2.3.7 Cardiac muscle isoenzymes
2.3.7 Cardiac muscle isoenzymes

The value of cardiac muscle isoenzymes in horses is contentious at present. There is little documented evidence which validates their use in horses; however, many anecdotal reports recommend their measurement as an aid to the diagof myocardial disease. The principle of isoenzyme measurements in horses is extrapolated from their use in detecting myocardial injury in humans. Myoinjury in humans is usually ischaemic in origin and results in much more extensive myocardial cell death than ever occurs in horses, except in a few uncommon conditions such as monensin toxicity. One of the reasons for the popularity of isoenzyme measurement in horses is that there is often no other form of evidence available to confirm or refute a diagnosis of myocarditis. However, there is no evidence that isoenzymes are likely to be of value except where acute myocardial injury has occurred, or in on-going disease The clinical signs of myocardial damage may only be evident some time after the initial cellular damage occurred, when isoenzyme levels have returned to normal. The extent of myocardial cell death due to myocarditis is seldom likely to be sufficient to result in high levels of cardiac isoenzymes.

Two isoenzymes have principally been used to evaluate myocardial damage in horses. Lactate dehydrogenase (LDH) has five isoenzymes, of which isoenzyme 1 and 2 have been reported by different authorities to originate from myocardial tissue. Creatinine kinase (CK) has two isoenzymes, the MM and MB fractions. It has been suggested that high levels of the MB fraction result from myocardial damage. However, there is a lack of specificity and sensitivity in these assays. Firstly, there is evidence that these isoenzymes can be produced from nontissue, therefore raised values are non-specific for myocardial damage. For example, in human athletes the CK MB fraction has been derived from skeletal muscle after hard exercise. Secondly, many animals in which myocarditis is diagnosed from clinical, echocardiographic or electrocardioevidence have normal isoenzyme levels, therefore the tests are relatively insensitive. In addition, because the levels seldom rise markedly, cardiac disease is often diagnosed when the isoenzyme level is only marginally outside a normal' range, making false positive diagnoses more likely.

With further research, it is possible that these assays will be clinically useful. This would be very helpful, in order that myocarditis could be detected by a routine screening test. However, there is insufficient evidence at present to ensure that the results are reliable and, although there may be individual cases in which elevated cardiac isoenzymes are helpful in pointing towards a diagnosis of myocardial disease, in the author's opinion they should be interpreted with caution.