{"id":208,"date":"2026-06-04T13:18:14","date_gmt":"2026-06-04T12:18:14","guid":{"rendered":"https:\/\/seniorsniffs.com\/index.php\/2026\/06\/04\/hypertrophic-cardiomyopathy-in-cats\/"},"modified":"2026-06-04T13:18:14","modified_gmt":"2026-06-04T12:18:14","slug":"hypertrophic-cardiomyopathy-in-cats","status":"publish","type":"post","link":"https:\/\/seniorsniffs.com\/index.php\/2026\/06\/04\/hypertrophic-cardiomyopathy-in-cats\/","title":{"rendered":"Hypertrophic Cardiomyopathy in Cats: What the Research Shows About HCM Symptoms, Diagnosis, and Treatment"},"content":{"rendered":"<h1>Hypertrophic Cardiomyopathy in Cats: What the Research Shows About HCM Symptoms, Diagnosis, and Treatment<\/h1>\n<div class=\"quick-answer\">\nHypertrophic cardiomyopathy (HCM) in cats is a disease where the muscular walls of the left ventricle thicken abnormally, reducing the heart&#8217;s ability to fill with blood during relaxation. HCM is the most common feline heart disease, affecting up to roughly 15% of domestic cats (Kittleson 2021). It often progresses silently until congestive heart failure or a blood clot occurs.\n<\/div>\n<figure>\n<img decoding=\"async\" src=\"https:\/\/seniorsniffs.com\/wp-content\/uploads\/2026\/06\/hypertrophic-cardiomyopathy-in-cats-vet-echocardiogram-examination-scaled.jpg\" alt=\"Veterinary cardiologist performing echocardiogram examination on Maine Coon cat for HCM diagnosis\" title=\"HCM in Cats - Vet Echocardiogram Examination\" \/><figcaption>An echocardiogram (cardiac ultrasound) is the gold-standard diagnostic tool for hypertrophic cardiomyopathy in cats, allowing cardiologists to measure ventricular wall thickness directly.<\/figcaption><\/figure>\n<p>If a veterinarian just told you your cat has hypertrophic cardiomyopathy, or that a heart murmur was detected during a routine exam, you need real information, not platitudes. HCM is the most common form of feline cardiomyopathy, and it is also the most commonly missed, because many affected cats look perfectly healthy until they suddenly are not. This article walks through what the disease actually does to the heart, who is at risk, how it is diagnosed and staged, what treatments work and which ones the evidence does not yet support, and what to watch for at home, drawing on peer-reviewed cardiology research and consensus statements from the American College of Veterinary Internal Medicine.<\/p>\n<h2>What Is Hypertrophic Cardiomyopathy in Cats?<\/h2>\n<p>HCM is a structural disease of the heart muscle. The left ventricle, the chamber that pumps oxygenated blood out to the body, develops walls that are abnormally thick. On an echocardiogram, the interventricular septum or the left ventricular free wall typically measures greater than 6 mm at end-diastole in an affected cat. That extra muscle is not stronger muscle. Thickened ventricular walls are stiffer and cannot relax fully between beats, which is called diastolic dysfunction. Less filling means less blood ejected per beat, less forward flow, and progressive back-pressure into the left atrium, which then enlarges.<\/p>\n<p>The Cornell Feline Health Center summarizes the cascade well: as the left atrium dilates to accommodate the back-pressure, blood flow within the atrium becomes turbulent and sluggish, which sets the stage for clot formation and for fluid to leak into the lungs or chest cavity. You can read their full overview on the <a href=\"https:\/\/www.vet.cornell.edu\/departments-centers-and-institutes\/cornell-feline-health-center\/health-information\/feline-health-topics\/hypertrophic-cardiomyopathy\" target=\"_blank\" rel=\"noopener noreferrer\">Cornell Feline Health Center HCM page<\/a>.<\/p>\n<p>Population studies suggest HCM affects approximately 15% of apparently healthy domestic cats, and the prevalence climbs in older animals and in certain breeds (Kittleson 2021, <a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC8642168\/\" target=\"_blank\" rel=\"noopener noreferrer\">feline cardiomyopathies review<\/a>). The disease tends to be diagnosed in middle-aged cats, although it can appear as early as a few months of age in genetically predisposed animals and as late as the geriatric years.<\/p>\n<h3>Primary HCM Versus Secondary Hypertrophy<\/h3>\n<p>True (primary) HCM is a disease of the heart muscle itself, often with a genetic basis. Several conditions can produce thickening of the ventricular walls that looks identical on echocardiogram, however, and these mimics must be ruled out before a cat is labeled with primary HCM:<\/p>\n<ul>\n<li><strong>Hyperthyroidism<\/strong>: Excess thyroid hormone drives a hyperdynamic cardiac state and can cause left ventricular hypertrophy that often regresses once the thyroid disease is treated.<\/li>\n<li><strong>Systemic hypertension<\/strong>: Chronically high blood pressure forces the left ventricle to push against greater resistance, producing concentric hypertrophy.<\/li>\n<li><strong>Acromegaly<\/strong>: Excess growth hormone, usually from a pituitary tumor, can cause organ enlargement including cardiac hypertrophy.<\/li>\n<li><strong>Subaortic stenosis or other structural lesions<\/strong>: Less common in cats but worth considering in young animals.<\/li>\n<\/ul>\n<p>Distinguishing primary from secondary disease matters enormously, because secondary hypertrophy may improve or fully resolve with treatment of the underlying cause.<\/p>\n<h3>HCM Versus DCM Versus RCM<\/h3>\n<p>Feline cardiomyopathy is an umbrella term. The major phenotypes differ in mechanism and prognosis:<\/p>\n<ul>\n<li><strong>Hypertrophic cardiomyopathy (HCM)<\/strong>: Thickened ventricular walls, impaired relaxation, normal-to-increased contractility early in disease.<\/li>\n<li><strong>Dilated cardiomyopathy (DCM)<\/strong>: Thin, weakly contracting ventricular walls. Once common in cats due to dietary taurine deficiency, DCM is now rare in cats eating commercial diets that supplement taurine.<\/li>\n<li><strong>Restrictive cardiomyopathy (RCM)<\/strong>: Endomyocardial fibrosis or scarring produces a stiff ventricle with normal wall thickness. Diagnosis can be challenging because echo findings overlap with end-stage HCM.<\/li>\n<li><strong>Arrhythmogenic right ventricular cardiomyopathy (ARVC)<\/strong>: Right ventricular involvement with fatty or fibrofatty replacement of myocardium; uncommon.