Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease affecting cats, characterised by concentric left ventricular hypertrophy, without an eliciting cause. Before the diagnosis is made, it is important to actively exclude other reasons for the concentric left ventricular hypertrophy phenotype1 (e.g. other reasons for a pressure overload on the left ventricle (e.g. aortic stenosis, systemic hypertension) and other reasons for left ventricular hypertrophy (e.g. hyperthyroidism, acromegaly, myocardial oedema (e.g. transient myocardial thickening), myocarditis (e.g. Toxoplasmosis) or myocardial infiltration (e.g. lymphoma). In both pedigree breeds and domestic shorthair / longhair cats, there is likely to be a genetic basis to the condition2, with different mutations reported in the Myosin Binding Protein C gene in Maine coon3 and Ragdoll4 cats. In Sphinx cats, a mutation in the ALMS1 gene has been associated with HCM.5 However, these may not be the only genetic causes of HCM in these breeds, and in most breeds and domestic cats, identification of the causal gene defects has proven elusive.


The overall prevalence of HCM has been estimated to be about 15% of the feline population.2,6,7 However, the prevalence increases with age, and in cats of 9 years of age and older, prevalence is 29.4%.6 So nearly one in three older cats might have HCM, and it is important to identify these cases especially if these senior cats have other co-morbidities which may prompt therapeutic intervention which potentially can result in decompensation of HCM into congestive heart failure (e.g. intravenous fluids, requirement for glucocorticoids, general anaesthesia or the stress of hospitalisation).


Most commonly, cats with preclinical HCM are initially suspected to have this condition because of the detection of a heart murmur. However, heart murmurs are common in cats and not all cats with heart murmurs have HCM;6 some have no identifiable cardiac disease at the time of examination (apparently innocent murmurs).
Other reasons for a heart murmur should be excluded (e.g. anaemia, other high output states such as hyperthyroidism).
Cats with heart murmurs and HCM usually have some form of left ventricular obstruction. Most commonly, this is dynamic left ventricular outflow tract obstruction (LVOTO). This is due to systolic anterior motion (SAM) of the septal mitral valve leaflet during ventricular systole, which has two consequences:
  • Variable degrees of obstruction across the left ventricular outflow tract (LVOT) (especially if significant basal septal hypertrophy), leading to increased velocity ofLVOT flow. Spectral Doppler indicates a biphasic acceleration of LVOT flow, the socalled scimitar or dagger shape, typical of dynamic LVOTO.
  • Mitral regurgitation: typically, this is an eccentric jet, coursing around the posteriorlateral wall of the left atrium.

HCM with this obstruction is sometimes called hypertrophic obstructive cardiomyopathy (HOCM). The two jets of turbulent flow on colour flow Doppler superimposed on a right parasternal 5-chamber view is typical of dynamic LVOTO and SAM.

The dynamic LVOTO can intensify leading to louder murmurs and more severe obstruction (higher velocity LVOT flow) when the cat is stressed, indicating the influence of catecholamines. The severity of obstruction can lead to a pressure overload across the LVOT. The velocity (v) indicates the instantaneous peak pressure gradient (PG) across this obstruction by the modified Bernoulli equation (PG ≈ 4v2). This pressure overload, if sustained, may contribute to the left ventricular hypertrophy. However, this does not impact on survival.8

The detection of the heart murmur which leads to subsequent diagnosis of HCM can be considered fortuitous. It can lead to the early diagnosis of HCM. This is the possible reason why younger cats, cats with louder heart murmurs and those with evidence mitral SAM and dynamic LVOTO appear to have a better prognosis and improved survival time.9


The diagnosis of HCM depends on echocardiography. Confirmation of left ventricular concentric hypertrophy depends on measurement of one or more left ventricular wall segments during diastole of ≥ 6.0 mm1 (Figure 1). As noted above, other potential causes of the HCM phenotype must be actively excluded. It is recommended that measurements of the LV wall thickness are done on 2D images. M-mode images may be inaccurate if papillary muscles or false tendons are included.


Cardiac biomarkers should not be considered as a sole screening test for HCM or other cardiomyopathies in cats. But they can be elevated in cats with preclinical HCM and therefore can be considered as a “pre-screening” tool to identify cats which would benefit from “gold-standard” screening by echocardiography after referral to a cardiologist. For example, these blood tests can be considered as part of health screening in a senior cat clinic. It is important to also appreciate that the cardiac biomarkers may be increased in systemic diseases (e.g. azotaemia).

  • Feline N-terminal pro-BNP: Increases with increased myocardial wall stress. Values of >100 pmol/L are consistent with cardiac disease with 100% specificity and 71% sensitivity.10 Values of >270 pmol/L are consistent with imminent or actual congestive heart failure if there are compatible clinical signs.
  • Troponin I: This increases with cardiomyocyte injury or death. This is not a species specific assay and there are many assays available, some high sensitivity. It is probably better to use a high sensitivity test for pre-screening of asymptomatic cats.
    For the Siemens Advia Centaur TnI ultra assay (ultra-sensitive), a cut-off of 0.06 ng/mL gives 95.4 % specificity and 87.8% sensitivity.11 High values (>0.7 ng/mL) in HCM cats are an independent predictor of poor prognosis.12


The risk of cats with HCM can be various. Many cats remain very stable for many years and some may never develop any complications or clinically relevant HCM. Risks to survival include:

  • Development of left sided or biventricular congestive heart failure (CHF)
  • Development of thromboembolic complications (feline arterial thromboembolism; FATE).
  • Sudden death

