Equine Congenital Cardiovascular Anomalies

Congenital cardiovascular malformations are rare in horses but can have serious implications.
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Congenital cardiovascular malformations are rare in horses with an estimated prevalence of 0.1-0.5%. Male and female horses are similarly affected, and a clear-cut breed predilection is not evident.

Cardiovascular malformations are broadly classified as either simple (a single anomaly) or complex (multiple coexisting anomalies). Each major category is further subdivided on the basis of the tissue affected: myocardium (heart muscle), blood vessels, or valves. Complex malformations typically involve multiple tissues and have the least favorable prognoses.

Clinical signs vary in severity and the age of onset. Typical clinical signs can include stunted growth, exercise intolerance, heart murmur, tachycardia (rapid heartbeat), respiratory distress, and cyanosis (a bluish discoloration of the skin and mucous membranes resulting from a deficiency of oxygen in the blood). Affected horses are frequently found dead; however, not all horses with cardiovascular malformations display clinical signs or die from the anomaly. In some cases, the cardiovascular defect is only identified at necropsy as an incidental finding and is not related to the cause of death.

Ventricular septal defect (VSD) is the most frequently reported congenital cardiac anomaly in the horse. This anomaly is represented by a patent channel in the interventricular septum that allows communication between the two ventricles, which play a critical role in pumping blood. The channel can result in altered pressures within the heart, the shunting of blood through the channel, compensatory hypertrophy (enlargement of the heart muscle), and systemic abnormalities (e.g. cyanosis) in severe cases. Horses with small defects can be asymptomatic or develop clinical signs at a later age. Further, VSDs can be components of complex cardiac anomalies such as tetralogy of Fallot (consisting of a ventricularseptal defect, pulmonic stenosis, rightward malpositioning of the origin of the aorta, and right ventricular hypertrophy/thickening), and truncus arteriosus (consisting of a ventricular septal defect and a single large arterial trunk exiting both ventricles)

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