Bacterial endocarditis is fairly uncommon in horses and is primarily thought to be secondary to bacteremia or thrombophlebitis.
Bacterial endocarditis is fairly uncommon in horses and is primarily thought to be secondary to bacteremia or thrombophlebitis. The number of horses with thrombophlebitis that actually develop bacterial endocarditis seems to be small. Clinical signs of endocarditis initially include fever, lethargy and depression. Recurrent pyrexia, poor appetite, weight loss, and varying degrees of cardiac compromise also can be seen.
In horses, there does not seem to be any predilection for lesions to occur on valves on the right or left side of the heart, and lesions tend to be less proliferative than they are in cattle. Because of this, blood flow alterations are less severe and incidence of thromboembolism is less in horses compared to cattle.
When there is sufficient proliferation on a valve to cause it to become regurgitant, a murmur can be heard. Cardiac function (or dysfunction) depends on the degree of regurgitation. Tricuspid valve regurgitation results in a systolic murmur heard best on the right side of the chest and a jugular pulse. Right heart failure leads to liver congestion, ascites, and peripheral edema. Mitral valve regurgitation results in a systolic murmur heard best on the left side of the chest in the 5th intercostal space. Significant mitral valve regurgitation results in pulmonary hypertension, pulmonary edema, and eventually right heart enlargement, liver congestion, ascites, etc. Pulmonic or aortic regurgitation result in diastolic murmurs.
If one suspects a horse has bacterial endocarditis, diagnostic tests should include CBC, serum chemistry panel, blood culture, and echocardiography. CBC may show evidence of chronic infection (increased white blood cell count, increased fibrinogen, etc.) Serum chemistry panel will only show evidence of organic disease (eg. renal or hepatic) if the horse is in heart failure or if primary organ disease is the source of the bacteremia. While positive blood cultures are indicative of bacteremia, negative blood cultures do not rule out bacterial endocarditis; the infection may have cleared by the time the diagnostics are performed, yet the changes on the valves remain.
Common isolates in equine bacterial endocarditis include Streptococcus zooepidemicus and Actinobacillus equuli. Cardiac ultrasonography should reveal which valve(s) are thickened and/or regurgitant. Cardiac ultrasonography also indicates degree of valve regurgitation, cardiac enlargement, contractility, etc. This information is useful prognostically. Treatment of bacterial endocarditis includes long-term administration of antibiotics (preferably based on culture and sensitivity) and supportive care for cardiac dysfunction.
Myocardial diseases include myocarditis and cardiomyopathy, both of which are rare in the horse. Myocarditis is defined as myocardial wall inflammation caused by bacteria, viruses, or parasites. Recognized causes of bacterial myocarditis include Streptococcus equi, Staphlococcus aureus, Clostridia chauvoei, Mycobacterium spp., and any other bacteria causing septicemia, pericarditis, or endocarditis.
Perhaps the most common cause of myocarditis is equine influenza virus, although other viral causes of myocarditis include equine infectious anemia, equine viral arteritis, foot-and-mouth disease, and African horse sickness. Parasitic causes of myocarditis include strongylosis, onchocerciasis, toxoplasmosis, cysticerciasis, Sarcocystis infection, and Borrelia burgdorferi.
Clinical signs of myocarditis include depression, lethargy, work intolerance, and increased resting heart rate. Arrhythmias are not uncommon. Clinical signs may be confused with mild colic. The most useful diagnostic tests include cardiac ultrasonography, ECG, and measurement of cardiac troponin. Cardiac ultrasonography shows poor contractility. The heart may or may not be enlarged, depending on the duration of the myocarditis. Additional useful diagnostic tests include CBC, serum chemistry panel, measurement of serum vitamin E concentration, Streptococcal titers, and viral titers.
Treatment includes treatment of any underlying cause of the myocarditis (eg antibiotics for a bacteremia, anthelmintics for parasites, vitamin E supplementation, etc) and supportive care for the decreased cardiac function (anti-arrhythmic drugs, positive inotropes, etc.). Steroids are often given for their anti-inflammatory effects, especially if an arrhythmia persists.
Cardiomyopathy is a subacute or chronic myocardial disease without congenital heart disease, valvular disease, or pulmonary disease. Only the dilated form has been reported in large animals. Causes of cardiomyopathy in the horse include toxins (ionophore antibiotics, eg monensin, gossypol, certain plants, eg Cassia occidentalis, Phalaris sp., and high dietary molybdenum and sulfate leading to a relative copper deficiency), deficiencies (vitamin E / selenium, copper), and other unknown causes.
