FRANK J. MILNE STATE-OF-THE-ART LECTURE


sue disorder affecting either elastin or collagen in the aortic media is suspected in affected horses.103 Although SCD can occur, most horses have a sub-


acute or chronic history of recurrent colic, anorexia, depression, repeated recumbency, poor performance, coughing, and epistaxis.101 Prior to diagnosis, pe- ripheral edema (intermittent), fever, tachycardia, and tachypnea may be present. Bounding arterial pulses would be expected, with the continuous shunting from the aorta to the pulmonary artery, and occurred in approximately 50% of affected horses.101 Cardiac murmurs (all on the left) and jugular pulses were reported in half of the horses in this retrospective study and a few had cardiac arrhythmias.


Echocardiographic Findings


Reported echocardiographic findings in affected Frie- sians include a dilated pulmonary artery and dilated right atrium and right ventricle; the latter two are prob- ably associated with the CHF that ensued.101 Pleural effusion, pericardial effusion,andpulmonaryedemamay also occur. With the use of nontraditional echocardio- graphic viewsandscanning out the aortaandpulmonary artery, the pseudoaneurysms104,105 can be imaged with 2D echocardiography, along with the turbulent flow in these structures using color-flow Doppler echocardiogra- phy. Transesophageal echocardiography has also visualized the aortic arch region better in affected horses.105,106


Significance/Prognosis


Friesian horses with aortic rupture or aortopulmo- nary fistulation have a grave prognosis for life, with most living only days to weeks following the onset of clinical signs.103 Right-sided CHF is common with pulmonary hypertension and right atrial and ventricular enlargement detected echocardio- graphically. Although treatment for CHF can be instituted, affected horses are not safe for ridden or driven work. Humane destruction is sug- gested due to the severity of the disease and the likely underlying genetic disorder.


5. Myocardial Disease with Emphasis on Diagnosis, Severity, and Impact on Performance, Life Expectancy, and Horse and Rider Safety


Myocarditis, myocardial necrosis, fibrosis, and fatty and fibrofatty infiltrates can cause SCD by trigger- ing fatal ventricular arrhythmias. At postmortem examination, there may be no other cause of death found or myocardial lesions are found that could have resulted in a fatal ventricular arrhythmia. This is reported most frequently in young racehorses that experience SCD.107 Infrequently, VT is docu- mented shortly before death.107 Multifocal myo- cardial necrosis or fibrosis has been documented histopathologically in some of these horses. These lesions were found close to the sinoatrial node, in the AV junction, and in the upper portion of the inter- ventricular septum in one study, along with vascular changes.107 Fibrous, fatty or fibrofatty infiltrates in


the myocardium have been found in horses of all ages with fatal ventricular arrhythmias/SCD and may be similar to changes seen with arrhythmogenic cardio- myopathy in humans.108–110 With the advent of echocardiography, myocardial disease is identified more frequently in horses with a variety of clinical presentations. Many young horses with suspected myocarditis have a history of fever in the days, weeks, or months preceding the onset of clinical signs. Myocardial disease may be associated with exercise intolerance, poor perfor- mance, collapse, tachycardia that is disproportion- ate to fever, arrhythmias, and/or murmurs or be clinically silent.111,112 The first indication of myo- cardial disease may be SCD in one or more horses.111 Myocardial disease can be associated with infection (viral, bacterial, or fungal), colic, sepsis, toxemia, drugs (ionophores), plants, envenomation, hypoxemia, amyloidosis, nutritional, glycogen storage disease, neoplastic infiltration, endocarditis, trauma, severe hemorrhage, catecholamines, cocaine, and cobalt, as well as other causes. Myocardial contusion should be considered as a possibility in horses with cranial tho- racic trauma.113 Cardiac auscultation may be normal or arrhyth-


mias or murmurs of MR or TR may be present. The valvular regurgitation usually develops second- ary to stretching of the AV valve annulus in a horse with primary myocardial disease. Frequent atrial or ventricular extrasystoles, sustained atrial tachy- cardia or VT, or multifocal arrhythmias are often indicative of primary myocardial disease.111,112 Resting, exercising, or continuous 24-hour electro- cardiography may be needed to identify arrhythmias in affected horses. Some arrhythmias associated with myocardial disease, such as multifocal VT, are life threatening. Resting heart rates in horses with myocardial disease may be normal or elevated, but affected animals usually have elevated exercising heart rates and prolonged heart rate recovery after exercise. cTnI or cTnT may be elevated in horses with active myocardial disease.114 Tachycardia and arrhythmias (both atrial and ventricular) are common problems in horses presenting with cardiac involvement associated with acute envenoma- tion.115,116 An elevated cTnI is also detected in a number of bitten horses, consistent with myocardial injury.116 In many horses with acute envenoma- tion, tachycardia persists through the time of dis- charge from the hospital.


Ionophore Toxicity


SCD of one or more horses may be the first indication of ionophore toxicity.117–125 Amyriad of other clinical signs, such as anorexia, lethargy, muscle weakness, colic, diarrhea, neurological signs, polyuria, and poly- dipsia, may also occur in horses with ionophore expo- sure.20,118–135 Arrhythmias are also reported in horses with monensin poisoning,117,118,121–123 as well


AAEP PROCEEDINGS  Vol. 64  2018 107


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