6.7.2 Specific myocardial conditions
6.7.2 Specific myocardial conditions


Myocarditis is a poorly defined condition characterised by reduced myocardial contractility and arrhythmias. Clinical signs include exercise intolerance, dysand sometimes episodic collapse or CHF. Myocarditis may follow a recent history of fever, anorexia, depression and respiratory disease that apparently responded to treatment. Pre- and post-exercise echocardiography, resting, 24-hour and exercise ECGs, and possibly isoenzyme assays are worthwhile invesprocedures in animals with poor exercise tolerance following a bout of respiratory disease. However, it is important that all body systems are examined thoroughly. Long-term respiratory dysfunction resulting in poor gaseous exchange is a much more common sequel to respiratory disease and may result in similar clinical signs.

Myocardial fibrosis

Myocardial fibrosis is thought to caused by ischaemia resulting from emboli, such as fibrin from vascular intima damaged by strongyles. These areas could act as ectopic foci and can be responsible for arrhythmias, but are more commonly seen as incidental findings at PM. More widespread fibrosis may follow myonecrosis.

Myocardial degeneration/necrosis

Conditions causing myocardial degeneration or necrosis are very uncommon. However, they have been reported to occur in outbreaks and may therefore have profound economic implications. The clinical significance of the conditions in an individual animal vary from sudden death to subclinical disease. The mechanisms of the diseases are poorly understood. The most well-known condition resulting in myocardial degeneration and necrosis is ingestion of ionophore antibiotics, such as monensin or salinomycin.

Monensin toxicity

This drug is used as a growth promoter in cattle feed and as a coccidiostat in poultry feed, but it is highly toxic to horses. A number of outbreaks of monensin poisoning associated with the accidental feeding of cattle feed to horses or contamination of horse feed at a feed mill have been reported in recent years. Monensin causes acute cellular necrosis, leading to fibrosis. In addition, hepatic, renal and skeletal muscle necrosis may result. When monensin toxicity is susspecialist analysis of the feed is required.

Clinical signs Clinical signs of monensin toxicity can vary from sudden death due to per-acute hypovolaemic shock, to mild inappetance. Anorexia, ataxia, sweating, increased urination, jugular pulses, tachycardia and dysrhythmias have been documented. CHF is a common feature. In some horses, the clinical signs may be delayed for weeks before the myocardial damage leads to the developof dysrhythmias. In animals which have been exposed to low doses, exercise intolerance may be the only abnormality observed.

Prognosis Echocardiography may show LV volume overload, and regional dyskinesis is common. Monitoring progress with ultrasound appears to be the best prognostic indicator. The outcome is largely dependent on the dose ingested. Some horses with mild disease may recover and return to normal athletic performance.

Treatment There is no specific treatment. Fluid therapy is indicated in the acute case; supportive treatment and strict rest is helpful. Vitamin E may have a cardio-protective effect because it scavenges free radicals produced by cellular necrosis and may be helpful in the treatment of monensin toxicity. Digoxin is contraindicated because it exacerbates the effect of monensin on ionic transport at the cellular level.

Nutritional causes of myocardial disease

Rarely, vitamin E and selenium deficiency can lead to myocardial degeneration in horses. This is very unlikely to be a problem in the UK, except in the most bizarre diets, and would most commonly be found in foals whose dams are malnourished. The condition has been reported in other parts of the world where local soil conditions result in a mineral inbalance. It is usually seen in association with skeletal muscle weakness.

Vitamin D toxicity due to over supplementation has been reported to produce a myopathy leading to valvular insufficiencies, in addition to tachycardia, anorweight loss, polyuria and polydipsia, and muscular stiffness. In some parts of the world, ingestion of toxic plants can result in hypervitaminosis D. Treatinvolves removal of the offending feed and fluid therapy. The prognosis is dependent on the degree of irreversible renal and cardiac damage, but recovery has been reported.

Idiopathic cardiomyopathy

Cardiomyopathy can be described as idiopathic if no other predisposing factor, such as viral infection, can be found. It is rare in the horse compared with small animals. However, it may be more common than has been thought; with the increasing use of echocardiography it may become a more common diagnosis. Cardiomyopathy should be considered in cases where murmurs and CHF develop fairly acutely and there are no signs of obvious valvular disease. Arrhythmias are frequently found in other species with cardiomyopathy and are likely to be common in horses with the condition also. Diagnosis is made on echocardiographic findings of poor myocardial contractility. Supportive treatinvolves the use of diuretics, such as frusemide, and positive inotropes, such as digoxin. However, the prognosis is likely to be poor.