<\/li>\n<li><strong>Unclassified or non-specific cardiomyopathy<\/strong>: A catch-all when echo findings do not fit a single category.<\/li>\n<\/ul>\n<p>Unlike DCM, which has a well-established nutritional cause in cats, HCM is overwhelmingly structural and genetic, and no dietary modification will reverse it.<\/p>\n<figure>\n<img decoding=\"async\" src=\"https:\/\/seniorsniffs.com\/wp-content\/uploads\/2026\/06\/hcm-cats-normal-vs-thickened-heart-wall-comparison-scaled.jpg\" alt=\"Side-by-side comparison of normal cat heart cross-section with thin walls versus HCM-affected heart with thickened ventricular walls\" title=\"HCM Cats - Normal vs Thickened Heart Wall Comparison\" \/><figcaption>In HCM, the left ventricular walls thicken significantly, leaving a much smaller chamber for blood to fill &#8211; reducing cardiac output with each heartbeat.<\/figcaption><\/figure>\n<h2>Which Cats Are Most at Risk? Breeds and Genetic Factors<\/h2>\n<p>Across published estimates, roughly 1 in 7 cats may develop some degree of HCM during their lifetime (Kittleson 2021; Merck Veterinary Manual). Males are over-represented in clinical case series and tend to present at younger ages with more severe disease, although females are certainly affected. Risk is strongly modified by breed.<\/p>\n<p>Two breeds have well-characterized causative mutations that can be tested directly by a DNA cheek swab or blood sample. The Maine Coon harbors the MYBPC3 A31P mutation, and the Ragdoll harbors a different MYBPC3 mutation, R820W. Both encode defective versions of cardiac myosin binding protein C, a structural protein in the contractile apparatus. Several other breeds appear to have elevated HCM prevalence but no single mutation has been identified to date.<\/p>\n<table>\n<thead>\n<tr>\n<th>Breed<\/th>\n<th>Estimated Prevalence<\/th>\n<th>Known Genetic Mutation<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>Maine Coon<\/td>\n<td>~26% in affected lines<\/td>\n<td>MYBPC3 A31P mutation<\/td>\n<\/tr>\n<tr>\n<td>Ragdoll<\/td>\n<td>~30% in affected lines<\/td>\n<td>MYBPC3 R820W mutation<\/td>\n<\/tr>\n<tr>\n<td>Sphynx<\/td>\n<td>Elevated (mutation unknown)<\/td>\n<td>None identified<\/td>\n<\/tr>\n<tr>\n<td>Scottish Fold<\/td>\n<td>High (often concurrent osteochondrodysplasia)<\/td>\n<td>None identified<\/td>\n<\/tr>\n<tr>\n<td>British Shorthair<\/td>\n<td>Elevated<\/td>\n<td>None identified<\/td>\n<\/tr>\n<tr>\n<td>Siberian<\/td>\n<td>Elevated<\/td>\n<td>Under investigation<\/td>\n<\/tr>\n<tr>\n<td>Domestic shorthair\/random-bred<\/td>\n<td>~5-10%<\/td>\n<td>Various polygenic factors<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>A critical caveat for breeders and worried owners: a negative DNA test for A31P or R820W reduces the probability of that specific form of inherited HCM, but it does not eliminate the risk of HCM altogether. Cats carrying neither known mutation can still develop the disease through other genetic or polygenic pathways that have not yet been mapped. For this reason, screening echocardiograms in high-risk breeds, especially before breeding, remain the most reliable way to identify affected cats.<\/p>\n<p>Indoor pet cats from random-bred backgrounds still develop HCM, and a high index of suspicion is warranted in any cat with a heart murmur, gallop rhythm, arrhythmia, or unexplained breathing changes regardless of pedigree.<\/p>\n<h2>HCM Symptoms in Cats: What to Watch For<\/h2>\n<p>HCM has earned its reputation as a silent killer. A significant proportion of cats show no detectable abnormalities at home until the day they collapse from congestive heart failure (CHF) or arterial thromboembolism (ATE). This is partly because cats are masters at hiding illness, and partly because the disease can advance to a dangerous stage while the cat&#8217;s daily routine looks unchanged.<\/p>\n<p>The earliest finding in most cases is an incidental heart murmur picked up at a routine veterinary exam. Not all cats with HCM have a murmur, however. Roughly half of cats with confirmed HCM on echo have an audible murmur on physical exam, and the loudness of the murmur does not correlate with how severe the underlying disease is (NC State Veterinary Hospital cardiology data). A grade 1 murmur can mask serious disease, and a grade 4 murmur can be associated with mild structural changes. This is one of the most important and counter-intuitive points in feline cardiology.<\/p>\n<h3>The Symptom Spectrum, From Subtle to Emergent<\/h3>\n<ul>\n<li><strong>Earliest signs<\/strong>: An incidental murmur on routine exam. A gallop sound (an extra heart sound during diastole) is more specific for cardiac disease than a murmur. Some owners report decreased activity, sleeping more, or reduced playfulness, although these are easy to attribute to age.<\/li>\n<li><strong>Intermediate signs<\/strong>: Mild exercise intolerance, occasional open-mouth breathing after exertion or stress, slight reduction in appetite. Cats do not generally cough with heart disease the way dogs do; coughing in a cat is more often a respiratory rather than a cardiac sign.<\/li>\n<li><strong>Late or CHF-stage signs<\/strong>: Rapid, labored breathing at rest. A sleeping respiratory rate persistently above 40 breaths per minute is a red flag. Open-mouth breathing in a cat that is not panting from heat or stress is an emergency. Abdominal distension from ascites is uncommon in cats with HCM but possible. Pleural effusion, fluid accumulating in the chest cavity around the lungs, is a frequent CHF presentation in cats and produces marked respiratory distress.<\/li>\n<li><strong>Emergency: arterial thromboembolism (ATE)<\/strong>: Sudden onset of hindlimb paralysis or weakness, loud vocalization from pain, cold and pale or blue-tinged paw pads, dragging or inability to use the back legs. ATE is a true cardiovascular emergency that needs same-hour intervention.