Category:Myocardial Pathology
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.
Steatosis
Hyaline Degeneration
Lipofuscinosis
Myocardial Mineralisation
Degenerative-Cardiomyopathy
The majority of cardiomyopahies in domestic species are idiopathic in aetiology. There are three forms if idiopathic cardiomyopathy:
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.
Pages in category "Myocardial Pathology"
The following 12 pages are in this category, out of 12 total.