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  • Cardiomyopathy is a disease of the heart muscle, either primary or secondary to another cardiac or systemic disease.
  • Cause: idiopathic, drugs, viral, immune-mediated, nutritional, hereditary.
  • Signs: depend on severity of myocardial dysfunction.
  • Diagnosis: echocardiography.
  • Treatment: cost prohibitive and limited treatment options available.
  • Prognosis: poor.



  • Nutritional causes leading to vitamin E and selenium deficiency Selenium and Vitamin E: white muscle disease.
  • There is a congenital form which occurs in calves and an acquired form. Skeletal muscle is usually affected concurrently.
  • Dilated cardiomyopathy is an inherited condition seen in Holstein-Friesian cattle Holstein Friesian.
  • Hypertrophic cardiomyopathy is rare in cattle but has been reported.
  • Infiltrative diseases like lymphoma can cause hypertrophic cardiomyopathy.
    • High-Mountain Disease (Brisket disease - seen in USA and South America add in links) causes hypertrophy of the right ventricular myocardium in the initial phases.
  • Restrictive cardiomyopathy is rare in cattle but any disease that leads to fibrosis of the cardiac muscle can result in restrictive cardiomyopathy.
  • Idiopathic.
  • Viral or immune-mediated.
  • Toxic- ingestion of cardiotoxic plants (such as Oleander Oleander toxicity/Yew Yew poisoning etc).


  •  There are 3 main types of Cardiomyopathy:

Dilated Cardiomyopathy

  • Metabolic or biochemical lesion affecting cardiac myocyte → failure of contractility/increased work for myocardium → chronic hypovolemic shock right-sided failure due to myocardial involvement or secondary to the left backward failure → ascites , hepatomegaly, jugular distention, 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.
  • 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 quality, 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 Dysrhythmias.
  • Poor myocardial contractility leads to low output failure.
  • Cardiac enlargement and areas of damaged myocardium predispose to dysrhythmias and results in poor ventricular filling and cardiac inefficiency.

Hypertrophic Cardiomyopathy

  • Characterized by hypertrophied non-dilated left (or less commonly, right) ventricle.
  • Left ventricular diastolic dysfunction → decreased distensibility of myocardium → increase in end-diastolic pressure with normal or reduced volume.
  • Increased muscle mass, myocardial fibrosis, disordered arrangement of myofibrils → decreased distensibility.
  • Abnormal myocardial relaxation → prolonged relaxation period and decreased rate of decline of left ventricular pressure.
  • Decreased capillary density in myocardium, abnormally narrowed intramural coronary arteries, increased resistance in large coronary arteries due to systolic pressures → myocardial ischemia.
  • Myocardial ischemia → abnormal relaxation, increased left ventricular filling pressures.
  • May be mild hypertrophy with severe left heart failure - probably due to abnormal myocyte function.

Restrictive Cardiomyopathy

  • Endocardial, subendocardial or myocardial fibrosis → prevents stretch (compliance), of left ventricle and ventricular filling.
  • Abnormal blood flows → predispose to formation of thromboemboli.
  • Lack of compliance of left ventricle and reduced ventricular filling → left atrial dilatation, decreased preload, decreased cardiac output and increased pulmonary venous pressure → pulmonary edema and pleural effusion.
  • Turbulence → damages cardiac endothelium → endocardial collagen induces platelet adhesion and aggregation, extrinsic pathway activation.
  • Circulation of blood through heart is abnormal → areas of sluggish flow allow aggregation of platelets particularly in dilated left atrium.


  •  Variable depending upon etiology.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Nart P, Thompson H, Williams W, Armstrong S C, Barrett D C, Innocent G, Morrison M & Nicolson L (2003) Investigation of bovine dilated cardiomyopathy in Holstein-Friesian cattle in the UK. Cattle Pract 11, 153-159 VetMedResource.

Other sources of information

  •  US department of health and human services. FDA US food and drug administration. CFR code of federal regulations Title 21.
  • Valberg S, Nutritional Myopathies in Ruminants and Pigs. MSD Veterinary Manual.
  •  Nart H, Thompson D C, Barrett S C, Armstrong & McPhaden A R. Clinical and pathological features of dilated cardiomyopathy in Holstein-Friesian cattle. Open Access Articles.

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