<\/li>\n<\/ul>\n<table>\n<thead>\n<tr>\n<th>Category<\/th>\n<th>Signs<\/th>\n<th>What to Do<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>Incidental finding (no symptoms)<\/td>\n<td>Heart murmur heard on routine exam<\/td>\n<td>Schedule echocardiogram<\/td>\n<\/tr>\n<tr>\n<td>Early concern<\/td>\n<td>Gallop rhythm, slightly reduced activity, mild breathing changes<\/td>\n<td>See cardiologist; echo to stage disease<\/td>\n<\/tr>\n<tr>\n<td>CHF onset<\/td>\n<td>Rapid breathing at rest (&gt;40\/min), labored breathing, open-mouth breathing, weakness<\/td>\n<td>Emergency vet immediately<\/td>\n<\/tr>\n<tr>\n<td>ATE (emergency)<\/td>\n<td>Sudden hindlimb paralysis, vocalization, cold paws, pale footpads<\/td>\n<td>Emergency vet immediately, time-critical<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>Owners often describe the transition from CHF onset to crisis as happening within hours. A cat that seemed slightly off in the morning may be in respiratory distress by evening. If you notice rapid breathing while your cat is sleeping or resting quietly, count the respiratory rate before deciding whether to wait or seek emergency care.<\/p>\n<h2>How HCM Is Diagnosed<\/h2>\n<p>Diagnosis rests on echocardiography. Every other test plays a supporting role.<\/p>\n<h3>Physical Examination<\/h3>\n<p>Auscultation may reveal a murmur, a gallop sound, an arrhythmia, or muffled heart sounds if pleural effusion is present. As noted above, a murmur is present in only about half of cats with HCM, so a normal auscultation does not rule out disease in a high-risk breed or in a cat with suspicious symptoms. The femoral pulse is checked in any cat with hindlimb weakness, because an absent femoral pulse is the bedside clue to aortic thromboembolism.<\/p>\n<h3>Echocardiogram<\/h3>\n<p>An echocardiogram, performed by a board-certified veterinary cardiologist when possible, is the gold standard. Two-dimensional, M-mode, and Doppler measurements quantify wall thickness, chamber sizes, the left atrium-to-aortic-root ratio (LA:Ao), valve function including the presence of systolic anterior motion (SAM) of the mitral valve, and flow patterns indicating diastolic dysfunction. Interventricular septal thickness or left ventricular free wall thickness greater than 6 mm at end-diastole is the conventional threshold, although context matters: a thinner-walled cat with severe atrial enlargement may still have advanced disease. The North Carolina State Veterinary Hospital provides a useful patient-facing overview of how echocardiograms guide HCM management on their <a href=\"https:\/\/hospital.cvm.ncsu.edu\/services\/small-animals\/cardiology\/cardiology-feline-hypertrophic-cardiomyopathy\/\" target=\"_blank\" rel=\"noopener noreferrer\">NC State Vet Hospital HCM page<\/a>.<\/p>\n<h3>NT-proBNP Blood Test<\/h3>\n<p>N-terminal pro B-type natriuretic peptide (NT-proBNP) is released by stretched cardiac muscle. Elevated levels in cats correlate with significant cardiac disease, and the test is useful as a screening tool, particularly to triage cats with a murmur for which an echocardiogram is not immediately available, and to monitor cats already diagnosed. A normal NT-proBNP does not exclude HCM completely, but it makes clinically meaningful disease less likely.<\/p>\n<h3>Chest Radiographs<\/h3>\n<p>Thoracic radiographs detect cardiomegaly, left atrial enlargement, pulmonary edema, and pleural effusion. X-rays are essential when CHF is suspected. They are less useful than echocardiography for staging preclinical disease, because a cat can have substantial structural HCM with relatively normal-looking chest radiographs.<\/p>\n<h3>Electrocardiogram (ECG)<\/h3>\n<p>ECG identifies arrhythmias including atrial fibrillation, ventricular premature complexes, and conduction abnormalities. ECG by itself does not diagnose HCM but can detect dangerous rhythm disturbances that change management.<\/p>\n<h3>Blood Pressure<\/h3>\n<p>Indirect blood pressure measurement, usually via Doppler, screens for systemic hypertension. Cats with concurrent kidney disease, hyperthyroidism, or unexplained ventricular hypertrophy need their blood pressure checked. Hypertension can both cause secondary hypertrophy and worsen primary HCM.<\/p>\n<h3>Thyroid Panel and Routine Bloodwork<\/h3>\n<p>A total T4 (and free T4 in middle-aged or older cats) is essential to rule out hyperthyroidism. A complete blood count, chemistry panel, and urinalysis evaluate kidney function, electrolytes, and the overall metabolic picture. These results also establish a baseline for cats who may need diuretics, which can alter renal values and potassium.<\/p>\n<h2>HCM Severity: Understanding the ACVIM Classification<\/h2>\n<p>The American College of Veterinary Internal Medicine (ACVIM) consensus statement on feline cardiomyopathy stages the disease using both structural findings on echocardiography and clinical signs. This framework standardizes communication between primary veterinarians, cardiologists, and owners, and it directly informs treatment decisions.<\/p>\n<table>\n<thead>\n<tr>\n<th>Stage<\/th>\n<th>Description<\/th>\n<th>Typical Management<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>Stage A<\/td>\n<td>High-risk breed, no structural disease on echo yet<\/td>\n<td>Periodic screening (echo every 1-2 years)<\/td>\n<\/tr>\n<tr>\n<td>Stage B1<\/td>\n<td>Structural disease present but no left atrial enlargement; no symptoms<\/td>\n<td>Monitoring; no medications proven to slow progression at this stage<\/td>\n<\/tr>\n<tr>\n<td>Stage B2<\/td>\n<td>Structural disease with left atrial enlargement (LA:Ao &gt;1.5); no symptoms yet<\/td>\n<td>Clopidogrel for ATE prevention; atenolol or diltiazem considered in some cases<\/td>\n<\/tr>\n<tr>\n<td>Stage C<\/td>\n<td>Current or historical CHF, fluid in or around the lungs, or pleural effusion<\/td>\n<td>Furosemide, pimobendan, ACE inhibitors; clopidogrel continued<\/td>\n<\/tr>\n<tr>\n<td>Stage D<\/td>\n<td>Refractory CHF despite standard therapies<\/td>\n<td>Adjusted diuretic regimen, specialist referral, palliative options<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>A few key points the staging system clarifies. Stage A cats may never develop disease at all, and breed-based screening is appropriate even in healthy-looking animals from high-risk lines. Stage B1 cats have structural hypertrophy but a still-normal-sized atrium and a low short-term risk of clot or CHF; no medication has been shown to slow progression in this stage in randomized trials, so monitoring is the standard. Stage B2 is the transition point where antithrombotic therapy with clopidogrel becomes appropriate because atrial enlargement raises the risk of thromboembolism. Stage C is symptomatic CHF, which requires diuretics and often additional agents. Stage D is refractory disease that continues to progress despite optimized therapy.