6.7.1 Diagnosis of myocardial disease
The clinical signs associated with myocardial disease vary from sub-clinical to fatal. Myocardial disease is most often a consideration in horses presented for poor athletic performance, but it can be difficult to diagnose with any degree of certainty. In horses with CHF it is important to distinguish primary myocardial disease from valvular heart disease. Some animals with CHF due to myocardial disease will recover, and may, in some instances, return to athletic use, but the prognosis is usually hopeless with CHF due to valvular heart disease. Myocardial failure may also occur secondary to severe valvular heart disease. In addition, horses with systemic disease may have myocardial dysfunction as a secondary complication. This is particularly common in foals with septicaemia, and in exhausted animals with profound electrolyte imbalance.
A thorough clinical examination is required in the evaluation of animals with suspected myocardial disease. Other causes of poor performance need to be investigated (see section 8.2). Examination of the cardiovascular system is performed along the lines previously described (Chapter 3). In animals with mild myocardial disease there may be no abnormal findings on clinical examination at rest. The disease may only be suspected after arrhythmias are detected during exercise. In other animals, arrhythmias at rest may be the only significant finding. This is most often the case with myocarditis. A raised pulse rate and poor pulse quality are common findings in animals with more severe myocardial disease. In cases in which there is a marked reduction in myocardial contractility, a weak apex beat and quiet heart sounds may be detected. Signs of CHF should also be noted if present. Abnormal heart murmurs should be classified and evaluated to determine whether they indicate the presence of primary valvular disease, and whether they alone are sufficient to account for the clinical signs. Animals with myocardial disease may develop cardiac murmurs, particuMR, as a result of dilatation of the valve annulus. Further diagnostic tests are usually required to determine the primary problem.
Echocardiography is a very important tool in the diagnosis of myocardial disease. It may allow a diagnosis to be made in those animals which have no abnormdetected on clinical examination. In horses which have obvious clinical signs, it is a helpful guide to the severity of the disease and is a useful prognostic indicator. Echocardiography may also allow the clinician to determine whether the primary problem is valvular or myocardial.
The heart should be carefully examined for evidence of valvular and myoabnormalities. In myocardial fibrosis, a diffuse or localised increase in echogenicity of the myocardium maybe noted. Care should be taken not to over- interpret artefactual changes in density which are very dependent on the gain settings and the angle of incidence of the ultrasound beam. The size of the cardiac chambers should be assessed.
Echocardiography is particularly useful for assessment of myocardial conAn impression of the effectiveness of myocardial contraction can be made from subjective assessment of the 2DE and M-mode image. A more quantitative method is to measure fractional shortening (FS%) of the LV from the M-mode image (see section 4.2.6). A marked reduction in contractility will result in a reduced FS%. A measurement of less than 26% can be regarded as abnormal (Figure 6.4). However, as with all echocardiographic measurements, this is a guideline rather than an absolute value and may be affected by meaerrors and the level of excitement of the animal. When there is dysof the ventricles, FS% may be of little value and a subjective assessment of contractility may be sufficient. Sedation affects FS% and should not be used in horses in which myocardial disease is suspected. In some animals, such as those with extensive myocardial fibrosis, diastolic dysfunction is the primary problem. This may be evident echocardiographically as a slow rate of filling and abnormal mitral valve motion on the M-mode trace (Figure 4.14), and may result in an increase in the relative size of the A wave compared with the E wave.
It is impossible to perform an echocardiographic investigation in the actively exercising horse; however, useful recordings can be made immediately after exercise. The examination is complicated by respiratory motion and is not easily performed. Animals with myocardial disease may show a reduction in FS% during this period which was not evident at rest. The consequences of other physiological changes which occur after exercise, such as the effects of dehyand cutaneous vasodilatation for thermoregulation, need to be conbut post-exercise echocardiograms may prove to be useful in selected cases.
Myocardial disease often causes arrhythmias. Detection of an abnormal arrhythmia may therefore indicate the presence of myocardial disease. Reduced athletic performance may result directly from the effect of the arrhythmia on ventricular filling and cardiac efficiency, or result from poor myocardial con
ECGs recorded at rest may show arrhythmias which are likely to result in poor athletic performance, or other signs of heart disease. Ideally, echocardiography and clinical pathological tests should be performed if frequent atrial premature beats (APCs), ventricular premature beats (VPCs), atrial or ventricular tachyor other abnormal rhythms are detected at rest. In many animals, the significance of arrhythmias detected at rest is unclear. It is helpful to assess their incidence during exercise in order to evaluate their likely effect on performance. ECGs recorded during exercise, either with the horse on a treadmill, or on the gallops if radiotelemetry is available, are therefore extremely useful in these cases. Some animals with poor athletic performance, but no evidence of cardiac disease at rest, will be shown to have significant arrhythmias during exercise which may explain the clinical signs. In other animals, arrhythmias such as APCs and VPCs, which were present at rest, may be abolished once the sinus rate is increased. 24-hour resting ECGs are also useful for assessment of the sigof arrhythmias detected intermittently at rest (Chapter 7).
In addition to identification of arrhythmias from the ECG, abnormalities in the morphology of the complexes and the intervals between them can result from myocardial damage. However, the changes are very non-specific and, because complexes may vary between different normal animals, these changes are difto interpret.
A variety of clinico-pathological tests are helpful in evaluating myocardial disDetails of each test are described in Chapter 2.
Haematology is helpful in assessing the possibility of viral infection, but is not helpful in specifically identifying the presence or absence of myocardial disease. Both haematology, viral antibody titres and virus isolation may be helpful if a viral cause for myocarditis is suspected; however, the clinical pathological evifor viral infection is most likely to be found in the active infection phase, and myocardial disease is seldom suspected or present until weeks or months later.
Abnormal electrolyte levels may be responsible for arrhythmias, and may be found following muscle damage. However, changes are seldom specific, and electrolyte measurements are of more help in ruling out other causes of arrhythmias than in evaluating the presence or absence of myocardial disease.
Isoenzymes of creatinine kinase (CPK) and lactate dehydrogenase (LDH) have been suggested as useful indicators of myocardial damage. However, a number of problems exist with the assays and in the author's opinion they should be interpreted with caution (see section 2.3).