Feline Hypertrophic Cardiomyopathy

Introduction #

Feline Hypertrophic Cardiomyopathy (HCM) is the most common cardiac disease affecting domestic cats, characterized by an abnormal thickening (hypertrophy) of the left ventricular myocardium without corresponding dilation of the ventricular chamber. This primary myocardial disease affects the heart’s ability to relax and fill properly during diastole, leading to various complications including congestive heart failure, arterial thromboembolism, and sudden death. HCM represents approximately 58-68% of all feline cardiac diseases diagnosed in clinical practice.

Pathogenesis #

The pathogenesis of feline HCM involves complex interactions between genetic predisposition, cellular abnormalities, and secondary compensatory mechanisms. At the molecular level, several mutations have been identified, particularly in genes encoding sarcomeric proteins. The most well-documented mutation occurs in the MYBPC3 gene (myosin binding protein C) in Maine Coon and Ragdoll breeds. These mutations result in disorganized myocardial architecture with myocyte hypertrophy, myofibrillar disarray, and interstitial fibrosis.

The hypertrophied myocardium demonstrates increased stiffness, reduced compliance, and impaired relaxation during diastole. This diastolic dysfunction leads to elevated left ventricular filling pressures, left atrial enlargement, and pulmonary congestion in advanced cases. Systolic function typically remains preserved until late in disease progression.

Secondary pathophysiological changes include myocardial ischemia due to increased oxygen demand, decreased coronary perfusion, and microvascular dysfunction. Mitral regurgitation commonly develops due to structural changes in the mitral valve apparatus and altered ventricular geometry. In some cases, dynamic left ventricular outflow tract obstruction occurs, further complicating the disease.

Signalment and Epidemiology #

HCM affects cats of all ages, with a median age of diagnosis between 5-7 years, though cases have been reported in cats as young as 3 months and as old as 17 years. Males are overrepresented with a male-to-female ratio of approximately 2:1 to 3:1. While any breed can develop HCM, certain breeds show increased predisposition:

• Maine Coon
• Ragdoll
• British Shorthair
• Persian
• Norwegian Forest Cat
• Sphynx
• American Shorthair
• Bengal

In Maine Coon and Ragdoll cats, an autosomal dominant inheritance pattern has been established. However, the majority of HCM cases occur in domestic shorthair cats, suggesting complex multifactorial inheritance patterns or spontaneous mutations in many affected individuals.

Clinical Variants #

Classic Hypertrophic Cardiomyopathy #

The classic form of HCM is characterized by concentric left ventricular hypertrophy, primarily affecting the interventricular septum and/or the free wall of the left ventricle. The papillary muscles are often prominently enlarged. The hypertrophy may be symmetrical or asymmetrical, with variable regional distribution patterns.

Hypertrophic Obstructive Cardiomyopathy (HOCM) #

Approximately 30-67% of cats with HCM develop dynamic left ventricular outflow tract obstruction (LVOTO), a condition termed hypertrophic obstructive cardiomyopathy (HOCM). This obstruction results from systolic anterior motion (SAM) of the mitral valve, where the mitral valve leaflet contacts the interventricular septum during contraction, creating a pressure gradient across the aortic outflow tract. SAM also produces concurrent mitral regurgitation, further complicating hemodynamics.

The obstruction is dynamic, varying with loading conditions, contractility, and heart rate. Factors that decrease preload (dehydration, vasodilators), increase contractility (sympathetic stimulation, positive inotropes), or decrease afterload can worsen obstruction.

End-Stage or Unclassified Cardiomyopathy #

Some cats with HCM progress to a “burnout” or end-stage form characterized by myocardial thinning, ventricular dilation, and systolic dysfunction. This progression blurs the distinction between hypertrophic and dilated cardiomyopathies, leading to classification as “unclassified cardiomyopathy.” This transition occurs in approximately 10-15% of HCM cases and carries a poor prognosis.

Medical Management #

Treatment strategies for feline HCM are tailored to the disease stage, presence of complications, and individual patient factors:

Asymptomatic HCM #

For cats with no clinical signs but echocardiographic evidence of HCM:

• Beta-blockers (atenolol, 6.25-12.5 mg/cat q12-24h) may be beneficial, particularly in cases with LVOTO, to reduce heart rate, contractility, and outflow obstruction.
• Calcium channel blockers (diltiazem, 7.5 mg/cat q8h or extended-release 30 mg/cat q24h) improve diastolic function by promoting myocardial relaxation.
• Prophylactic antithrombotic therapy (clopidogrel, 18.75 mg/cat q24h) may be considered in cats with severe left atrial enlargement.