<\/p>\n<h2>Treatment Options by Stage<\/h2>\n<p>There is currently no cure for primary HCM. Treatment goals are concrete: slow progression where evidence supports it, prevent and manage CHF, and reduce the risk of thromboembolism. Every cat is treated as an individual, based on echocardiographic findings, clinical signs, comorbidities, and tolerability of medications. A specific protocol that suits one Stage C cat may be wrong for another.<\/p>\n<table>\n<thead>\n<tr>\n<th>Drug<\/th>\n<th>Drug Class<\/th>\n<th>When Used<\/th>\n<th>Evidence Level<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>Furosemide (Lasix)<\/td>\n<td>Loop diuretic<\/td>\n<td>Stage C\/D (active CHF), reduces fluid accumulation<\/td>\n<td>Strong (standard of care for CHF)<\/td>\n<\/tr>\n<tr>\n<td>Clopidogrel (Plavix) 18.75 mg\/day<\/td>\n<td>Antiplatelet<\/td>\n<td>Stage B2, C, D, ATE prevention<\/td>\n<td>Strong (FATCAT trial 2015)<\/td>\n<\/tr>\n<tr>\n<td>Atenolol<\/td>\n<td>Beta-blocker<\/td>\n<td>Systolic anterior mitral valve motion (SAM); tachyarrhythmias<\/td>\n<td>Moderate (used in specific indications, not all HCM)<\/td>\n<\/tr>\n<tr>\n<td>Diltiazem<\/td>\n<td>Calcium channel blocker<\/td>\n<td>Heart rate control; may improve diastolic function<\/td>\n<td>Limited (evidence is mixed)<\/td>\n<\/tr>\n<tr>\n<td>Enalapril \/ Benazepril<\/td>\n<td>ACE inhibitor<\/td>\n<td>Stage C\/D; Merck notes no apparent benefit before CHF onset<\/td>\n<td>Moderate (pre-CHF use controversial)<\/td>\n<\/tr>\n<tr>\n<td>Pimobendan<\/td>\n<td>Cardiac inotrope\/vasodilator<\/td>\n<td>Stage C\/D CHF (use in HCM cats is growing but differs from dog protocols)<\/td>\n<td>Growing evidence in feline CHF<\/td>\n<\/tr>\n<tr>\n<td>Spironolactone<\/td>\n<td>Aldosterone antagonist\/diuretic<\/td>\n<td>Stage D, adjunct diuresis<\/td>\n<td>Limited in cats<\/td>\n<\/tr>\n<tr>\n<td>Torsemide<\/td>\n<td>Loop diuretic (potent)<\/td>\n<td>Stage D refractory cases<\/td>\n<td>Limited<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<h3>What the Evidence Actually Supports<\/h3>\n<p>The pillar of CHF management in cats is furosemide. It is the most evidence-supported drug in feline cardiology and the foundation of treatment for any cat with current or historical CHF. Dosing is highly individualized, titrated to respiratory rate and clinical signs while monitoring kidney values and electrolytes. Owners typically learn to recognize when a dose adjustment is needed, in close consultation with their veterinarian.<\/p>\n<p>The FATCAT trial published by Hogan and colleagues in 2015 in the Journal of Veterinary Internal Medicine compared clopidogrel to aspirin for prevention of recurrent ATE in cats. Clopidogrel substantially outperformed aspirin, reducing recurrence and extending survival. The standard dose used clinically is 18.75 mg per cat once daily, and the drug is well tolerated. Because of this trial, clopidogrel has become the standard antithrombotic in cats with significant left atrial enlargement (Stage B2 and beyond), even before any ATE event has occurred.<\/p>\n<p>Beta-blockers such as atenolol are useful in specific situations: cats with significant systolic anterior motion of the mitral valve causing dynamic left ventricular outflow tract obstruction, and cats with sustained tachyarrhythmias. The historic practice of starting every HCM cat on atenolol is no longer supported, because randomized data have not shown a survival benefit in cats without those specific indications.<\/p>\n<p>Calcium channel blockers such as diltiazem have been used to improve diastolic relaxation and slow heart rate. Evidence is mixed, and they are no longer first-line for most cats. Some cardiologists still use diltiazem in selected cases where rate control is needed and a beta-blocker is contraindicated.<\/p>\n<p>ACE inhibitors (enalapril, benazepril) are commonly used in Stage C and D cats. The Merck Veterinary Manual notes that there is no clear evidence of benefit in cats before CHF onset, and pre-CHF use remains controversial. You can read their full discussion in the <a href=\"https:\/\/www.merckvetmanual.com\/circulatory-system\/cardiomyopathy-in-dogs-and-cats\/hypertrophic-cardiomyopathy-in-dogs-and-cats\" target=\"_blank\" rel=\"noopener noreferrer\">Merck Veterinary Manual HCM entry<\/a>.<\/p>\n<p>Pimobendan, a positive inotrope and vasodilator widely used in canine heart disease, has historically been used cautiously in HCM cats because of concern about worsening dynamic outflow obstruction in cats with SAM. Recent evidence suggests pimobendan can be beneficial in cats with CHF, particularly when systolic function is impaired or in end-stage disease, although the protocols differ from those used in dogs. It is increasingly part of the toolkit for Stage C and D feline patients.<\/p>\n<p>Spironolactone provides modest additional diuresis and aldosterone antagonism but evidence in cats is limited. Some Stage D protocols include it. Torsemide is a more potent loop diuretic reserved for refractory cases where furosemide is no longer producing adequate diuresis.<\/p>\n<p>Whatever the specific regimen, your cardiologist tailors the drug list to your cat&#8217;s echocardiogram, ECG, blood pressure, and bloodwork. A protocol pulled from the internet, or copied from another cat, is not a substitute for that individualized plan.<\/p>\n<h2>Aortic Thromboembolism (ATE): The Complication That Changes Everything<\/h2>\n<p>Of every aspect of feline HCM, aortic thromboembolism deserves the most careful attention from owners, because it is the single complication most likely to end your cat&#8217;s life or quality of life suddenly. Most consumer-facing HCM articles cover ATE in a sentence or two, which does owners a disservice.