimension at end-systole

LVFWs - Left Ventricular Free Wall during systole

SF - Shortening Fraction. This is a direct measurement of the muscular contractility of the heart. An impairment of the heart’s ability to discharge blood occurs when the shortening isn't at least 28%.

Ao - Aorta, a very large artery that takes blood from the heart out into the rest of the body

LA - Left Atrium, one of four chambers in the heart that receives oxygenated blood and moves it into the left ventricle

LA/Ao - Left Atrial to Aortic Ratio

RCM - Restrictive Cardiomyopathy. This occurs when the muscles stiffen and prevent the proper filling of blood in the heart.

Subjective left atrial size - the cardiologists visual evaluation of the heart’s left atrium.

Systolic anterior motion of the mitral valve (SAM) - a narrow pathway after LVOT is created due to the enlarged ventricle and papillary muscles that help prevent leakages between the atrium and ventricles when blood is pumped from the heart chambers into the arteries). This event is typically what is identified as a heart murmur.

End-systolic Cavity Obliteration- “angiographic [a view of the blood vessels and flow of blood) phenomenon in which apical (in the apex or top of the) intracavitary space becomes totally occupied in systole by the contracting left ventricular muscle.”

Papillary Muscles- muscles in the heart ventricles that can be a first indicator of HCM or other heart issues.

The following are the Normal Values of various heart structures in 2-D Mode measured in millimeters (some veterinarians may use centimeters) on an echocardiogram.


The following are the Normal Values of various heart structures in M Mode measured in millimeters (some veterinarians may use centimeters) on an echocardiogram.

Unfortunately there is no cure for HCM. The aim primarily is to reduce symptoms and manage the progression of the disease. Medications are typically prescribed to help reduce or prevent the accumulation of fluid around the heart and lungs. In addition, controlling the heart rate and reducing the risk of blood clots.

Treatment is heavily dependent on obstructive vs. non obstructive HCM and the symptoms that are present (23). Typical medication includes:

Beta Blockers such as Atenolol are used to control blood pressure (which also can be controlled with calcium channel blockers), chest pain and heart rhythm. These are typically prescribed for cats that have signs of heart disease but are not considered severe enough; however their use is debatable at this stage (32, 33). Atenolol specifically can help reduce heart rate as well as Left Ventricle diastolic and Left Atrial systolic function when used at doses of 6.25 mg or 12.5 mg (34, 35).

Anticoagulants and Antiplatelet therapy is recommended in cats with severe HCM as they are at a higher risk for blood clots. These drugs are important for trying to prevent their development that would otherwise result in a blockage. The current drug of choice is Clopidogrel. At doses of 18.75 mg/cat orally every 24 hour. This drug has been shown to have the highest success rate (36, 37).

At this time Diltiazem is no longer recommended as its efficacy has been put to question and tends to have several gastrointestinal side effects (38).

If pulmonary embolism is already present, Loop Diuretics such as Furosemide (orally every 8-12 hours up to 12 mg/kg/day) or Torsemide (orally at 0.1-0.3 mg/kg) (39, 40) are usually recommended) The patient should also receive oxygen treatment in a low stress environment (41). Loop diuretics typically will need to be administered for the life of the cat. Dosing will depend on the severity of the embolism and is typically higher when starting the medication to get things under control therefore starting dose of Furosemide for example may be 0.2 mg/kg orally every 24 hours or higher if there is severe heart failure.

Stress reduction is equally as important as pharmaceutical therapies. SAM as well as LVOT is influenced by the amount of stress a cat is under INCLUDING stress induced administering medications.