As noted above, the cat with a heart murmur due to SAM and dynamic LVOTO is not at increased risk of these complications, perhaps surprisingly in view of the additional contribution of pressure load to left ventricular hypertrophy. This is likely because left ventricular systolic function is still preserved. In fact, the disappearance of a heart murmur may be an ominous sign since the cat with impaired systolic function may no longer demonstrate LVOT obstruction. From the physical examination findings, the following are associated with poor prognosis: older age, absence of a murmur, presence of diastolic gallops, presence of an arrhythmia (and presentation with either CHF or FATE).9 Cats with a history of syncope and with arrhythmias are at increased risk of sudden death.13

Echocardiographic findings are of major prognostic significance and findings which indicate a poor prognosis include: extreme left ventricular (LV) hypertrophy (≥9.0 mm diastolic wall thickness), impaired LV systolic function (FS <30%) or wall hypokinesis,
increased left atrial (LA) size (e.g. LAmax >21.1 mm) and reduced LA function (LA FS reference 25.1 ± 5%),14 spontaneous echocontrast, restrictive diastolic dysfunction and / or increased left sided filling pressures.9


There is very little evidence base for any of the medication used in cats with cardiac disease including both clinical and preclinical HCM, and we tend to extrapolate from what is known in humans or dogs. There is no available evidence that medication influences progression or survival time in cats with preclinical HCM.


Giving any medication to cats is challenging for many, and so we need to have evidence that it makes a difference, especially for the asymptomatic cat. Daily medication may impact on the pet-owner bond.

  • Clopidogrel: In cats with left atrial dilatation and / or reduced LA function, anti-platelet medication to reduce the risk of thromboembolic complications is logical.
  • ACE-inhibitors: In preclinical HCM, at this time there is no available evidence that ACE inhibitors will influence progression of HCM or survival time. The author may start an ACE-I if the left atrium is dilated (evidence of remodelling) so an active reninangiotensin-aldosterone system (RAAS)15 is inferred.
  • Spironolactone: Histologically, HCM is associated with myocardial fibrosis. However, an MRI study showed no significant impact of spironolactone in Maine coon cats with preclinical HCM.
  • Diltiazem: Although Diltiazem is (was) licensed in some countries to treat HCM, following some experimental evidence of efficacy, it is now rarely prescribed for HCM unless as an antiarrhythmic drug.
  • Beta blockers (Atenolol): It is known that beta blockers will reduce tendency for SAM and reduce dynamic LVOTO16 by counteracting the effect of catecholamines and their negatively inotropic effects. Beta blockers should be considered contra-indicated in cats with congestive heart failure, and even in preclinical HCM cats with left atrial dilatation, they are potentially risky. However, since LVOTO can increase the pressure load on the LV with a stimulus to further LV hypertrophy, their use might seem logical in a cat without left atrial enlargement and with preserved systolic function. However, this did not influence 5-year outcome, survival or quality of life and activity scores in two separate studies.17,18

At the current time, we do not have any strong evidence that any medication in cats with preclinical HCM makes any difference to their outcome or progression of HCM (except clopidogrel). There is a real need for well-designed prospective studies in cats with HCM to assess the potential role for pharmacological intervention.


Cats with HCM are more likely to be larger, overweight and male. They may have increased insulin, blood glucose and IGF1 suggesting insulin resistance.19 Dietary intervention may therefore influence progression of asymptomatic HCM. Furthermore,
congestive heart failure is an inflammatory state in all species, but it is not known at what stage during progression of preclinical disease an inflammatory state develops. However, in cats with preclinical HCM, an association between serum amyloid A (SAA), an acute phase protein in the cat, and some echocardiographic measurements consistent with severity of HCM has been noted. 19 Dietary intervention with high omega-3 fatty acids (fish-oil supplementation) in dogs reduces the inflammatory cytokines associated with CHF and diets with anti-inflammatory effect may also influence progression of disease. In a one-year study with cats with preclinical HCM, randomised to receive a test diet (restricted starch; higher protein; supplemented with fish oil (eicosapentaenoic acid + docosahexaenoic acid; EPA+ DHA)) compared with a control diet, the test diet group showed significant decreases in maximal LV wall thicknesses and IGF1 at 12 months, and Troponin I at 6 months.20 In the linear mixed model, there was no significant difference between diet groups, but a possible explanation is that LV wall thicknesses tended to decline in both groups (only significant in the test diet), possibly reflecting the diet change that the control group also had, compared to each cat’s original food. The changes in the test diet group were more marked for cats at an earlier stage of HCM,
without left atrial enlargement.20 There is therefore some preliminary evidence that nutritional intervention may influence progression of preclinical HCM in cats. This is a reason for hope, but longer-term studies with more cats followed over their lives are required to investigate whether any changes offer improved prognosis and survival time and quality of life.


Since development of CHF is likely the most common consequence of progression of HCM, owner monitoring of sleeping or resting respiratory rate is the most sensitive method of monitoring

Serial echocardiographic monitoring will indicate progression of HCM, and it is especially important to monitor left atrial size, since this will indicate likely risk of onset of CHF or FATE. However, many cats remain echocardiographically stable for many years and it is difficult to predict which cats may progress and at what rate. The frequency of echo reassessments will be influenced by the feline and owner compliance with travelling and toleration of echocardiography. Stress should be avoided.


Preclinical HCM is common in cats affecting about 15% of the overall population. Only a small proportion progress to develop devastating sequelae such as congestive heart failure, feline arterial thromboembolism or sudden death. The difficulty is predicting which cats will progress and when. There is no currently available evidence that any medication makes a difference to outcome and medication is often a matter of extrapolation from other species or personal opinion.21 However, we now have evidence that dietary intervention may modify progression of HCM and result in some reverse remodelling as well as decreasing IGF1 and Troponin I.19,20