<\/p>\n<h3>What Actually Happens<\/h3>\n<p>As the left atrium enlarges, blood flow inside it becomes turbulent and slow, similar in principle to atrial fibrillation in humans. Slow flow plus endothelial changes set up the classic Virchow conditions for clot formation. A thrombus forms inside the left atrium or the left auricle. At some point, a piece breaks off and travels through the aorta until it wedges, most commonly at the aortic trifurcation where the aorta divides into the iliac arteries supplying the hind legs. This is the saddle thrombus. Blood flow to the hindlimbs is abruptly cut off. Muscle tissue downstream of the clot becomes ischemic within minutes, releasing potassium and other inflammatory mediators that can affect cardiac rhythm and kidney function.<\/p>\n<h3>What You Will See<\/h3>\n<p>The presentation is dramatic and almost unmistakable once you know what to look for: sudden onset of hindlimb paralysis or severe weakness, often affecting both legs but sometimes one, intense vocalization from pain (a cat in ATE pain often howls or screams), cold paws on the affected limbs, pale or blue-tinged paw pads, and absent femoral pulses. Cats may also breathe rapidly because of pain, shock, or concurrent CHF.<\/p>\n<p>Front limb ATE happens occasionally, and the right brachial artery is the most common site. Affected cats present with a cold, painful, paretic forelimb.<\/p>\n<h3>The Grim Reality<\/h3>\n<p>Acute ATE carries roughly a 30 to 40 percent in-hospital mortality even with aggressive care. For cats who survive the initial 48 to 72 hours, prognosis improves but remains guarded, because the underlying heart disease that caused the clot is still present and a second ATE can occur. Historical recurrence rates without antithrombotic therapy were high, with many cats experiencing a second event within six months.<\/p>\n<p>The FATCAT trial changed this picture. Cats treated with clopidogrel after a first ATE had significantly lower recurrence and longer survival than those on aspirin. This is the reason cats with significant atrial enlargement (Stage B2) are now started on clopidogrel preemptively, before any ATE has occurred, and it is also why every cat who survives a first ATE should be on clopidogrel indefinitely.<\/p>\n<h3>The Decision Owners Face<\/h3>\n<p>ATE is excruciatingly painful in the acute phase. Many emergency clinicians will offer adequate analgesia (often a constant rate opioid infusion) and time to see whether the cat stabilizes. Some owners, after honest conversation with the veterinarian about prognosis, choose humane euthanasia at the time of first ATE rather than pursue aggressive treatment. This is not a wrong choice, and there is no universal right answer; the decision involves the individual cat, the underlying cardiac stage, comorbidities, the owner&#8217;s resources, and the cat&#8217;s likely quality of life if it survives. A veterinary cardiologist or emergency clinician should walk you through the realistic outcomes for your cat specifically.<\/p>\n<h3>Recovery, When It Happens<\/h3>\n<p>Cats who survive ATE often regain partial limb function over weeks to months as collateral circulation develops. Some cats walk again with mild residual weakness or a stiff gait, while others have permanent paresis or paralysis of one or both legs. Bandaging may be needed for skin sloughs over pressure points. Long-term antiplatelet therapy is non-negotiable in survivors.<\/p>\n<h2>The HCM-Hyperthyroidism Connection<\/h2>\n<p>One of the most important diagnostic crossroads in middle-aged and older cats is the relationship between thyroid disease and cardiac disease. Hyperthyroidism is the most common endocrine disorder in older cats, and it routinely produces left ventricular hypertrophy that mimics primary HCM on echocardiogram.<\/p>\n<p>The mechanism: thyroid hormone has direct effects on cardiac muscle, increasing contractility and heart rate, and indirect effects through increased metabolic demand and adrenergic sensitivity. The heart compensates by hypertrophying. Cats with hyperthyroidism may also develop systemic hypertension, which adds another stimulus to ventricular thickening.<\/p>\n<p>The clinical implication is enormous: when hyperthyroidism is treated, whether by methimazole, radioactive iodine, surgery, or a prescription iodine-restricted diet, the cardiac hypertrophy often regresses substantially or fully. A cat that looks like it has primary HCM may actually have reversible secondary hypertrophy. This is why a thyroid panel is mandatory in any newly diagnosed feline cardiomyopathy case, especially in cats over seven years of age.<\/p>\n<p>There is a further nuance worth understanding. Many cats with hyperthyroidism also have underlying chronic kidney disease that is masked by the hyperdynamic state. Treating the thyroid disease can unmask azotemia and prompt initiation of kidney-protective measures. The interplay is covered in more depth in our article on <a href=\"https:\/\/seniorsniffs.com\/index.php\/2026\/06\/02\/hyperthyroidism-in-cats\/\">hyperthyroidism in cats<\/a>, which we suggest reading alongside this one for any senior cat with both cardiac and thyroid findings.<\/p>\n<h2>HCM and Kidney Disease: Managing Two Conditions at Once<\/h2>\n<p>Many senior cats arrive at the cardiologist already carrying a diagnosis of chronic kidney disease (CKD), or the diagnosis emerges as CHF management progresses. These two diseases interact in ways that make co-management one of the most challenging scenarios in feline internal medicine.<\/p>\n<p>The core problem is the diuretic dilemma. Furosemide and other loop diuretics are essential for managing CHF, because they pull fluid out of the lungs and chest cavity. Diuresis simultaneously reduces effective circulating volume, however, and the kidneys depend on adequate perfusion to filter waste. A cat with marginal kidney function and significant cardiac disease often sits on a tightrope: too little diuretic and the lungs fill with fluid, too much diuretic and the kidneys decompensate.<\/p>\n<p>Practical implications:<\/p>\n<ul>\n<li><strong>Frequent monitoring<\/strong>: BUN, creatinine, electrolytes (especially potassium), and urine specific gravity should be checked regularly in any cat on diuretics. The frequency depends on disease severity, but every few weeks at the start of therapy and at every dose change is reasonable.