Hypertrophic Cardiomyopathy (HCM)

HCM is the master of disguise. Many affected cats maintain normal activity, appetite, and weight for months to years — the first noticeable sign is often a murmur or gallop rhythm found incidentally on a wellness exam. When the disease advances, signs can escalate abruptly:

• Rapid or labored breathing at rest — often the first sign owners notice at home; the cat may breathe with an open mouth, extend their neck forward, or breathe using their abdominal muscles
• Elevated resting respiratory rate — counting breaths per minute while the cat is in a deep, relaxed sleep; a rate persistently above 30 breaths per minute is a warning sign
• Open-mouth breathing or panting — cats almost never pant from heat; any panting in a cat is a potential cardiac or respiratory emergency
• Reduced activity or hiding — cats instinctively conceal illness; a cat that is quieter than usual or less willing to jump deserves a closer look
• Aortic thromboembolism (ATE, "saddle thrombus") — a blood clot that forms in the dilated left atrium travels to where the aorta divides (the saddle point) and blocks blood flow to the hind limbs; this is a cardiac emergency. Signs include sudden inability to use the back legs, crying in pain, cold and pale or blue hind paw pads, and muscle rigidity.
• Heart murmur or gallop sound — detected during a veterinary exam; a gallop rhythm (an abnormal extra heartbeat sound, S3 or S4) is particularly concerning in cats
• Weight loss and reduced appetite — more common in advanced or concurrent disease

Because ATE strikes without warning and causes extreme pain and rapid deterioration, any cat suddenly unable to move its hind legs requires emergency care immediately.

The cause of HCM in most cats is not fully known, but genetic factors play a central role in several breeds, and increasing age is the most consistent risk factor across all cats:

• Maine Coon cats — carry a specific mutation in the cardiac myosin binding protein C gene (MYBPC3 A31P) that is directly linked to HCM; genetic testing is commercially available; homozygous cats (two copies of the mutation) tend to develop more severe disease earlier in life
• Ragdoll cats — have their own distinct MYBPC3 mutation (R820W); HCM in Ragdolls can appear at a younger age and may progress differently from Maine Coon HCM; genetic testing is also available for this mutation
• Other predisposed breeds — British Shorthairs, Sphynx, Norwegian Forest Cats, and Persians are also over-represented, though the specific genetic drivers in these breeds are less well characterized
• Male cats — statistically more likely to be diagnosed with HCM and tend to develop more severe disease than females, though females are not exempt
• Age — prevalence increases substantially in cats over six years old; many cases are detected for the first time in middle-aged or senior cats
• Domestic shorthair and longhair cats — HCM is common across all breeds and mixed-breed cats; genetic testing applies only to Maine Coons and Ragdolls

Because HCM is so prevalent and so often silent, echocardiographic screening is the only reliable way to detect it before complications arise. At-risk breeds and older cats benefit most from proactive evaluation:

• Echocardiogram (cardiac ultrasound) — the definitive diagnostic test; performed on-site by Dr. D'Urso; measures left ventricular wall thickness, chamber dimensions, and diastolic function (how well the heart relaxes and fills); detects HCM before any symptoms appear and grades its severity. It is the only way to distinguish HCM from hyperthyroidism-associated cardiac hypertrophy, which looks identical on auscultation.
• NT-proBNP blood test (cardiac biomarker) — a protein released when the heart wall is under stretch; elevated levels suggest HCM is present and clinically significant; valuable for screening cats before an echocardiogram and for monitoring disease progression over time
• Chest radiographs (X-rays) — detect heart enlargement and the left atrium dilation that raises the risk of clot formation; also the quickest way to identify pleural effusion (fluid around the lungs) when a cat is in respiratory distress
• Blood pressure measurement — systemic hypertension causes the same concentric thickening of the left ventricle as HCM; distinguishing between the two is critical, as hypertension is treated differently. Blood pressure is measured at every cardiac visit.
• Thyroid hormone level (T4) — hyperthyroidism causes secondary cardiac hypertrophy that resolves with treatment; ruling it out is essential before labeling a cat with primary HCM
• Genetic testing (Maine Coons and Ragdolls) — a cheek swab identifies MYBPC3 mutation carriers; positive cats are prioritized for echocardiographic screening; negative cats still require monitoring, as not all HCM mutations are covered by current tests

There is currently no treatment proven to stop or reverse the thickening of the heart muscle in cats with HCM. Treatment instead focuses on managing fluid accumulation, preventing blood clots, and controlling any arrhythmias. The specific medications used depend on the clinical presentation:

• Diuretics (furosemide or torasemide) — the cornerstone of treatment when congestive heart failure is present; remove fluid from the lungs or chest cavity to restore comfortable breathing. Home resting respiratory rate monitoring helps detect early fluid reaccumulation between visits.
• Clopidogrel (Plavix) — an antiplatelet medication (prevents blood cells called platelets from clumping) recommended for cats with moderate to severe left atrial enlargement, which is the primary risk factor for ATE; the FATCAT trial showed clopidogrel significantly reduced the recurrence of thromboembolism compared to aspirin
• Atenolol (a beta-blocker) — slows the heart rate and may reduce dynamic obstruction of the outflow tract (LVOTO) in cats with a subset of HCM called hypertrophic obstructive cardiomyopathy (HOCM); also used to manage tachyarrhythmias (abnormally rapid heart rhythms)
• ACE inhibitors and other vasodilators — less universally agreed upon in feline HCM than in canine heart disease; used in cats with concurrent hypertension or heart failure on a case-by-case basis
• Anxiolytic and pain management during ATE — immediate hospitalization with pain control, warmth, and supportive care is the first priority when a cat arrives with an acute saddle thrombus; heparin may be used acutely to prevent further clot extension

Cats with mild HCM and no symptoms or left atrial enlargement may require no medication initially — monitoring with repeat echocardiograms every six to twelve months is appropriate to watch for progression.

Maine Coon and Ragdoll owners should pursue genetic testing and baseline echocardiography early — ideally by one to two years of age — regardless of whether a murmur has been detected. All cats over seven years old benefit from an NT-proBNP screen at their annual wellness visit to catch HCM before symptoms emerge. If your cat is breathing faster than usual at rest, panting without obvious cause, hiding more than normal, or has suddenly lost the use of their hind legs, call Dog & Cat Hospital Calabasas immediately — do not wait for a scheduled appointment. ATE especially demands emergency care within minutes to hours. Dr. D'Urso's on-site cardiology practice means echocardiographic evaluation, a treatment plan, and a monitoring schedule can all be established during a single Calabasas visit. Book an appointment to screen your cat today.