Feline cardiomyopathies

The first report describing acquired cardiac lesions which culminated in congestive heart failure was published in 1970. Over the subsequent decade, various reports were published detailing the gross anatomical and histological features of the feline cardiomyopathies. At that time, cardiomyopathy was detected in 8.5% of cats that underwent post-mortem examination. In addition, it was found that the classification system described in human beings suitably differentiated the disease groups described in cats, namely; Dilated Cardiomyopathy (DCM), Hypertrophic Cardiomyopathy (HCM), Restrictive Cardiomyopathy (RCM), Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC), Unclassified Cardiomyopathy (UCM) and persistent moderator band cardiomyopathy. Initially, DCM and HCM were reported to be the most prevalent of the feline cardiomyopathies. However, in 1987, Pion and colleagues discovered a causal relationship between decreased plasma taurine levels and feline myocardial failure.  With the supplementation of commercial cat food with taurine, the incidence of feline ‘DCM’ has decreased.  Today, the most prevalent feline cardiomyopathy is HCM.

- Hypertrophic Cardiomyopathy
HCM accounts for approximately 27% of all feline cardiac disease. In 1999, Kittleson and colleagues identified a family of Maine Coon cats with HCM and an autosomal dominant mode of inheritance, where 100% penetrance was demonstrated. Further studies have demonstrated left ventricular hypertrophy in a closed colony of Persian cats, a familial predisposition for HCM and aortic thromboembolism (AT) in a family of (American) domestic shorthaired cats, and a predisposition to severe HCM in the Ragdoll breed.  In addition, a family of American shorthaired cats has been identified with a familial tendency for HCM and/or abnormal motion of the mitral valve. In all these studies the pattern of inheritance was consistent with that of an autosomal dominant trait. In addition, there are anecdotal reports of the disease occurring with an increased incidence in many other breeds (see breed predispositions above). Polymorphisms of both the feline TnT gene and the feline myosin regulatory light chain gene (MYL2) have been identified. Furthermore, it has been found that Myomesin (an M-band sarcomeric protein) was decreased or absent in Maine Coon cats with HCM, compared to control cats.  Recently it has been discovered that some Maine Coon or Maine Coon cross cats with HCM have a mutation of the Myosin Binding Protein C. In addition, a different mutation of the same gene has also been identified in Ragdoll Cats with HCM, although as yet, it is not known what proportion of Ragdolls with HCM has this mutation.
Feline HCM is a highly heterogeneous disease and therefore, the associated clinical signs are highly variable. Since many cats are asymptomatic (cause no signs of ill health), apparent unexpected sudden death may occur. In others, stress may induce breathing difficulties due to acute pulmonary oedema or pleural effusion. Other reported clinical signs include rapid breathing, anorexia, vomiting, fainting or paralysis, which is typically of the hind limbs, lethargy and occasionally ascites (fluid on the abdomen). 

- Restrictive Cardiomyopathy
The term restrictive cardiomyopathy (RCM) is applied to cases of cardiomyopathic disease that restricts the diastolic ventricular function (relaxation) and excludes HCM. Pathologically, there are two forms described, one affecting the myocardium only, and one affecting the endomyocardium (which is more common). There are no sex predilections, and the age of affected cats is highly variable, but typically middle to old aged animals are affected. RCM has not been reported as an inherited disease.  However, it has been hypothesised that endomyocardial fibroelastosis (EMF), a fibrosis thickening of the endocardium may be a form of RCM. An increased incidence of EMF has been reported in the Burmese and possibly the Siamese breeds.

Paasch LH, Zook BC (1980) Pathogenesis of endocardial fibroelastosis in Burmese cats. Laboratory-Investigation; 42(2): 197-204

- Dilated Cardiomyopathy
Since the discovery of taurine deficiency in cats, the incidence of DCM has decreased, with now only ~3% of cats with cardiomyopathy suffering from systolic myocardial failure (DCM). Whilst some of these cats remain taurine deficient, either through poor diet, or metabolic anomalies, others appear to suffer from a familial DCM. In addition, isolation of parvoviral DNA (e.g. from Feline Panleukopenia Virus) has been isolated from cats hearts with DCM, and it has been hypothesised that some cases may be caused by an infectious myocarditis. It remains unclear as to whether the reported ‘breed predispositions’ to DCM (ie the Burmese and Abyssinian and Siamese breeds) are truly at an increased risk of primary DCM, have an increased taurine requirement or whether feeding differences in these breeds previously predisposed them to DCM.