<\/li>\n<li><strong>SDMA<\/strong>: Symmetric dimethylarginine is a more sensitive early marker of glomerular filtration than creatinine, useful for picking up worsening kidney function before BUN and creatinine rise.<\/li>\n<li><strong>Hydration<\/strong>: Subcutaneous fluids, sometimes given in mild CKD, are problematic in advanced HCM because volume loading can precipitate CHF. Any decision to add fluids requires close coordination between primary vet and cardiologist.<\/li>\n<li><strong>ACE inhibitors<\/strong>: ACE inhibitors are kidney-protective in proteinuric CKD by lowering intraglomerular pressure. In cats with HCM, their role is less clear: evidence of benefit in pre-CHF stages is limited, and they may be more useful in Stage C and D animals. Decisions to use enalapril or benazepril balance cardiac and renal considerations.<\/li>\n<li><strong>Diet<\/strong>: Renal diets and cardiac diets sometimes diverge (sodium restriction is shared, but protein restriction is debated). The decision is highly individualized.<\/li>\n<\/ul>\n<p>Owners managing both conditions benefit from explicit communication between their primary vet, internist if involved, and cardiologist. For background on the kidney side of this equation, see our articles on <a href=\"https:\/\/seniorsniffs.com\/index.php\/2026\/05\/28\/kidney-disease-in-cats\/\">kidney disease in cats<\/a> and the early <a href=\"https:\/\/seniorsniffs.com\/index.php\/2026\/05\/29\/signs-of-kidney-disease-in-cats\/\">signs of kidney disease in cats<\/a> that may overlap with or be masked by cardiac signs.<\/p>\n<h2>Omega-3 Fatty Acids and Cardiac Support<\/h2>\n<p>Omega-3 fatty acids, specifically EPA and DHA from fish or algal sources, have been studied across cardiovascular conditions in multiple species. In dogs with cardiac disease, omega-3 supplementation has shown benefits including reduced arrhythmia frequency, anti-inflammatory effects, and possible preservation of muscle mass in cardiac cachexia. In cats, the data are thinner, but the general cardiac and anti-inflammatory rationale carries over.<\/p>\n<p>We suggest discussing omega-3 supplementation with your cardiologist before starting on your own. Important caveats:<\/p>\n<ul>\n<li>Dose matters. High doses of omega-3s can have antiplatelet effects, which become a consideration in cats already on clopidogrel.<\/li>\n<li>Quality matters. Fish oil products vary widely in EPA\/DHA concentration and in oxidation; rancid oil can be pro-inflammatory.<\/li>\n<li>Source matters in cats specifically. Cats can be sensitive to certain oils and to high-mercury fish sources.<\/li>\n<\/ul>\n<p>For a deeper discussion of fish-oil chemistry and dosing in pets, we have a companion piece on <a href=\"https:\/\/seniorsniffs.com\/index.php\/2023\/12\/22\/fish-oil-for-dogs\/\">fish oil for dogs<\/a> that covers EPA\/DHA fundamentals applicable across species, and a more general article on <a href=\"https:\/\/seniorsniffs.com\/index.php\/2023\/12\/22\/omega-3-for-dogs\/\">omega-3 for pets<\/a> that walks through evidence quality and dosing frameworks.<\/p>\n<figure>\n<img decoding=\"async\" src=\"https:\/\/seniorsniffs.com\/wp-content\/uploads\/2026\/06\/cat-owner-monitoring-resting-respiratory-rate-hcm.jpg\" alt=\"Cat owner monitoring senior cat's resting respiratory rate at home using phone timer as part of HCM management\" title=\"Cat Owner Monitoring Resting Respiratory Rate - HCM Home Management\" \/><figcaption>Monitoring your cat&#8217;s sleeping respiratory rate at home is one of the most valuable tools for early detection of fluid buildup. A rate consistently above 40 breaths per minute during sleep warrants a call to your vet.<\/figcaption><\/figure>\n<h2>Monitoring Your Cat at Home and With Your Vet<\/h2>\n<p>The single most useful home monitoring tool in feline cardiology is the resting respiratory rate. The number of breaths your cat takes per minute while sleeping or resting quietly is one of the earliest and most sensitive signals of impending CHF, and it is something any owner can measure with a watch or a phone timer.<\/p>\n<h3>How to Measure Resting Respiratory Rate<\/h3>\n<ol>\n<li>Wait until your cat is genuinely asleep or deeply resting, not panting, not just having played, not in a hot room.<\/li>\n<li>Watch the chest or abdomen. One breath equals one full rise and fall.<\/li>\n<li>Count the breaths for 30 seconds and multiply by 2, or for 60 seconds for a direct count.<\/li>\n<li>Record the number and the date.<\/li>\n<\/ol>\n<h3>What the Numbers Mean<\/h3>\n<ul>\n<li><strong>Normal sleeping rate<\/strong>: Fewer than 30 breaths per minute.<\/li>\n<li><strong>Watch closely<\/strong>: Sustained rates of 30 to 40 breaths per minute warrant a call to your veterinarian if this is a change from baseline.<\/li>\n<li><strong>Emergency threshold<\/strong>: A sleeping rate persistently above 40 breaths per minute is a strong signal of pulmonary edema or pleural effusion, and is an indication for immediate veterinary evaluation.<\/li>\n<\/ul>\n<p>Several apps exist to help owners log resting respiratory rate over time, and many cardiologists welcome a phone-photo or screenshot of the log at recheck appointments. The trend matters as much as any single reading; a cat creeping from a baseline of 22 to 35 over a few weeks may be in early CHF even though no single number looks alarming.<\/p>\n<table>\n<thead>\n<tr>\n<th>HCM Stage<\/th>\n<th>Echo Recheck Frequency<\/th>\n<th>Additional Tests<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>Stage A (high-risk breed, no disease)<\/td>\n<td>Every 1-2 years<\/td>\n<td>NT-proBNP, physical exam<\/td>\n<\/tr>\n<tr>\n<td>Stage B1 (mild structural changes)<\/td>\n<td>Every 12-18 months<\/td>\n<td>NT-proBNP, blood panel<\/td>\n<\/tr>\n<tr>\n<td>Stage B2 (LA enlargement, preclinical)<\/td>\n<td>Every 6-12 months<\/td>\n<td>NT-proBNP, chest X-ray, blood panel<\/td>\n<\/tr>\n<tr>\n<td>Stage C (CHF)<\/td>\n<td>Every 3-6 months or as needed<\/td>\n<td>Chest X-ray, blood panel, electrolytes<\/td>\n<\/tr>\n<tr>\n<td>Stage D (refractory)<\/td>\n<td>As directed by cardiologist<\/td>\n<td>Frequent bloodwork to monitor kidneys and electrolytes<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<h3>When to Call Your Vet, and When to Go to the ER<\/h3>\n<p>Same-week appointment for any of the