Congestive Heart Failure #

For cats with pulmonary edema or pleural effusion:

• Furosemide (1-4 mg/kg q8-12h, adjusted based on response) reduces congestion.
• ACE inhibitors (benazepril, 0.25-0.5 mg/kg q24h) help manage neurohormonal activation.
• Pimobendan (0.1-0.3 mg/kg q12h) may benefit cats with systolic dysfunction or refractory CHF.
• Spironolactone (1-2 mg/kg q12-24h) provides additional diuresis and anti-fibrotic effects.

Arterial Thromboembolism #

For prevention and management of thromboembolism:

• Clopidogrel (18.75 mg/cat q24h) has demonstrated superiority to aspirin in preventing recurrent events.
• Low molecular weight heparins (dalteparin, 100 IU/kg q12h) or factor Xa inhibitors (rivaroxaban, 1 mg/kg q24h) represent newer anticoagulant options.
• Combination therapy may be considered for high-risk cases.

Anesthetic Considerations #

Anesthesia in cats with HCM requires careful consideration to avoid hemodynamic decompensation:

Preoperative Assessment #

• Comprehensive cardiac evaluation including echocardiography to assess disease severity.
• Optimization of medication regimen and resolution of any decompensation before elective procedures.
• Laboratory evaluation of renal function, as many HCM cats have concurrent renal disease.

Anesthetic Protocol #

• Avoid drugs with significant negative inotropic effects
• Maintain adequate preload while avoiding volume overload.
• Ketamine should be used cautiously due to sympathomimetic effects that can worsen LVOTO.
• Opioids (e.g., methadone, buprenorphine) provide relatively stable hemodynamics.
• Alpha-2 agonists (dexmedetomidine) should generally be avoided or used at very low doses.
• Blood pressure is often very effected by heart rate since diastolic filling is impaired. High heart rates can limit filling time while low heart rates (coupled with poor ventricular compliance) can lead to decreased cardiac output since CO=SVxHR
• Anticholinergics should be used cautiously since they may uncontrollably increase heart rate and significantly increase oxygen consumption
• Vasoconstrictors (phenylephrine) are often recommended for management of blood pressure, however they also can decrease tissue perfusion and should be used cautiously, and at the lowest effective dose.
• Dobutamine is often listed as a contraindicated drug due to the increased risk of outflow obstruction in cats during vigourous systolic contraction. However, dobutamine is an effective and titratable chronotrope and has been successfully used to adjust heart rate and contractility to maintain adequate blood pressure without the use of vasoconstricting drugs. Dopamine may also be effective, but cat kidneys don’t have the same vasodilatory response to dopamine as other species so the lowest effective dose should be used.

Perioperative Management #

• Continuous ECG monitoring for arrhythmia detection.
• Adequate pain management to minimize sympathetic stimulation.
• Careful fluid management, typically at conservative rates (2-3 ml/kg/hr). However, small (1-2 mL/kg) boluses may be needed in cats that are dehydrated due to comorbidities such as diabetes or renal disease to maintain adequate preload
• Blood pressure monitoring with intervention for significant hypotension.
• Position patients to optimize venous return and cardiac output.

References #

1. Payne JR, Brodbelt DC, Luis Fuentes V. Cardiomyopathy prevalence in 780 apparently healthy cats in rehoming centers (the CatScan study). J Vet Cardiol. 2015;17:S244-S257.
2. Maron BJ, Fox PR. Hypertrophic cardiomyopathy in man and cats. J Vet Cardiol. 2015;17:S6-S9.
3. Kittleson MD, Meurs KM, Harris SP. The genetic basis of hypertrophic cardiomyopathy in cats and humans. J Vet Cardiol. 2015;17:S53-S73.
4. Fox PR, Schober KE. Management of asymptomatic (occult) feline cardiomyopathy: challenges and realities. J Vet Cardiol. 2015;17:S150-S158.
5. Gordon SG, Côté E. Pharmacotherapy of feline cardiomyopathy: chronic management of heart failure. J Vet Cardiol. 2015;17:S159-S172.
6. 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:S306-S317.
7. Robertson SA, Gogolski SM, Pascoe P, Shafford HL, Sager J, Griffenhagen GM. AAFP Feline Anesthesia Guidelines. J Feline Med Surg. 2018;20(7):602-634.
8. Luis Fuentes V, Abbott J, Chetboul V, et al. ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats. J Vet Intern Med. 2020;34(3):1062-1077.