Etiology

• 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).

Pathophysiology

•  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.

Timecourse

•  Variable depending upon etiology.