Hypertrophic cardiomyopathy (HCM) in cats

What is HCM?

Hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats, with a prevalence of 15 to 37% depending on the population studied [1]. The condition is characterised by pathological thickening of the heart muscle (myocardial hypertrophy), which reduces the filling space of the left ventricle and can cause heart failure or dangerous blood clots.

HCM in cats resembles the human variant closely in terms of clinical presentation and genetics, which also makes feline HCM scientifically interesting as an animal model [1][4].

Cause and genetics

The condition is predominantly genetic in origin. Known mutations in the MYBPC3 gene occur in Maine Coons (variants A31P, present in 22–42%) and Ragdolls (variant R820W, ~27%). Additionally, variants in ALMS1, MYH7 and TNNT2 have been described [4]. Genetic screening exists, but a negative test does not completely rule out HCM — the genetic architecture is more complex than a single mutation.

Diagnosis

Echocardiography is the diagnostic gold standard: only this method allows reliable measurement of the heart wall thickness [2]. Additionally, blood markers NT-proBNP and cardiac troponin-I are useful for population screening and disease monitoring, although they do not replace echocardiography [1][2].

Conventional treatment by stage

The ACVIM 2020 consensus divides HCM into stages [2]:

In cats with a previous aortic thromboembolism, clopidogrel is demonstrably superior to aspirin for preventing recurrence: the randomised FAT CAT trial showed a median difference of 443 versus 192 days to recurrence [3].

What does NOT work: the taurine myth

Taurine deficiency plays a role in dilated cardiomyopathy in some dogs, which is sometimes extrapolated to cats. This is incorrect for feline HCM. Contemporary feline HCM is a genetic and not a nutritional condition; taurine supplementation has no proven therapeutic effect [1]. Cats fed a complete cat food receive sufficient taurine as standard.

Supplementary and natural options: what does the evidence say?

There is no clinical evidence from controlled trials for supplementary or natural agents (including omega-3 fatty acids, co-enzyme Q10, herbal preparations or homeopathy) in feline HCM. Extrapolations from human cardiology or in-vitro studies are scientifically insufficient to base recommendations on.

Emerging, still experimental therapies such as myosine ATPase inhibitors (mavacamten, aficamten) and rapamycin show early promise in research, but are not yet available as standard treatment [1].

Supplementary is never a substitute. HCM requires echocardiographic monitoring and — once symptoms occur — immediate veterinary treatment. Delay of diagnosis or treatment can have life-threatening consequences.

Prevention and monitoring

At-risk breeds (Maine Coon, Ragdoll, but also British Shorthair, Sphynx and Persians) deserve regular cardiological screening, even without complaints. Genetic tests can be considered, but do not rule out disease [4].