Page 1018 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Cardiovascular system 993

VetBooks.ir (20,000 IU/kg i/v q6 h [sodium/potassium penicil- echocardiography, a normal leucogram and resolu-
tion of hyperfibrinogenaemia. Antimicrobials should
lin] or q12 h [procaine penicillin]) and gentamicin
(6.6 mg/kg i/v q24 h) provide good initial broad-
beyond the time that fibrinogen levels return to nor-
spectrum coverage. Antimicrobial therapy should be continued for at least 4 weeks or for 2 weeks
be re-evaluated once culture and sensitivity reports mal. Potential sequelae are relapse on withdrawal of
are available. Failure to improve clinically within antimicrobials and scarring and deformity of valves,
5 days should result in re-evaluation of antimicro- resulting in stenosis or insufficiency.
bial therapy. Non-steroidal anti-inflammatory drug
(NSAID) therapy may also be of benefit, particularly Prognosis
in depressed or pyrexic animals. Repeated clini- The prognosis in horses with endocarditis is poor
cal examination, ultrasonography and haematology both for survival and for return to performance.
are recommended. Indications of a response to The onset of heart failure is a poor prognostic indi-
therapy can include the resolution of clinical signs, cator and euthanasia should be considered in such
decreased size or smoother appearance of lesions on animals.

MYOCARDIAL DISEASES

Cardiomyopathies, where cardiac dysfunction is asso- only be reached through histological examination.
ciated with myocardial disease, are not extensively Therefore, in clinical cases only a suspicion of myo-
documented in horses. Heritable cardiomyopathies, carditis can be reached.
such as those documented in cattle, have not been
reported. However, changes in the myocardium (e.g. Aetiology/pathophysiology
focal fibrosis) have been well documented at necropsy Primary myocarditis occurs as a consequence of
in horses. Myocardial disease or damage may occur viral or bacterial respiratory disease. Inflammation
as a result of a toxic insult, an infectious process, and infiltration of myocardial cells disrupt cell func-
neoplasia, trauma, degeneration or inflammation. tion, myocardial contraction and the conduction of
Cardiomyopathy as a result of vitamin E/selenium electrical signals.
deficiency has not been well documented in the horse.
The occurrence of systolic failure (poor contractility) Clinical presentation
or diastolic failure (increased stiffness) has not been Reduced myocardial contractility and arrhythmias
explored in the horse. True structural anomalies, are the main abnormalities. Exercise intolerance,
such as VSD, are addressed elsewhere (see p. 982). respiratory signs, congestive heart failure and col-
Clinical signs associated with myocardial disease lapse are possible. Recent respiratory disease, fever
(not including congenital anomalies) consist of tachy- or anorexia may precede signs.
cardia, arrhythmias and heart failure. In all instances,
cardiac function is affected. Focal lesions are more Differential diagnosis
likely to be associated with arrhythmias, while exten- Ionophore toxicity, cantharidin toxicity, vitamin D
sive lesions more commonly lead to heart failure. toxicity and chronic respiratory disease have a simi-
lar appearance.
PRIMARY MYOCARDITIS
Diagnosis
Definition/overview A history of recent viral/bacterial disease and
Myocarditis is defined as inflammation of the car- potential exposure to toxic agents should be inves-
diac muscle. This inflammation is characterised tigated. Cardiac isoenzyme or cardiac troponin
by myocardial cell damage/death and infiltration analysis may suggest active myocardial inflamma-
by inflammatory cells. A definitive diagnosis can tion. No radiographic abnormalities are present.