If you are a breeder it is 100% essential to handle this situation with care. Education and sensitivity is completely key. As long as you are purchasing from ethical and responsible breeders and screening annually there is nothing to be ashamed of. HCM even in tested lines can occur but it's how you handle this situation. The following is highly recommended in the case of a positive HCM diagnosis. 1. Submit your test results to Bengal-Data or other HCM tracking database or groups 2. Inform any kitten owners who have offspring from this parent including people you have sold breeding cats too

3. Inform breeders of this line of the situation

4. Retire the cat from your program If one of your kitten owners or breeders have a Positive HCM Diagnosis again be kind and sympathetic. This person just got some devastating news. Do your due diligence and ask for veterinarian notes, tests and documentation of the diagnosis and treatment plan. In addition you should follow through on your health guarantees and HCM clauses. If you are a buyer, it is equally important to handle this situation delicately. You will want to reach out to your breeder to let them know about the situation. Your ethical and responsible breeder has worked hard to do everything they can to select the best cats and keep their lines healthy. This will be a sad time and loss for them as well . Be mindful this will dictate decisions in their program and since they do not live with you and your cat anymore they may have questions. It is important you provide them with documentation of the diagnosis, test results, doctor’s notes as well as your cardiologist’s information. Make sure you also review your breeder’s health guarantees and HCM guarantees to familiarize yourself with what is covered and how to proceed with your breeder..

Health guarantees and clauses protect both you and your buyer. It is essential to detail them in your contract and for buyers to understand what they mean so everyone is on the same page. Of course you never have intentions to sell an ill cat but what happens if your kitten has a congenital or genetic condition even years down the road? This is where your contract comes in handy. Breeders will have various clauses covering several illnesses and diseases as well as different time spans these clauses are applicable. Some clauses you may consider adding or a buyer may see could include All kittens have a lifetime congenital health guarantee” “All kittens have a lifetime hypertrophic cardiomyopathy (HCM) guarantee IF buyers agree to annually HCM screen and provide the results to the breeder.” “We offer a FIVE year guarantee against congenital defects as well as a FIVE year guarantee against Hypertrophic Cardiomyopathy (HCM)”

“We guarantee our breeder kittens against HCM for 2 years”

“We will replace your Bengal for a period of One year from the date of birth if it develops a life-threatening hereditary/genetic or congenital defect which would affect this Bengal's quality of life or if it dies of HCM.”

“HCM. There is no genetic test in Bengals for this condition, but screenings are performed to monitor the heart’s development; however we cannot guarantee 100% the absence of HCM in the future.”

To learn more about contracts check out this article

HCM is not the only cause for heart disease, congestive heart failure or the thickening of the heart walls. Other conditions that should be ruled out include hyperthyroidism and high blood pressure as well as acromegaly (growth hormone abnormalities) and dehydration need to be considered.

What if a heart murmur is heard in a young cat

Keep in mind murmurs can be the result of other problems than HCM such as other defects, age, stress and more. Often in young kittens a baby murmur can be heard and often goes away. Its best to re-evaluate in 6 months before jumping to conclusions. An understanding of feline cardiology is important for breeders and pet owners, not only of the general population of cats, but for several specific purebred breeds like the Bengal, Persian and Ragdoll. Often we generally know what Hypertrophic Cardiomyopathy or HCM is but have a limited understanding of how to read reports, importance of scanning regularly and what is involved in diagnosis and treatment. Furthermore it can seem daunting tackling how to deal with a positive case not only as a breeder but a pet owner. HCM is a sensitive and very serious topic but doesn't need to be intimidating or complicated to understand.

It should be noted Elysian Bengals and its authors are not veterinarians in any capacity. Our information is for education purposes only but should not replace trained professionals and is not responsible for how readers use this information.


  1. Kittleson MD, Côté E. The Feline Cardiomyopathies: 2. Hypertrophic cardiomyopathy. J Feline Med Surg. 2021 Nov;23(11):1028-1051. doi: 10.1177/1098612X211020162. PMID: 34693811; PMCID: PMC8642168.

  2. Payne, JR, Brodbelt, DC, Luis Fuentes, V. Cardiomyopathy prevalence in 780 apparently healthy cats in rehoming centres (the CatScan study). J Vet Cardiol 2015; 17 Suppl 1: S244–S257.

  3. Baty, CJ, Malarkey, DE, Atkins, CE, et al. Natural history of hypertrophic cardiomyopathy and aortic thromboembolism in a family of domestic shorthair cats. J Vet Intern Med 2001; 15: 595–599.

