Category:Myocardial Pathology

Functional Anatomy

The myocardium provides the bulk of the heart tissue, and enables the co-ordinated contraction needed for efficient pumping of blood to the body.

Cardiac muscle is intermediate in appearance between skeletal muscle and visceral muscle with characteristics of both:

• Contracts with the force of skeletal muscle.
• Contracts continually like visceral muscle.

Cardiac muscle cells are long, striated, cylindrical cells with one or sometimes two nuclei. Cells contain a sarcoplasmic reticulum which slowly leak calcium ions into the cytoplasm, allowing automatic contractions without the need for external input. The rate of contractions is modulated by external autonomic and hormonal inputs. The sino-atrial node is the pace-maker of the heart as its rate of automatic firing is the greatest.

Intercellular junctions are known as intercalated discs and provide anchorage. They also allow the rapid progression of contractile stimuli throughout the heart muscle, making a functional syncytium.

The ventricular muscle is much thicker than that of the atria, and the atrial myocardium has a more fibrous component.

Blood supply is from the coronary arteries, sinuses beind the leaflets of the aortic valve allow entry of blood into the coronary system at diastole.

Disease of the myocardium may be incidental at post mortem and cause no clinical signs, or may be clinically evident. Disease must be severe and widespread to lead to observable clinical signs. Myocardial disease most often leads to heart failure.

The heart cannnot regenerate by hyperplasia and so responds with hypertrophic change in order to maintain normal function.

Hypertrophy

Increased bulk of myocardium due to increased cell size. Estimated most accurately by chamber wall thickness.

Right sided hypertrophy results in increased heart width.

Left sided hypertrophy results in increased heart length.

Bilateral hypertrophy results in a round heart shape.

• Physiological: In resposnse to exercise in athletic animals E.g. racing greyhounds.
• Pathological:
  • Concentric: Due to pressure overload E.g. restrictive pericarditis. Thickened chamber walls with a decreased chamber lumen, often will result in myocardial hypoxia. Fibrosis of the myocardium will restrict chamber expansion and filling at diastole leading to diastolic failure.
  • Eccentric: Due to volume overload. Increased wall thickness, which may be variable, with a dilated chamber. E.g. mitral regurgitation will result in eccentric hypertrophy of the left atrium.

When the disease progress occurs too rapidly to allow the heart to adapt dilation will occur. Dilation is also seen at the onset of decompensation of a previously compensating failing heart.

Metabolic pathology

Cloudy swelling

An early stage of toxic degenerative change of the protein component of tissues. Tissues appear swollen and opaque but will return to normal once the insult is removed. Occurs with toxaemia and septicaemia.

Fatty change

Deposition of fatty globules within an organ or tissue, indicative of myocardial hypoxia or toxicity. Seen therefore with myocardial ischaemia, anaemia and poisons such as chloroform, phosphorous and tetrachloride. Heart is grossly pale, soft, greasy and friable.

Steatosis

Replacement of muscle bundles with fat without an inflammatory response. Congenital condition which may also affect skeletal muscle. Usually found in cattle, sheep and pigs and poses a problem at meat inspection only.

Hyaline degeneration

Hyalisation of muscle fibrils of skeletal, intercostal, diaphragmatic and cardiac muscles. Histologically there is Zenker degeneration and occasionally also dystrophic calcification.

Grossly the condition is seen as grey/yellow streaks on the innermost part of the myocardium.

The condition is associated with Vitamin/Selenium deficiency. Also known as nutritional myopathy or White muscle disease. The myocardium of the left ventricle is most affected as it has the largest metabolic demand and so the largest production of anti-oxidants and the greatest need for Vitamin E/Selenium. This manifests clinically as left sided heart failure with clinical signs:

• Pulmonary oedema.

Also:

• Acute ataxia and collapse with the skeletal muscles affected.

Also associated with a diet over-rich in unsaturated fatty acids seen in pigs (Vitamin E/Selenium unavailable as used up by the unsaturated fats).

Lipofuscinosis

Also known as Brown atrophy. Lipofuscins are a class of fatty pigments formed when a pigment is dissolved in fat. Known as wear and tear pigments, they become deposited with advancing age and Vitamin E/Selenium deficiency. Also ay be breed related, seen in Ayreshires.

Mineralisation

• Dytrophic: Calcium is deposited due to damage of the myocyte. Myocyte damage may be:
  • Hypoxia.
  • Vitamin E/Selenium deficiency.
• Metastatic: Occurs with elevated serum calcium for example will occur with:
  • Vitamin D toxicity.
  • Secondary hyperparathyroidism.

Degenerative-Cardiomyopathy

The majority of cardiomyopahies in domestic species are idiopathic in aetiology. There are three forms if idiopathic cardiomyopathy:

• Dilated
• Hypertrophic
• Restrictive

Dilated cardiomyopathy

Incidence:

Most common form in the dog. Seen in young to middle aged dogs of large breeds:

• St Bernard
• Great Dane

Clinical signs:

Disease is a slowly progressive dilation of the ventricles with a loss of contractility. This is seen histologically as random myofibrillar thinning and degeneration of myocyte mitochonria, although it is possible that no histological lesions are present.

Clinical signs will appear as a sudden onset disease as there will be an acute decompensation for the pathology that had accumulated gradually. Signs include those of a congestive heart failure:

• Pulmonary oedema.
• Ascites.
• Hepatomegaly and splenomegaly.

