
Feline Hypertrophic Cardiomyopathy (HCM)
🫀 Feline Hypertrophic Cardiomyopathy (HCM) is the most prevalent form of heart disease in cats and a critical condition to understand for NAVLE preparation. It is characterized by primary concentric hypertrophy of the left ventricular myocardium, typically in the absence of other systemic causes such as hypertension or hyperthyroidism. HCM can lead to diastolic dysfunction, left atrial enlargement, congestive heart failure (CHF), and predisposition to arterial thromboembolism (ATE)—particularly saddle thrombus formation. Commonly affected breeds include Maine Coons and Ragdolls, often with an autosomal dominant genetic mutation in the myosin-binding protein C (MYBPC3) gene. Clinical manifestations range from asymptomatic murmurs to severe respiratory distress and sudden death. Diagnosis is based on echocardiography, and treatment focuses on controlling heart rate, improving diastolic filling, and preventing thromboembolic events.
Comprehensive Information on Feline Hypertrophic Cardiomyopathy (HCM) for NAVLE Preparation
Definition
Hypertrophic Cardiomyopathy (HCM): The most common form of feline cardiomyopathy, characterized by concentric left ventricular hypertrophy (LVH) without another cardiac or systemic disease capable of producing this magnitude of hypertrophy.
Etiology
Genetic Basis:
Identified mutations in Maine Coons and Ragdolls, specifically in the myosin binding protein C gene (A31P and R820W mutations).
Likely hereditary in Sphynx cats and suspected in other breeds like Bengal, American Shorthair, British Shorthair, Persian, and Siberian.
Unidentified causes: In many cases, particularly in mixed-breed cats.
Pathophysiology
Myocardial Hypertrophy: The LV wall thickens due to abnormal sarcomere function, which increases myocardial contractility, leading to diastolic dysfunction.
Diastolic Dysfunction: A stiff LV results in elevated left atrial (LA) pressure, causing LA enlargement and increased pulmonary venous pressure, leading to pulmonary edema (PE) and pleural effusion (PLE).
Systolic Anterior Motion (SAM): Common in HCM, where the anterior mitral valve leaflet moves into the LV outflow tract (LVOT) during systole, causing dynamic LVOT obstruction (DLVOTO) and contributing to mitral regurgitation.
Clinical Signs
Asymptomatic: Many cats remain subclinical.
Symptomatic:
Heart Failure Signs: Dyspnea, PE, PLE, tachypnea.
Arterial Thromboembolism (ATE): Hindlimb paralysis, pain, and cold extremities.
Sudden Death: In some cases, without prior signs.
Diagnosis
Echocardiography: Gold standard for diagnosing HCM, showing LV hypertrophy, SAM, LA enlargement, and reduced diastolic function.
Radiography: Useful for identifying severe LA enlargement and signs of left heart failure.
Cardiac Biomarkers:
NT-proBNP: Elevated in severe HCM but not reliable as a standalone diagnostic test.
Cardiac Troponin I (cTnI): Elevated in HCM, especially in cases with myocardial injury or heart failure.
Electrocardiography (ECG): Can reveal arrhythmias but is not sensitive enough to detect all cases.
Treatment
Asymptomatic Cats (Stage B1):
No medical treatment recommended if there is mild hypertrophy and normal to mildly enlarged LA.
Monitoring: Regular follow-ups to detect progression to severe LA enlargement or heart failure.
Avoidance of triggers: Anesthesia, surgery, and fluid therapy should be carefully managed to prevent heart failure.
Beta Blockers (e.g., Atenolol): May be considered in cats with severe SAM and DLVOTO, although evidence of efficacy is limited.
Symptomatic Cats (Heart Failure/ATE):
Furosemide: Diuretic therapy to reduce pulmonary edema.
ACE Inhibitors (e.g., Enalapril): To reduce afterload and mitigate heart failure symptoms.
Antithrombotic Therapy (e.g., Clopidogrel, Aspirin): To prevent ATE.
Beta Blockers (e.g., Atenolol): For cats with severe SAM or ventricular arrhythmias.
Calcium Channel Blockers (e.g., Diltiazem): Previously used but now less favored due to gastrointestinal side effects and lack of clear efficacy.
Prognosis
Varies: Many cats with subclinical HCM may live a normal life span, while others progress to heart failure or suffer sudden death.
Severe Cases: Poor prognosis, especially in cats with heart failure or ATE.
Complications
ATE: Common in cats with LA enlargement and sluggish blood flow, often leading to hindlimb paralysis.
Sudden Death: Possible, especially in cases with severe myocardial disease or ventricular arrhythmias.
Breed-Specific Considerations
Maine Coon and Ragdoll: Genetic testing for specific mutations is recommended, and affected cats should not be bred.
Sphynx: Possible genetic predisposition to HCM, though not fully confirmed.

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