Hypertrophic Cardiomyopathy (HCM) in Cats

A Multi-Source Review

Note on the textbook library: The medical library available here contains human medicine textbooks only (Braunwald's Heart Disease, Robbins Pathology, Goldman-Cecil Medicine, etc.) — no veterinary textbooks are indexed. The review below therefore draws from the best available peer-reviewed veterinary literature across multiple authoritative sources: the landmark Kittleson & Côté series (J Feline Med Surg, 2021), a 2025 comprehensive review (Vet Sci), a 2024 genetics review (Curr Issues Mol Biol), and specialized 2023 reviews from Vet Clin North Am Small Anim Pract — effectively the "different books" of veterinary cardiology.

1. Overview & Epidemiology

• Cats of any age from 3 months upward, either sex, and any breed can be affected
• Males and domestic shorthair cats show higher prevalence
• Breed predispositions: Maine Coon, Ragdoll, British Shorthair, Sphynx, Persian
• Mixed-breed cats are numerically the most commonly affected

2. Pathology & Pathophysiology

• Disordered alignment (disarray) of cardiomyocytes
• Excessive collagen deposition (myocardial fibrosis)
• Reduced intracavitary internal diameter due to wall thickening

1. Elevated LV end-diastolic pressure → elevated left atrial (LA) pressure → pulmonary edema and/or pleural effusion (left heart failure)
2. Sluggish LA blood flow → atrial thrombus formation → aortic thromboembolism (ATE)

• Systolic anterior motion (SAM) of the mitral valve is the most common cause of dynamic left ventricular outflow tract obstruction (DLVOTO) and the most common cause of a cardiac murmur in HCM cats
• Diastolic dysfunction is the primary driver of clinical signs and death
• The distinction between obstructive HCM (HOCM) and non-obstructive HCM is of limited clinical importance in cats, since SAM can be induced in most HCM cats under certain conditions

3. Genetic Basis

• Myosin-binding protein C (MYBPC3) mutations are the most well-characterized
• These parallel the dominant sarcomeric mutations seen in human HCM (MYBPC3 and MYH7)
• However, many cats develop HCM without any known mutation, indicating undiscovered genetic factors and possibly polygenic inheritance
• The disease shows variable penetrance and expressivity — even cats carrying the same mutation may have very different disease courses

4. Clinical Signs

• No overt signs
• May or may not have a heart murmur or gallop sound (S3 or S4)
• Detected incidentally on physical exam or screening echo

• Dyspnea / tachypnea (left heart failure, pulmonary edema, pleural effusion)
• Acute posterior paresis/paralysis with cold, painful limbs (ATE — "saddle thrombus" at the aortic trifurcation)
• Syncope (less common)
• Sudden death

5. Diagnosis

Echocardiography (gold standard)

• LV wall thickness ≥ 6 mm (diastole) in the absence of other causes is the diagnostic threshold
• Asymmetric hypertrophy, SAM of the mitral valve, LA enlargement, reduced LV internal diameter
• Left atrial dysfunction is an early phenotypic abnormality and an important prognostic marker
• Newer techniques: tissue speckle-tracking echocardiography and contrast-enhanced echocardiography add information on myocardial function

• LA dysfunction on echo predicts both the risk of developing HCM in susceptible cats and the risk of cardiovascular events in cats already diagnosed

Biomarkers

• NT-proBNP: useful screening tool; elevated in cats with significant cardiomegaly; should NOT be used as the sole diagnostic test
• Troponin I: elevated in myocardial injury
• Galectin-3: under active investigation as a novel biomarker of fibrosis

Cardiac MRI

• Emerging tool providing information on myocardial fibrosis (late gadolinium enhancement)
• Valuable for risk stratification

Important exclusion criteria (HCM is a diagnosis of exclusion for mild-moderate cases):

• Hyperthyroidism — can cause reversible LV hypertrophy
• Systemic hypertension — same
• Acromegaly (excess GH)
• Dehydration/hemoconcentration

6. Complications

Congestive Heart Failure (CHF)

• Supplemental oxygen
• Furosemide (IV/IM) — first-line diuretic
• Thoracocentesis for large pleural effusions
• Anxiolytic support (butorphanol)

Arterial Thromboembolism (ATE)

• Most commonly involves the terminal aorta ("saddle thrombus") → bilateral hindlimb paralysis, cold extremities, absent femoral pulses
• Also affects forelimbs, kidneys, mesenteric vessels
• Pathogenesis involves Virchow's triad: sluggish LA flow + endothelial dysfunction + hypercoagulable state
• Recurrence rate is high despite treatment
• Active research into the roles of immunothrombosis and procoagulant platelets

7. Treatment

Heart Failure Management

• Loop diuretics (furosemide): cornerstone of CHF management
• ACE inhibitors / atenolol: used in various scenarios; no survival benefit proven
• Treatment is aimed at controlling signs, not reversing the myopathy

Pimobendan

• Pimobendan (0.25 mg/kg PO q12h) is a phosphodiesterase III inhibitor and calcium sensitizer
• Potential benefits: improved LV systolic and diastolic function, reduced platelet aggregation, reduced LA size, improved LA systolic function
• Indicated for CHF associated with systolic dysfunction (dilated, restrictive, arrhythmogenic RV cardiomyopathy)
• Also used in CHF secondary to HCM, though evidence is more limited
• Contraindicated in fixed LVOT obstruction (aortic stenosis)
• Not licensed for cats in most countries, but widely used off-label

Antithrombotic Therapy

• Clopidogrel (antiplatelet) reduces risk of ATE recurrence and is standard-of-care after a first ATE event
• As primary prevention in severe HCM: absolute risk reduction is modest (~3–4%)
• Clopidogrel is unpalatable, making consistent administration challenging
• Clinicians should weigh realistic benefit against administration difficulty on a per-patient basis
• Aspirin (81 mg q72h) may be used as alternative or in combination (FATCAT trial data)

Novel / Investigational Therapies

• Small molecule myosin inhibitors (e.g., mavacamten — now used in human HCM) are under investigation in cats
• Rapamycin (mTOR inhibitor): clinical trials underway exploring anti-hypertrophic effects
• Cats serve as a valuable naturally occurring large animal model for human HCM drug development
• No current therapy has demonstrated reversal or slowing of the underlying cardiomyopathic process

8. Prognosis

Summary Table by Source