Diagnosis:

Gross cardiomegaly with cardiac hypertrophy, dilation and decreased contractility. Histopathologically; increased attenuated wavy fibres within the myocardium. Fibres are thinner than normal and have a wavy appearance. May develop due to a chronic volume overload.

• Ventricular dilation, particularly the left ventricle, distorts the AV-valves which often become incompetant.
• Fibrillation is a common finding as dilation of the myocardium induces abnormal electrical activity and arrhythmias.

Variations of the disease exist in specific breeds:

• Doberman: Present with arrhythmias. Histologically there are lymphocytic infiltrates within the ventricular myocardium. See focal degeneration of the bundle of His, probably due to narrowing of small vessels near the conductive tissue.
• English Cockers: Familial with many dogs having sub-clinical disease.

View images courtesy of Cornell Veterinary Medicine

Hypertrophic cardiomyopathy

Incidence:

The cat is most commonly affected. There is some evidence of inheritance, as in man, and the disease is said to be more common in male cats. There is a wide age range of 7 months to 24 years.

Inherited in Maine Coon cats.

Clinical signs:

Grossly there is disproportionate hypertrophy of the left ventricle and often the interventricular septum. The chamber size is dramatically reduced.

Histologically there is haphazard hypertrophy of the myocardial fibres.

The reduction in left ventricular volume and the stiffened ventricular wall results in diastolic dysfunction, the stroke volume is reduced resulting in congestive heart failure and the following clinical signs:

• Tachycardia.
• Arrhythmia (abnormal myocardium)
• Dyspnoea.

The force of the left ventricular contraction reduces afterload and reduces end-systolic volume to zero in some cases. This is cavity obliteration.

• Thromboembolic disease is a frequent complication. The thromboemboli most often impact in the femoral arteries manifesting as an acute hindlimb paralysis.

Restrictive cardiomyopathy

Described clinically in cats and cattle. There is fibrosis and thickening of the left ventricle which allows decreased filling and so diastolic dysfunction. There is left atrial dilation to cope with the increased difficulty in filling the left ventricle and this predisposes to thromboembolic disease. Atrial fibrillation is also a common finding.

Clinical signs:

Left sided heart failure and so:

• Pulmonary oedema, plus...
• Thromboembolism, usually hindlimb paralysis.

In cattle the disease appears to have an inherited pathogenesis. Disease is seen in:

• Polled Herefords with curly hair coats.
• Friesian Holsteins with a common sire.

Other Cardiomyopathies

Feline Hyperthyroidism

A hypertrophic cardiomyopathy is seen secondary to this disease in elderly cats. Thyroid hormones induce the growth of the myocardium.

Secondary to toxic agents

Includes:

• Dilated myopathy in horses with monensin toxicity.
• Dilated myopathy in dogs with long term administration of doxorubicin.
• Dilated myopathy in cats due to taurine deficiency.

Inflammatory-Myocarditis

Most often due to an infective agent. In most cases myocarditis is a result of a generalised infection, myocarditis is rarely an isolated primary condition. Classified as:

Acute Suppurative

Follows from the dissemination of septic emboli form suppurative foci therefore always follows pyaemia. Original septic foci may be:

• Joint ill.
• Umbilical abcess.
• Metritis.
• Mastitis.
• Valvular endocarditis.

May also be a result of extension from the endocarium or pericardium.

Acute non-suppurative

Usually results from a septicaemia or viraemia E.g Parvovirus infection in puppies. Also includes:

• Foot and Mouth Disease.
• Leptospirosis.
• Pasteurellosis.

Parvovirus Infection of puppies:

Parvovirus affects rapidly dividing cells which are found in the GI tract, and in the growing pup, the myocardium. Myocardial cells divide up to approximately 2 weeks of age and so this is when the infection has an effect although clinical signs may not become apparent until later in life.

Two cardiac syndromes exist:

• Sudden death, 3-8 weeks: Cardiac failure with pulmonary oedema etc. Histologically see multifocal myocardial necrosis due to viral replication within the myocardium. May see large basophilic intranuclear inclusion bodies.
• Puppies >8 weeks: See dyspoea, weakness, collapse and death within 24 hours. In this case cardiac failure occurs due to myocardial fibrosis.

Chronic

Myofibrils replaced by fibrous tissue during healing. May be a sequale of previous acute myocarditis.

Parasites

Parasites also may cause myocarditis. parasitic larvae may encyst in the myocardium, including:

• Cysticercosis.
• Sarcocystis.
• Toxoplasmosis.

Vascular pathology

Haemorrhage

Haemorrhage into the myocardium is seen with septicaemic disease. Also seen with:

Mulberry Heart Disease.

Occurs in pigs fed a diet deficient in Vitamin E/Selenium. Exact aetiology unknown but the lack of free radical scavenging allows haemorrhage into the myocardium. Characteristic linear and ecchymotic haemorrages are seen under the visceral pericarium and haermorrhage extends between the fibres, leading to myocardial degeneration.

Clinically seen as sudden death in pigs 3-4 months of age. The fastest growing pigs are affected the most so disease is seen in those with the best condition.

Thrombosis

Myocardial infarction rare in animals. May be seen with septicaemias.