Dilated Cardiomyopathy - Feline Cardiomyopathies

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Dilated cardiomyopathy (DCM) is now an uncommon feline cardiomyopathy, representing ~10% of cardiomyopathies. Previously, DCM was associated with taurine deficiency. However, the discovery of this in 1987 led to supplementation of commercial feline diets with adequate taurine. The rare cases of taurine deficiency observed since then are generally the consequence of vegetarian, vegan or canine diets to cats. It is difficult to differentiate idiopathic DCM, which is a primary systolic failure of the myocardium, from other forms of cardiac pathology which may result in a 'DCM phenotype'. Examples include the end stage of undiagnosed valvular diases (mitral dysplasia), ischaemic myocardial disease (HCM) or sustained tachycardia (tachycardia-induced cardiomyopathy). Idiopathic DCM is a diagnosis of exclusion of other causes of secondary myocardial failure.


Reduced myocardial contractility, predominantly involving the left ventricle (LV), will result in reduced stroke volume and increased ventricular filling pressure.

Taurine Deficiency

In 1987, a reversible form of myocardial failure associated with low plasma taurine levels was identified in cats. Taurine is an essential amino acid in cats. Taurine is found at the highest levels in the body within the myocardium and retina. Taurine is important in modulating cardiac contractility, metabolic and osmotic regulation of the myocardium, membrane stabilisation of retinal photoreceptors and neuroinhibitory actions within the central nervous system. Chronic dietary taurine deficiency (months) can lead to central retinal degeneration and DCM.

Clinical Signs


DCM is most commonly diagnosed in middle-aged and older cats. Cats are typically diagnosed at the end-stage phase of disease when they have clinical signs referable to heart failure.

Physical Exam

  • May present with signs of systolic failure (low output failure;cardiogenic shock): hypotension, hypothermia, bradycardia, weak femoral pulses
  • Murmurs are quiet or absent
  • Gallop rhythm may be present
  • Arterial thromboembolism (ATE) is common

Left-sided Congestive Heart Failure

  • Dyspnoea, tachypnoea, crackles (pulmonary oedema)
  • Dyspnoea, restrictive pattern (rapid,shallow breathing), muffled heart and ventral lung sounds (pleural effusion)

Right-sided Congestive Heart Failure

  • Jugular venous distension and jugular pulses
  • Hepatojugular reflux
  • Hepatomegaly
  • Ascites

Arterial Thromboembolism

The enlarged left atrium, stasis of blood within the left atrium, and reduced atrial function predispose to thrombus formation, and emboli may result. Typically these cases present with paresis or paralysis of one or both rear limbs due to occlusion at the aorta-iliac trifurcation. In some cases, emboli can involve other areas and can cause complex neurological manifestations, forelimb paralysis or acute renal ischemia.



Radiographs are important to evaluate for congestive heart failure, but do not diagnosed the underlying cardiac disease. Radiographic signs typically include generalised cardiomegaly and atrial dilation. Loss of abdominal detail would suggest ascites as a result of right-sided congestive heart failure. One case series of cats with DCM suggested that pleural effusion (91%) and ascites (55%) are more common than pulmonary oedema (36%).


Two dimensional (2D) and M-mode

DCM is defined as primary myocardial failure, which can be diagnosed by a reduced fractional shortening and increased LV end-systolic diameter. Eccentric hypertrophy, which occurs as a result of volume overload, results in an increased end-diastolic diameter. Left atrial (LA) dilation occurs secondary to elevated LV filling pressures. Global systolic dysfunction resulting in dilation of all-four cardiac chambers is frequently observed in cases of DCM. Mild atrioventricular valve (mitral, tricuspid) insufficiency is common. This occurs secondary to dilation of the valve annulus and distortion of the papillary muscles, such that the valve no longer seals closed within the dilated heart during systole. Spontaneous echocontrast and thrombi within the dilated atria are common findings. Mild pericardial effusion is also frequently identified.

Taurine Levels

Although taurine deficiency is now a rare cause of DCM, it is worth ruling out due to its potentially reversible nature. Taurine levels are measured in plasma or whole blood.

Differential Diagnoses

The differentials for systolic myocardial failure in the cat include:

  • Taurine deficiency-induced cardiomyopathy
  • Idiopathic DCM
  • Tachycardia - induced cardiomyopathy
  • Severe volume overload (mitral insufficiency, large left to right shunt)
  • Doxorubicin toxicity


Treatment should aim to control clinical signs of congestive heart failure (CHF) and aim to prevent arterial thromboembolism (ATE). In addition to this, consideration should be given to positive inotropic therapy. Treatment with positive inotropes, such as Pimobendan is indicated for severe systolic dysfunction and heart failure.

Taurine Deficiency

Treatment with taurine improves and often normalises systolic function. It may require several weeks to months of supplementation before improvement occurs. Initial treatment with positive inotropes as well as treatment for congestive heart failure is necessary until this improvement occurs. Clinical signs usually improve within 2 weeks, and echocardiographic evidence of improvement can be expected with 3-6 weeks of therapy. Improvements in fractional shortening may continue for up to a year after taurine supplementation.


Prognosis for cats with idiopathic DCM is grave. One case series of 11 cats with DCM reported a median survival time of just 11 days. Prognosis for DCM associated with taurine deficiency is generally good with appropriate therapy.


  • Ferasin L. Feline myocardial disease. 1: Classification, pathophysiology and clinical presentation. J Feline Med Surg 2009;11:3-13.
  • Pion, P.D, Kittleson MD et al. Myocardial failure in cats associated with low plasma taurine:a reversible cardiomyopathy. Science 1987; 237:764-68.