Sophy A. Jesty
Congenital Cardiovascular Conditions
The horse is thought to have the lowest prevalence of congenital heart disease among domestic animals, with estimates ranging from less than 1% to 3.5%. The clinical consequence of these defects varies considerably, from incidental to immediately life threatening. Most congenital heart defects can be correctly identified with auscultation and a complete and thorough echocardiogram. In addition to two-dimensional, M-mode, and Doppler echo, contrast echocardiography can be very useful for the diagnosis of congenital heart disease. Agitated saline can be injected into the jugular vein and will appear as echogenic bubbles in the right chambers of the heart. Right-to-left shunts are especially easy to detect by use of this technique because a right-to-left shunt is the only way echogenic bubbles can be visualized in the left chambers of the heart. An estimation of the prognosis for each defect must be formulated so that decisions can be made regarding purchase, sale, performance capacity, safety, and life expectancy. This chapter reviews the most common congenital heart defects, which are listed alphabetically. All of the defects listed under Simple Congenital Cardiac Defects may also be seen as part of complex congenital cardiac defects.
Clinical Signs
Regardless of the specific defect, congenital heart disease may result in left-sided congestive heart failure (manifested by tachypnea, dyspnea, nostril flare, cough, exercise intolerance, cool extremities and skin, decreased pulse intensity, inappetence, and lethargy), right-sided congestive heart failure (ventral subcutaneous pitting edema, abdominomegaly secondary to hepatomegaly and ascites, jugular distension or pulsation, weakness, and lethargy), or signs of cyanotic heart disease (failure to thrive, exercise intolerance, lethargy, tachypnea, dyspnea, inappetence, syncope, and altered mental state). In the discussion of each congenital defect, the syndromes that develop as a consequence of the defect (e.g., left-sided heart failure, right-sided heart failure, cyanotic heart disease) are described, but the specific clinical signs are not reiterated.
Congenital Defects
The most common congenital heart defects reported in horses are described in the following section. There are, however, many more congenital heart defects that have been described in only one or a few horses, including anomalous pulmonary venous connection, aortic arch abnormalities, aorticopulmonary window, atrial septal defect, double-inlet left ventricle, double-outlet right ventricle, hypoplastic left heart syndrome, situs inversus, pentalogy of Fallot, and transposition of the great arteries. Readers are encouraged to search for more information about these rare conditions if an echocardiography examination reveals abnormalities not described in this text.
Simple Congenital Cardiac Defects
Patent Ductus Arteriosus
Even though the ductus arteriosus usually closes slowly after birth, the murmur characteristic of patent ductus arteriosus (PDA) often is gone by the time the foal is 3 days old. However, a fair number of foals still have ductal murmurs and shunt flow evident on color Doppler echocardiography at 7 weeks of age. Unless there is severe pulmonary hypertension, the ductus shunts blood from left (aorta) to right (pulmonary artery). Classically, the physical examination will reveal a continuous murmur heard best over the left heart base and bounding facial pulses. Echocardiography will not clearly show the ductus because it connects to the descending aorta, which cannot be seen on a transthoracic echocardiogram. It may be possible to observe where the ductus connects to the main pulmonary artery, and main pulmonary artery dilation should be visible. If the shunt volume is large, left atrial and left ventricular dilation will also be seen. Color Doppler echocardiography will show continual high-velocity flow entering into the main pulmonary artery. The prognosis is variable, depending on the degree of partial closure of the ductus. If the shunt is large enough, PDA can lead to left-sided congestive heart failure, although there have been reports of horses living into their 20s with a PDA. If a PDA is documented in a weanling or older horse and there is significant remodeling of the heart indicating a likelihood of heart failure developing, surgical ligation of the duct by means of a thoracotomy can be considered.
Mitral, Tricuspid, Aortic, or Pulmonic Valve Dysplasia
Valve dysplasia is an unusual congenital defect in horses, particularly as a simple defect. Dysplasia of any of the four valves may cause regurgitation, stenosis, or both. In horses, mitral, tricuspid, and aortic dysplasias are more likely to be regurgitant, whereas pulmonic dysplasia is more likely to be stenotic. Pulmonic stenosis is seen more commonly in complex congenital malformations, such as tetralogy of Fallot. The murmur will depend on the valve involved: mitral and tricuspid dysplasia causing regurgitation and pulmonic dysplasia causing stenosis will all be associated with a systolic murmur (mitral regurgitation over the left side of the apex, tricuspid regurgitation over the right side of the apex, and pulmonic stenosis over the left side of the heart base), whereas aortic dysplasia causing regurgitation will be associated with a diastolic murmur (over the left side of the heart base). Echocardiography will reveal thick, stunted, or redundant valves; abnormal chordae tendineae (mitral and tricuspid); or abnormal papillary muscles (mitral and tricuspid). Color Doppler echocardiography will show high velocity, turbulent regurgitation, or stenosis associated with the affected valve. Although the case reports of valve dysplasias in the equine literature portray a guarded prognosis, in the author’s opinion there is a range of valve dysplasia severity and therefore a range of prognoses. Performance and life expectancy vary depending on the degree of regurgitation or stenosis. The degree of regurgitation can be assessed on the basis of size of the regurgitant jet, dilation of the receiving atrium and ventricle, and any decrease in contractility. The degree of stenosis can be assessed using the outflow velocity, the size of the post-stenotic dilation, and the degree of ventricular thickening. If valve dysplasia is causing only mild regurgitation or stenosis, performance and life expectancy may never be affected, but if valve dysplasia is causing severe regurgitation or stenosis and there is obvious cardiac remodeling, the horse may be at risk for early heart failure.
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