following:<\/p>\n<ul>\n<li>Resting respiratory rate consistently rising above baseline<\/li>\n<li>Decreased appetite over several days<\/li>\n<li>Increased lethargy that is sustained<\/li>\n<li>Weight loss that you can feel along the spine or hips<\/li>\n<\/ul>\n<p>Same-hour ER for any of the following:<\/p>\n<ul>\n<li>Resting respiratory rate above 40 breaths per minute<\/li>\n<li>Open-mouth breathing<\/li>\n<li>Sudden hindlimb weakness or paralysis<\/li>\n<li>Collapse, fainting, or severe lethargy<\/li>\n<li>Cold or pale paw pads<\/li>\n<li>Vocalization that suggests pain<\/li>\n<\/ul>\n<h2>Prognosis and Life Expectancy<\/h2>\n<p>Prognosis in HCM is highly stage-dependent. Generalized survival figures hide enormous individual variation, and your cardiologist&#8217;s estimate, based on your cat&#8217;s specific echocardiogram, is more accurate than any web average. With that caveat, the following figures from published case series and university referral hospitals offer a sense of the range.<\/p>\n<ul>\n<li><strong>Preclinical Stage B1<\/strong>: Many cats live for years with minimal disease progression. A meaningful subset never advance to CHF and ultimately die of unrelated causes.<\/li>\n<li><strong>Preclinical Stage B2<\/strong>: Prognosis is guarded. Roughly 20% of these cats develop CHF within five years of diagnosis (NC State data). The risk of ATE is also non-trivial, which is why clopidogrel becomes standard at this stage.<\/li>\n<li><strong>Stage C (active or historical CHF)<\/strong>: Median survival is approximately 12 months from CHF onset with appropriate management (NC State and Merck Veterinary Manual data). Some cats live considerably longer; others have a much shorter course.<\/li>\n<li><strong>Stage D (refractory CHF)<\/strong>: Survival is measured in weeks to months. The goal at this stage is comfort and quality of life.<\/li>\n<\/ul>\n<p>An ATE event substantially shortens median survival, regardless of stage at the time it occurs.<\/p>\n<h3>Factors Associated With Shorter Survival<\/h3>\n<ul>\n<li>Severe left atrial enlargement (LA:Ao ratio above 2.0)<\/li>\n<li>Atrial fibrillation or other sustained tachyarrhythmias<\/li>\n<li>History of ATE<\/li>\n<li>Male sex<\/li>\n<li>Older age at diagnosis<\/li>\n<li>Concurrent CKD or hyperthyroidism poorly controlled<\/li>\n<li>Persistent pleural effusion despite therapy<\/li>\n<\/ul>\n<h3>Factors Associated With Longer Survival<\/h3>\n<ul>\n<li>Stage B1 at diagnosis<\/li>\n<li>Mild atrial enlargement or LA:Ao ratio below 1.7<\/li>\n<li>Well-controlled heart rate<\/li>\n<li>Good response to initial CHF therapy (rapid resolution of edema or effusion)<\/li>\n<li>No history of ATE<\/li>\n<li>Compliant home monitoring of resting respiratory rate<\/li>\n<\/ul>\n<h2>When Is It Time? End-of-Life Considerations<\/h2>\n<p>For cats whose disease has advanced into Stage D, or who have suffered ATE, or who are no longer responding to maximal therapy, the decisions facing owners shift. Treatment becomes less about extending survival and more about preserving the daily experience of the cat. Most consumer-facing HCM articles avoid this topic; we think that does owners a disservice, because the question of &#8220;when is it time&#8221; is often the hardest part of caring for a cat with HCM.<\/p>\n<h3>Signs the Disease Is Advancing Despite Treatment<\/h3>\n<ul>\n<li>More frequent CHF episodes requiring increases in diuretic dose<\/li>\n<li>Diuretic doses approaching ceiling without adequate response<\/li>\n<li>Worsening kidney values that limit further diuretic adjustment<\/li>\n<li>Weight loss, especially loss of muscle along the back and hips<\/li>\n<li>Persistent reduced appetite<\/li>\n<li>Reluctance to engage with the household, hiding more than usual<\/li>\n<li>Visible labored breathing even at rest, despite medication adjustments<\/li>\n<li>Repeated ATE events<\/li>\n<\/ul>\n<h3>A Practical Quality-of-Life Framework<\/h3>\n<p>Several validated quality-of-life scales exist; what they share is a focus on the cat&#8217;s experience over a typical day. We suggest asking yourself the following weekly:<\/p>\n<ul>\n<li>Is my cat breathing comfortably at rest most of the time?<\/li>\n<li>Is my cat eating and drinking voluntarily?<\/li>\n<li>Can my cat rest comfortably without distress?<\/li>\n<li>Does my cat still seek out interaction, even briefly?<\/li>\n<li>Is my cat using the litter box without difficulty?<\/li>\n<li>Does the cat seem to have more good moments than difficult ones?<\/li>\n<\/ul>\n<p>When several of those answers shift from yes to no over a sustained period, it is time to have an honest conversation with your veterinarian.<\/p>\n<h3>When to Initiate That Conversation<\/h3>\n<p>You do not need to wait until the cat is suffering. Open dialogue is better held early, while you and your veterinarian still have options. Consider initiating it when:<\/p>\n<ul>\n<li>Hospitalizations are becoming more frequent<\/li>\n<li>The cat is not fully recovering between episodes<\/li>\n<li>You are unsure whether the cat is comfortable at home<\/li>\n<li>You are anticipating a stage transition (B2 to C, or C to D)<\/li>\n<\/ul>\n<p>There is no universal right answer to when to elect humane euthanasia, and there is no badge for waiting longer. The standard is the individual cat&#8217;s lived experience, not just survival time. Palliative care options, focused on keeping the cat comfortable at home with adjusted medications and minimized stress, are appropriate to discuss with your cardiologist if you prefer to manage at home for as long as feasible.<\/p>\n<h2>Frequently Asked Questions About HCM in Cats<\/h2>\n<h3>Can cats live a normal life with HCM?<\/h3>\n<p>Many cats with preclinical HCM (Stage B1) live an essentially normal life and die from unrelated causes. As disease advances into Stage B2 and beyond, normalcy gradually erodes: medications enter the daily routine, activity may decline, and monitoring becomes part of life. With committed home monitoring and appropriate medical care, many cats maintain good quality of life for years even after a diagnosis. Cats in Stage C or D will have meaningful limitations on activity and a guarded prognosis.<\/p>\n<h3>What is the life expectancy for a cat with HCM?