Clinical signs following ionophore antibiotic ingestion depend on amount of toxin ingested. In more severe cases, arrhythmias or sudden death may be the only signs. In more chronic cases, cardiac chamber sizes becomes enlarged and the wall thicknesses decrease. Stretching of the atrioventricular valve annuluses results in tricuspid and mitral regurgitation.
Treatment for cardiomyopathy includes identification and removal of the underlying cause and supportive care for arrhythmias, pulmonary edema, heart failure and shock. Prognosis is guarded to poor once the horse exhibits signs of heart failure.
Treatment of heart failure caused by valvular and myocardial diseases
Moderate to severe valvular disease, myocarditis and cardiomyopathy can result in decreased cardiac contractility (decreased fractional shortening), cardiac chamber dilation, arrhythmias, pulmonary edema, heart failure, and shock. Treatment includes correction of any underlying deficiency or toxicity, treatment of specific arrhythmias as needed (see above) and support of cardiac function as needed (see below). Corticosteroid administration may also be indicated in cases of myocarditis, depending on severity and response to initial treatment.
Treatment for heart failure:
Furosemide-0.5-3.0 mg/kg q 12 hour (IV, IM, or PO) (note - oral absorption may be erratic, so parenteral administration is preferred)
Digoxin-Loading dose (rarely used) 0.0044-0.0075 mg/kg IV q12h (2 doses only)
Maintenance dose--IV:0.0022-0.00375 mg/kg q 12h; Oral:0.011-0.0175 mg/kg q12h (oral used more commonly); peak concentrations of digoxin in plasma should not exceed 2.5 ng/ml. Increases vagal activity, which slows ventricular rate in atrial fibrillation; signs of digoxin toxicity: anorexia, diarrhea, colic, weakness, depression, cardiac arrhythmias, and conduction disturbances.
Pericarditis is fairly rare in the horse. When present, it is usually secondary to bacterial infection, pleuritis, influenza, or equine viral arteritis. In these cases the fluid is most often a transudate and the volume is often not great. Fibrinous pericarditis has more recently been associated with mare reproductive loss syndrome. Horses with pericarditis may also have myocarditis.
Clinical signs of pericarditis include depression and lethargy, with or without a fever. The horse may stand with a wide-based stance or may be reluctant to lie down. Ventral edema or a jugular pulse may be present. Auscultation of the heart may reveal a pericardial friction rub or muffled heart sounds, depending on the acuteness or chronicity of the problem and the amount of fluid accumulation. Heart rate is often increased and may be irregular. Fluid accumulation in the pericardial sac is initially effusive. More chronically it can become constrictive. Epicardial fibrin accumulation can constrict the chambers and limit cardiac filling.
Pericardial effusion is confirmed by echocardiography. Echocardiography also allows assessment of the character of the fluid, whether or not there is fibrin accumulation on the epicardial surfaces (increased thickness of free walls, most evident on the right ventricle), can guide pericardiocentesis if needed, and is used to monitor progression or resolution of disease. If the amount of pericardial fluid is small, appears serous, and is not affecting cardiac function, pericardiocentesis is not immediately necessary. Treatment of the presumed underlying cause is initiated, while the amount and character of pericardial fluid is monitored.
If the amount of fluid is large enough to be interfering with cardiac output, pericardiocentesis can be performed to drain the fluid. Cytology and culture of the fluid obtained can be used to guide continued treatment. In chronic cases, surgical pericardiotomy or pericardiectomy may be indicated to remove fibrin accumulation, but prognosis is much worse. Prognosis is also extremely guarded if the horse is showing signs of heart failure. Additional diagnostics should include CBC, serum chemistry panel, cardiac troponin (to rule out accompanying myocarditis), and virus titers.
A sample of pericardial fluid can be aspirated for bacterial culture and sensitivity if the cause appears to be bacterial. However, the latter is often not the case in horses. Treatment should include cardiac support as well as treatment for the presumed underlying cause (virus, etc.). Administration of anti-inflammatory steroids should be considered if pericardial fluid is not resolving rapidly, if there is evidence of moderate to severe myocarditis, or if the horse is experiencing continuing arrhythmias.
Steroids are not necessary if the pericardial effusion is trivial, and may be contra-indicated if the horse has a viral respiratory infection. If the amount of pericaridial fluid is small, appears hypoechoic on ultrasound, and is thought to be secondary to viral disease, the likelihood that it will resolve without drainage is good. However, the prognosis is guarded if the horse is showing signs of heart failure.
Mesothelioma, melanoma, and hemangiosarcoma have been reported on the pericardium of horses, but these tumors are extremely rare. Probably the most common cardiac neoplasm is lymphosarcoma, which can invade the atria.