  4. Trehiou-Sechi, E, Tissier, R, Gouni, V, et al. Comparative echocardiographic and clinical features of hypertrophic cardiomyopathy in 5 breeds of cats: a retrospective analysis of 344 cases (2001-2011). J Vet Intern Med 2012; 26: 532–541.

  5. Silverman, SJ, Stern, JA, Meurs, KM. Hypertrophic car-diomyopathy in the Sphynx cat: a retrospective evaluation of clinical presentation and heritable etiology. J Feline Med Surg 2012; 14: 246–249.

  6. Granström, S, Nyberg Godiksen, MT, Christiansen, M, et Prevalence of hypertrophic cardiomyopathy in a cohort of British Shorthair cats in Denmark. J Vet Intern Med 2011; 25: 866–871.

  7. Schober, KE, Chetboul, V. Echocardiographic evaluation of left ventricular diastolic function in cats: hemodynamic determinants and pattern recognition. J Vet Cardiol 2015; 17 Suppl 1: S102–S133.

  8. Patata, V, Caivano, D, Porciello, F, et al. Pulmonary vein to pulmonary artery ratio in healthy and cardiomyopathic cats. J Vet Cardiol 2020; 27: 23–33.

  9. Fox, PR, Keene, BW, Lamb, K, et al. International collaborative study to assess cardiovascular risk and evaluate long-term health in cats with preclinical hypertrophic cardiomyopathy and apparently healthy cats: The REVEAL Study. J Vet Intern Med 2018; 32: 930–943.

  10. Rush, JE, Freeman, LM, Fenollosa, NK, et al. Population and survival characteristics of cats with hypertrophic cardio-myopathy: 260 cases (1990-1999). ] Am Vet Med Assoc 2002; 220: 202–207.

  11. Laste, NJ, Harpster, NK. A retrospective study of 100 cases of feline distal aortic thromboembolism: 1977-1993. J Am Anim Hosp Assoc 1995; 31: 492–500.

  12. Meurs, KM, Williams, BG, DeProspero, D, et al. A deleterious mutation in the ALMS1 gene in a naturally occurring model of hypertrophic cardiomyopathy in the Sphynx cat. Orphanet J Rare Dis 2021; 16: 108. DOI: 10.1186/s13023-021-01740-5.

  13. Meurs, KM, Norgard, MM, Ederer, MM, et al. A substitution mutation in the myosin binding protein C gene in Ragdoll hypertrophic cardiomyopathy. Genomics 2007; 90: 261–264.

  14. Meurs, KM, Sanchez, X, David, RM, et al. A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy. Hum Mol Genet 2005;14: 3587–3593

  15. Fuentes, Virginia Luis. “Feline Cardiomyopathy-Establishing a Diagnosis - WALTHAMOSU2002 - Vin.” Powered By VIN, Waltham/OSU Symposium, Small Animal Cardiology, 2002, Ohio State University , 2002,

  16. Levine, RA, Vlahakes, GJ, Lefebvre, X, et al. Papillary-muscle displacement causes systolic anterior motion of the mitral valve. Experimental validation and insights into the mechanism of subaortic obstruction. Circulation 1995; 91: 1189–1195.

  17. Sherrid, MV, Balaram, S, Kim, B, et al. The mitral valve in obstructive hypertrophic cardiomyopathy: a test in context. J Am Coll Cardiol 2016; 67: 1846–1858.

  18. Abbott, JA, MacLean, HN. Two-dimensional echocardio-graphic assessment of the feline left atrium. J Vet Intern Med 2006; 20: 111–119.

  19. Linney, CJ, Dukes-McEwan, J, Stephenson, HM, et al. Left atrial size, atrial function and left ventricular diastolic function in cats with hypertrophic cardiomyopathy. J Small Anim Pract 2014; 55: 198–206.

  20. Duler, L, Scollan, KF, LeBlanc, NL. Left atrial size and volume in cats with primary cardiomyopathy with and without congestive heart failure. J Vet Cardiol 2019; 24: 36–47.

  21. Luis Fuentes, V, Abbott, J, Chetboul, V, et al. ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats. ] Vet Intern Med 2020; 34: 1062–1077.

