Introduction

• Cause: unknown. Heritable in Maine Coon, Ragdolls, and probably Persians and Sphynx cats.
• Signs: sudden onset in apparently well cat, acute dyspnea, lethargy or signs of thromboembolism.
• Diagnosis: biomarkers, ultrasound, radiography, ECG.
• Treatment: diuresis, vasodilators, beta-blockers (in certain cases of HOCM and not when decompensated heart failure).
• Prognosis: variable.

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Pathogenesis

Etiology

• Two forms of HCM occur:
  • Primary:
    • Largely unknown in idiopathic form.
    • Ragdoll (R820W) and Maine Coon (A31P) can have inheritable form associated with myosin binding protein C.
    • Other inherited predispositions likely as in humans.
    • Oversensitivity to circulating catecholamines may be involved.
  • Secondary:
    • Hyperthyroidism Hyperthyroidism.
    • Outflow obstruction, eg congenital aortic stenosis Heart: aortic stenosis.
    • Possibly related to hypertension Hypertension, eg in renal disease.
    • Possibly related to growth hormone disorders Acromegaly.

Pathophysiology

• Characterized by hypertrophied non-dilated left ventricle.

• Left ventricular diastolic dysfunction   →   decreased distensibility of myocardium   →   increase in end-diastolic pressure with normal or reduced volume.
• Increased muscle mass, myocardial fibrosis, disordered arrangement of myofibrils   →   decreased distensibility.
• Abnormal myocardial relaxation   →   prolonged relaxation period and decreased rate of decline of left ventricular pressure.
• Decreased capillary density in myocardium, abnormally narrowed intramural coronary arteries, increased resistance in large coronary arteries due to systolic pressures   →   myocardial ischemia.
• Myocardial ischemia   →   abnormal relaxation, increased left ventricular filling pressures.
• May be mild hypertrophy with severe left heart failure - probably due to abnormal myocyte function.
• Systolic anterior motion of the mitral valve (SAM) might be present due to abnormal mitral valve apparatus/papillary muscle geometry resulting in hypertrophic obstructive cardiomyopathy (HOCM).

Systemic thromboembolism

• Turbulence   →   damages cardiac endothelium   →   endocardial collagen induces platelet adhesion and aggregation, extrinsic pathway activation Hemostatic disorders: acquired.
• Circulation of blood through heart is abnormal   →   areas of sluggish flow allow aggregation of platelets.
• Higher levels of serotonin in felines due to larger platelets than dogs and humans, felines more sensitive to effects of serotonin   →   higher susceptibility to aggregation.

Timecourse

• Onset can appear rapid.
• Survival can be months to years.

Diagnosis

Treatment

Outcomes