- Moderator Band Cardiomyopathy
Increased numbers or enlarged moderator bands (fibrous stands spanning the heart chambers) have been reported in various breeds of cats. There is anecdotal evidence that Burmese cats may be predisposed to the development of a large bridging moderator band, whilst Siamese cats may be predisposed to the development of multiple moderator bands spanning the ventricle.

HCM discussed on Susan Little’s website www.catvet.homestead.com - Selected Inherited Diseases of the Cat.

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A paper based on a study published originally in the Journal of Veterinary Internal Medicine 1993, 7 383-387.
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Congenital heart defects

A variety of congenital heart defects have been reported in cats. These may occur by themselves or in combination with other congenital abnormalities. Congenital heart defects can develop as a result of toxic, environmental, genetic, nutritional or chromosome related abnormalities. In cats, the estimated incidence of congenital heart disease is 0.2-1%. The most commonly reported abnormality is an atrioventricular defect (a hole between two or more of the cardiac chambers), this group of diseases included ventricular septal defects, atrial septal defects and endocardial cushion defects. Malformation of the atrioventricular (mitral and/or tricuspid) valves is the second most commonly reported congenital cardiac disease in the cat, followed by endocardial fibroelastosis (see Restrictive Cardiomyopathy: a predisposition to this disease has been reported in the Burmese and Siamese breeds, see specific breed predispositions), patent ductus arteriosis, aortic stenosis (a predisposition has been reported in the Siamese breed), and tetralogy of fallot (a combination of pulmonic stenosis, right ventricular hypertrophy, ventricular septal defect and dextrorotation of the aorta). Pulmonic stenosis has been reported occasionally in the cat.

Bonagura J.D., Lehmkuhl L.B. Congenital Heart Disease, 2nd Edition. Philadelphia, W.B. Saunders Company, 1999, pp 621-678
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Stamoulis, M.E., Fox, P.R. Mitral Valve Stenosis in 3 Cats, Journal of Small Animal Practice 34:452-456, 1993.
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Bush, M., Pieroni, D.R., Goodman, D.G., White, R.I., Thomas, V., James, A.E. Tetralogy of fallot in a cat, Journal of the American Veterinary Medical Association 161:1679-1686, 1972.

Congenital portosystemic shunt

It has been reported that Colour Point Persian cats are predisposed to a vascular anomaly by which the blood from the intestines bypasses the liver, a so called portosystemic shunt. They may therefore develop signs of hepatic encephalopathy caused by the systemic accumulation of ammonia, and numerous other neurotoxins. Most affected kittens have clinical signs from ~10-12 weeks of age, typically presenting with intermittent visual disturbances, pupillary dilation, ataxia, behavioural changes (eg. aggression), seizures, lethargy, depression, and ptyalism (excessive salivation). Stunted growth occurs rarely in cats. There is not usually any clear relationship between clinical signs and recent feeding. Diagnosis is made on finding raised bile acids in the blood and visualising the shunting vessel with ultrasound or contrast radiography. Medical and/or surgical treatment options are available.

Hunt GB. (2004) Effect of breed on anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet J. 82(12):746-9.

Peritoneopericardial diaphragmatic hernia (*)

Not truly a cardiac disease, peritoneopericardial diaphragmatic hernia (PPDH) is a congenital abnormality by which the abdominal cavity, directly communicates with the pericardium (the sac that the heart sits in).  Colour point Persians and Persian cats have frequently been identified with peritoneal pericardial diaphragmatic hernia. Anecdotally, British Short hair cats and blue colour or colour point cats may be at an increased risk.

Skrodzki, M et al (1997) Congenital peritoneopericardial hernias in 16 cats - part 1 - literature review and cases [German], Kleintierpraxis 42:973 ff
Neiger, R (1996) Peritoneopericardial diaphragmatic hernia in cats, Compendium on Continuing Education for the Practicing Veterinarian 18:461
Frye, F.L & Taylor D (1968) Pericardial and diaphragmatic defects in a cat, Journal of the American Veterinary Medical Association 152:1507-1510
Reimer SB, Kyles AE, Filipowicz DE, Gregory CR. (2004) Long-term outcome of cats treated conservatively or surgically for peritoneopericardial diaphragmatic hernia: 66 cases (1987-2002). J Am Vet Med Assoc. 224(5):728-32