The equine heart occupying the ventral middle mediastinal space extends between ribs 2 and 6. It is surrounded by a pericardium attached to the sternum. The weight of the heart depends on breed, sex, and age. Generally, it averages 0.6% of the total body weight (3.45 kg average heart weight) in horses without exercise training. It can reach 1.04% of body weight in horses under training and exercise. Small horses have relatively heavier hearts than large horses. The shape of the equine heart is that of a cone with the sharp apex formed by the left ventricle.
The equine heart, as in all mammals, has three physiologic features: (1) it is a pump supplying oxygenated blood to the dependent organs of the body and returning venous blood to the lungs for oxygenation; (2) it contains a conduction system associated with specialized cardiocytes receiving and supplying electrical stimuli; and (3) as an endocrine organ it contains hormone-producing cardiocytes to secrete a peptide hormone defined as atrial natriuretic factor.
A healthy heart is especially important for the equine athlete. Cardiac markers such a troponins are used for the clinical diagnosis of myocardial disease in the horse.
An orderly dissection of the heart is necessary to avoid mutilation of anatomic structures for the assessment of pathologic processes. Several techniques have been proposed. The method used at the University of Florida is described in Chapter 1.
I. Heart
Figure 5.1. Horse. Normal Heart. The apex is exclusively formed by the left ventricle in the healthy equine heart.
1. Congenital cardiovascular anomalies
In the horse, these anomalies have been reported as ventricular septal defect (VSD) and less frequently as atrial septal defect (ASD), patent ductus arteriosus (PDA), common truncus arteriosus, tetralogy of Fallot, vascular ring anomaly, complete transposition of greater vessels, and double-outlet right ventricle and tricuspid valve atresia.
a. Ventricular septal defect
VSD is the most frequently occurring single defect in the horse. It is usually a membranous defect high in the ventricle, but apical muscular defects can be encountered. A small VSD often remains unnoticed clinically, but in larger ones there may be evidence of pulmonary edema in the case of a left-to-right blood shunt due to overflooding of the lungs, or there may be cyanosis in the case of a shunt reversal from right to left. The right ventricle undergoes hypertrophy in the latter case. Animals with VSD range in age from neonates to 2 years.
Figure 5.2. Horse. Heart. Ventricular Septal Defect. There is evidence of both a high ventricular and apical septal defect in this 2-month-old thoroughbred colt. (Reprinted with permission from Cambridge University Press.)
b. Common truncus arteriosus
This anomaly is defined as one major vessel leaving the ventricular part of the heart. The single vessel receives unoxygenated blood through a high ventricular ventricular defect. The condition leads to cyanosis.
Figure 5.3. Horse. Heart. Common Truncus Arteriosus. One large vessel overriding a ventricular septal defect exits the heart. A high VSD is present.
c. Patent ductus arteriosus
The ductus arteriosus is a tubular muscular structure of the fetal circulation that connects the pulmonary trunk with the ascending aorta and allows blood to bypass the lungs. In the horse it closes physiologically within 3 days after birth to obliterate and to become the ligamentum arteriosum. There is usually a left-to-right shunting of blood with pulmonary circulatory overload. Pulmonary hypertension in long-standing cases may lead to shunt reversal, cyanosis, and aneurysm of the pulmonary artery as in this case.
Figure 5.4. Horse. Heart. Major Vessels. Patent Ductus Arteriosus. An aneurysm of the pulmonary artery is indicated by the red discoloration of the wall.
d. Vascular ring anomaly and megaesophagus
Figure 5.5. Horse. Vessel. Persistent Right Fourth Aortic Arch. A vascular ring over the esophagus has created a compression of the esophagus at that site with cranial distension of the esophagus creating a megaesophagus. (Courtesy Dr. J. Roberts, National Zoo, Washington, DC.)