  22. Burris, Shauntay. “How to Read an Echocardiogram Form – Sphynx Cat.” Sphynx Info, 6 Aug. 2021,

  23. Mitevksa, Irena Peovska. “Focus on Echocardiography in Hypertrophic Cardiomyopathy - Fourth in Series.” European Society of Cardiology, e-Journal of Cardiology Practice, 14 Apr. 2015,

  24. Lu, T, Côté Kuo, Y, et al. Point-of-care N-terminal pro B-type natriuretic peptide assay to screen apparently healthy cats for cardiac disease in general practice. J Vet Intern Med 2021; 35: 1663–1672.

  25. “Idexx Snap Feline Probnp Test Now Use NT-Probnp.” Idexx, Idexx Laboratories, Feb. 2019,

  26. Liu, SK, Peterson, ME, Fox, PR. Hypertrophic cardio-myopathy and hyperthyroidism in the cat. J Am Vet Med Assoc 1984; 185: 52–57.

  27. “Docs Cardiology.” NC State Veterinary Medicine, 31 Oct. 2016,

  28. Waals, Meghan, and Corrie Barker DVM, DACVIM (SAIM). “Cardiology/Echocardiogram Questions for Dr. Barker.” 14 June 2022.

  29. Egner B, Carr AJ, Brown S, et al: Essential Facts of Blood Pressure in Dogs and Cats. Germany, BE Vet Verlag, 2003.

  30. Detweiler DK: Control mechanisms of the circulatory system, in Swenson MJ, Reece WO (eds): Duke's Physiology of Domestic Animals. Ithaca, NY, Cornell University Press, 1993, pp 184-226.

  31. Haggstrom, J, Luis Fuentes, V, Wess, G. Screening for hypertrophic cardiomyopathy in cats. J Vet Cardiol 2015;17 Suppl 1: S134–S149.

  32. Ommen, SR, Mital, S, Burke, MA, et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hyper-trophic cardiomyopathy: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. ] Am Coll Cardiol 2020; 76: e159–240.

  33. Ammirati, E, Contri, R, Coppini, R, et al. Pharmacological treatment of hypertrophic cardiomyopathy: current practice and novel perspectives: pharmacological treatment of HCM. Eur J Heart Fail 2016; 18: 1106–1118.

  34. Sugimoto, K, Aoki, T, Fujii, Y. Effects of atenolol on left atrial and left ventricular function in healthy cats and in cats with hypertrophic cardiomyopathy. J Vet Med Sci 2020; 82: 546–552.

  35. Riesen, SC, Schober, KE, Cervenec, RM, et al. Comparison of the effects of ivabradine and atenolol on heart rate and echocardiographic variables of left heart function in healthy cats. J Vet Intern Med 2011; 25: 469–476.

  36. Hogan, DF, Fox, PR, Jacob, K, 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). J Vet Cardiol 2015; 17 Suppl 1: S306–S317

  37. Lo, ST, Walker, AL, Georges, CJ, et al. Dual therapy with clopi-dogrel and rivaroxaban in cats with thromboembolic disease. J Feline Med Surg. Epub ahead of print 10 May 2021. DOI: 10.1177/1098612X211013736.

  38. Wall, M, Calvert, CA, Sanderson, SL, et al. Evaluation of extended-release diltiazem once daily for cats with hyper-trophic cardiomyopathy. J Am Anim Hosp Assoc 2005; 41: 98–103.

  39. Giatis, IZ, Nguyenba, TP, Oyama, MA, et al. Use of torsemide in 17 cats with advanced congestive heart failure [abstract]. ACVIM Forum, 2014.

  40. Poissonnier, C, Ghazal, S, Passavin, P, et al. Tolerance of torasemide in cats with congestive heart failure: a retrospective study on 21 cases (2016-2019). BMC Vet Res 2020; 16: 339. DOI: 10.1186/s12917-020-02554-6.

  41. Ohad, DG, Segev, Y, Kelmer, E, et al. Constant rate infusion vs. intermittent bolus administration of IV furosemide in 100 pets with acute left-sided congestive heart failure: a retrospective study. Vet J 2018; 238: 70–75.


bottom of page