Felis ISSN 2398-2950

Heart: dilated cardiomyopathy (DCM)

Synonym(s): DCM Taurine responsive cardiomyopathy, Congestive cardiomyopathy, COCM

Contributor(s): Serena Brownlie, Phil Fox, Philip K Nicholls, Penny Watson


  • Cause: taurine deficiency; idiopathic.
  • Signs: dyspnea, lethargy, reduced activity, inappetence.
  • Diagnosis: radiography, ultrasound.
  • Treatment: rest, diuretics, vasodilators, digoxin; taurine.
  • Prognosis: good if taurine related; very poor if idiopathic.
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  • Taurine deficiency Taurine deficiency: canned/dried foods   →   destruction of taurine. Feeding an unfortified diet, eg dog food, can   →   low blood levels which have been associated with DCM, retinal degeneration Taurine.
  • Need 1000-1500 mg/kg dry matter taurine in dry foods and 2000-2500 mg/kg dry matter taurine in canned foods.

Predisposing factors


Factors which worsen congestive failure

  • Exertion.
  • Stress.
  • Sudden increase in salt intake.


  • Age.


  • Poorly understood or unknown.
  • Metabolic or biochemical lesion affecting cardiac myocyte   →   failure of contractility/increased work for myocardium   →   chronic hypovolemic shock response Shock:
    • Right-sided failure due to myocardial involvement or secondary to the left backward failure   →   ascites, hepatomegaly, jugular pulse, pleural effusion, pericardial effusion.
    • Salt and water retention by kidney due to poor renal perfusion   →   sympathetic drive and RAAS (aldosterone) leads to increased venous return (preload) and venous pressure, further stretch of myocardium and predisposition to edema.
    • Increased end-diastolic left ventricular volume and pressure   →   dilation and non-compensatory hypertrophy (La Place relationship) of left ventricle   →   compromized papillary muscle function and passive dilation of atrioventricular annulus causing mitral regurgitation   →   increased left atrial pressures   →   left atrial enlargement   →   increased pulmonary venous (capillary wedge) pressure and pulmonary edema +/- pleural effusion   →   pleural effusion.
      Note pleural effusion will occur with left-sided as well as right-sided failure in cats.
    • Poor cardiac output (CO) due to decreased stroke volume (SV)   →   sympathetic drive   →   increased heart rate (HR).
    • Reduced cardiac output with arteriolar contraction to increase vascular resistance (mediated through sympathetic tone, active renin-angiotension-aldosterone system (RAAS) and increased vasopressin release); also venoconstriction   →   increased venous return   →   increased stretch of myocardium (preload).
    • Arteriolar constriction increases afterload (left ventricle wall stress) and myocardial workload   →   further myocardial dysfunction, further dilation.
  • Signs of poor systolic function and vasoconstricted state: poor pulse, pale mucous membranes, delayed capillary refill time, cold extremities, etc.
  • Left atrial stretch may   →   supraventricular dysrhythmias, eg atrial fibrillation.
  • Increased myocardial wall stress, poor coronary perfusion of myocardium and diseased myocytes may result in ventricular dysrhythmias.


  • Weeks-months from onset of signs.
  • Usually weeks-months survival after diagnosis.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Van Israël N (2004) Feline cardiomyopathies: diagnostic approach. UK Vet (5), 35-42.
  • Bright J M, Herrtage M E & Schneider J F (1999) Pulsed Doppler assessment of left ventricular diastolic function in normal and cardiomyopathic cats. JAAHA 35 (4), 285-291 PubMed.
  • Bright J M, Mears E (1997) Chronic heart disease and its management. Vet Clin North Am Small Animal Pract 27 (6), 1305-1329 PubMed.
  • Novotny M J, Hogan P M, Flannigan G (1994) Echocardiographic evidence for myocardial failure induced by taurine deficiency in domestic cats. Can J Vet Res 58 (1), 6-12 PubMed.
  • Lawler D F, Templeton A J, Monti K L (1993) Evidence for genetic involvement in feline dilated cardiomyopathy. J Vet Intern Med (6), 383-387 PubMed.