<\/h3>\n<p>It depends heavily on stage. Cats with preclinical, mild disease (Stage B1) may live a normal lifespan. Stage B2 cats have a guarded prognosis with roughly 20% progressing to CHF within five years (NC State data). Cats in CHF (Stage C) have a median survival around 12 months from CHF onset with treatment, although individual variation is large (Merck Veterinary Manual). Cats who experience an ATE event typically have shorter survival regardless of stage.<\/p>\n<h3>Is HCM in cats painful?<\/h3>\n<p>The structural changes of HCM themselves are not generally painful. Cats in CHF can be uncomfortable due to difficulty breathing, and this distress is significant and should be addressed promptly. Aortic thromboembolism is severely painful in the acute phase, which is one of the strongest arguments for clopidogrel prophylaxis in eligible cats and for prompt veterinary care if ATE occurs. Adequate pain control, usually with opioids, is essential in any cat with ATE.<\/p>\n<h3>Can HCM in cats be cured?<\/h3>\n<p>No. Primary HCM cannot be cured. Treatment manages symptoms and reduces complication risk. There is an important exception: cats with secondary cardiac hypertrophy from hyperthyroidism, systemic hypertension, or acromegaly can sometimes show substantial reversal of cardiac changes when the underlying cause is treated. This is why every newly diagnosed HCM cat should have thyroid testing and a blood pressure measurement.<\/p>\n<h3>Is HCM in cats hereditary?<\/h3>\n<p>Yes, in many cases. Two specific mutations are well-documented: MYBPC3 A31P in Maine Coons and MYBPC3 R820W in Ragdolls. DNA tests for these mutations are widely available. Other breeds with elevated prevalence, including the Sphynx, Scottish Fold, British Shorthair, and Siberian, do not yet have identified causative mutations, but a strong genetic component is suspected. Domestic shorthair cats can also develop HCM through polygenic or as-yet-unidentified genetic mechanisms.<\/p>\n<h3>What should I feed a cat with HCM?<\/h3>\n<p>For preclinical cats, a high-quality complete and balanced commercial diet is appropriate. Specific dietary modifications enter the picture as disease advances: sodium restriction is reasonable in CHF, and protein quality may need attention if concurrent CKD develops. Cardiac diets specifically formulated for cats are available, and your cardiologist can guide selection based on your cat&#8217;s stage and comorbidities. Avoid sudden diet changes during active CHF, when appetite is already fragile. Maintaining caloric intake is critical to prevent cardiac cachexia, the muscle wasting that can occur with advanced heart disease.<\/p>\n<h3>Can I breed a cat that has tested positive for HCM mutations?<\/h3>\n<p>The mainstream view in feline cardiology is that cats homozygous for known HCM mutations should not be bred, and breeders should screen breeding cats with both DNA testing (for A31P or R820W where applicable) and periodic echocardiography. Heterozygotes also have elevated risk, and many breed registries have moved toward selecting against the mutation entirely in affected breeds. Even a negative genetic test does not guarantee a cat will not develop HCM, so screening echocardiograms in breeding programs remain important alongside DNA testing.<\/p>\n<h3>How do I know if my cat is going into heart failure?<\/h3>\n<p>The earliest and most reliable home signal is a rising resting respiratory rate. Sleeping rates persistently above 40 breaths per minute, or open-mouth breathing in a cat that is not stressed or overheated, indicate possible pulmonary edema or pleural effusion and warrant emergency evaluation. Other signs include lethargy, decreased appetite, weakness, hiding, and in some cats a slightly hunched posture suggesting respiratory effort. By the time external signs are obvious, the cat is usually well into CHF, which is why daily or near-daily counts of sleeping respiratory rate are so valuable.<\/p>\n<p><script type=\"application\/ld+json\">\n{\n  \"@context\": \"https:\/\/schema.org\",\n  \"@type\": \"Article\",\n  \"headline\": \"Hypertrophic Cardiomyopathy in Cats: What the Research Shows About HCM Symptoms, Diagnosis, and Treatment\",\n  \"description\": \"Evidence-based guide to HCM in cats: symptoms, ACVIM staging, echocardiogram diagnosis, treatment options, ATE risk, and prognosis from a senior pet care perspective.\",\n  \"author\": {\"@type\": \"Organization\", \"name\": \"SeniorSniffs.com\"},\n  \"publisher\": {\"@type\": \"Organization\", \"name\": \"SeniorSniffs.com\"},\n  \"datePublished\": \"2026-06-04\",\n  \"dateModified\": \"2026-06-04\",\n  \"mainEntityOfPage\": {\"@type\": \"WebPage\", \"@id\": \"https:\/\/seniorsniffs.com\/index.php\/2026\/06\/04\/hypertrophic-cardiomyopathy-in-cats\/\"}\n}\n<\/script><\/p>\n<p><script type=\"application\/ld+json\">\n{\n  \"@context\": \"https:\/\/schema.org\",\n  \"@type\": \"FAQPage\",\n  \"mainEntity\": [\n    {\n      \"@type\": \"Question\",\n      \"name\": \"Can cats live a normal life with HCM?\",\n      \"acceptedAnswer\": {\n        \"@type\": \"Answer\",\n        \"text\": \"Many cats with preclinical HCM (Stage B1) live an essentially normal life and die from unrelated causes. 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HCM is the most common feline heart disease, affecting up to roughly 15% [&hellip;]<\/p>\n","protected":false},"author":2,"featured_media":205,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"om_disable_all_campaigns":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":""},"categories":[9],"tags":[],"aioseo_notices":[],"_links":{"self":[{"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/posts\/208"}],"collection":[{"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/comments?post=208"}],"version-history":[{"count":0,"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/posts\/208\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/media\/205"}],"wp:attachment":[{"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/media?parent=208"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/categories?post=208"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/seniorsniffs.com\/index.php\/wp-json\/wp\/v2\/tags?post=208"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}