2. Pericardial diseases
Two types of pericardial inflammatory processes are distinguished: effusive, often nonseptic, and fibrinous septic pericarditis. The cause of the effusive form is unknown; bacteria are frequently isolated from the fibrinous form. The principal bacterial isolates are Actinobacillus sp., Streptococcus sp., Enterococcus sp., and Klebsiella pneumoniae. Bacterial inflammation of the pericardium usually is hematogenous in origin as to the portal of entry. A special form of fibrinous pericarditis has been reported in adult horses in conjunction with the mare reproductive loss syndrome since its occurrence in 2001 (see Chapter 12, “Diseases of the Reproductive System”).
Figure 5.6. Horse. Heart. Septic Pericarditis. The severely distended pericardium is the result of the accumulation of a brown septic exudate. Arcanobacterium pyogenes was isolated in this case.
Hydropericardium and hemopericardium from cardiac tamponade or cardiac hemangiosarcoma are other types of fluid accumulation in the pericardium.
3. Myocardial diseases
Diseases of the myocardium can be divided into primarily degenerative and primarily inflammatory entities.
a. Necrosis/degeneration
Nutritional or toxic factors need to be taken under consideration as etiology. Vitamin E/selenium deficiency is an example of a nutritional disorder. Ionophore antimicrobials (e.g., monensin, lasalocid), Cassia occidentalis, blister beetle cantharidin, oleander cardenolides (Nerium oleander), adonis cardenolides (Adonis aestivalis), and mycotoxins are etiologic examples for toxic cardiomyopathies.
Figure 5.7. Horse. Heart. Myocardium. Necrosis. Blister Beetle. The gray foci in the myocardium represent myocyte necrosis. (Courtesy J. Roberts, National Zoo, Washington, DC.)
Figure 5.8. Horse. Heart. Myocardium. Vitamin E/Selenium Deficiency. This nutritional myopathy is rare in horses and usually affects foals. Patches of white foci are present in the myocardium of the left ventricle. (Reprinted with permission from Cambridge University Press.)
b. Myocarditis
Myocarditis is relatively rare in horses. Viruses such as the alphavirus of eastern equine encephalitis or equine infectious anemia, bacteria such as Streptococci, fungi such as Aspergillus sp. or nematodes such as Halicephalobus gingivalis are recognized etiologic causes for myocarditis.
Figure 5.9. Horse. Heart. Parasitic Myocarditis. This horse had a granulomatous parasitic myocarditis due to Halicephalobus gingivalis as an incidental finding at necropsy. A few larvae are embedded within granulomatous inflammation. (H&E)
Figure 5.10. Horse. Heart. Myocardial Fibrosis. Very old horses develop myocardial fibrosis as end-stage lesions of previous inflammation or degeneration, replacing myocardium with collagen (myocardial scar). In this heart major areas of the myocardium have been replaced by gray streaks of collagen tissue.
Figure 5.11. Horse. Heart. Myocardial Fibrosis. Dense layers of collagen have encircled Purkinje myocytes potentially interfering with the function of the conduction system. Such a change may result in sudden death of the animal. (Trichrome)
4. Endocardial disorders
The endocardium as a thin membrane lines the ventricles, atria, and valves. It is susceptible to degenerative and inflammatory changes.
a. Fibrosis and mineralization
Focal endocardial fibrosis may be the result of blood regurgitation and circulatory disturbance due to valvular insufficiency. Endocardial fibroelastosis denotes diffuse thickening of the entire endocardium along ventricles. This may lead to congestive heart failure due to interfering with ventricular myocardial contraction. A few such cases have been reported in the horse.
Endocardial mineralization is metastatic as the result of pseudohypervitaminosis D from consumption of toxic plants such as Cestrum diurnum. Similar mineralization occurs in the intima of the aorta and in tendons and ligaments. It has to be differentiated from hypercalcemia as a paraneoplastic syndrome secondary to lymphoma.
Figure 5.12. Horse. Heart. Endocardial Mineralization. White gritty streaks cover the apical endocardium in this case of Cestrum diurnum toxicity.
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