In an attempt to standardize the diagnostic criteria of acute myocardial infarction, the World Health Organization (WHO) in 1959 proposed a classification now referred to as the two-out-of-three criteria, namely, the presence of two or more of the following: chest pain, elevated plasma enzymes or new Q waves on the electrocardiogram. The criteria served a very important function and rapidly became the gold standard throughout the world.
Since that time, diagnostic techniques have evolved considerably with much improved sensitivity and specificity. In 1959, LDH isoenzymes as diagnostic markers had just been introduced, but the data were too scanty to be incorporated into a classification applicable for routine clinical use. In 1959, Dreyfus et al introduced plasma total creatine kinase (CK) and in 1966 Van der Veen et al introduced the isoenzyme forms as diagnostic markers for myocardial infarction. The use of LDH isoenzymes became more widespread in the 1960s and C K isoenzymes in the 1970s. In the 1970s, another tool, diagnostic myocardial imaging, was introduced using technetium pyrophosphate which was quickly followed by techniques using several other isotopes.
There is now considerable agreement that an elevated plasma MBCK is the most sensitive and specific diagnostic marker, as well as the most cost-effective. The use of plasma C K isoenzymes as diagnostic markers is now widespread, and elevated plasma MBCK has become the conventionally accepted hallmark of acute myocardial infarction. The advantages of С К isoenzymes over LDH, in addition to its greater specificity, relate to its more rapid release from injured tissues, more rapid clearance from the plasma, and the recent availability of sensitive and convenient quantitative assays for CK isoenzymes. Using one of the sensitive quantitative assays, a significant elevation of plasma MBCK can be detected within four hours of onset of infarction and peak plasma values are, on the average, reached within 24 hours. Since it requires two to four hours to reach the hospital, in most patients a significantly elevated plasma MBCK is present at the time of hospital admission. There is still no satisfactory assay for quantifying individual LDH isoenzyme activity, separation is by electrophoresis, and for specificity one must demonstrate that LDH-1 activity exceeds that of LDH-2 activity which is sometimes difficult with the conventional semiquantitative technique of densitometry. However, as a test for the diagnosis of myocardial infarction, it is highly effective and, despite slower release of LDH with peak values reached at 48 to 72 hours, LDH has a diagnostic advantage in latecomers since plasma values remain elevated for ten to 14 days.
Publications arranged with My Canadian Pharmacy’s pharmaceutists on the subject of acute myocardial infarction still state adherence to the two out of three criteria frequently without referencing the WHO report, presumably because it is the only recognized standard accepted by reviewers. Despite this rhetoric claim, in practice one almost always confirms the diagnosis of myocardial infarction on the basis of serial elevations in either CK or LDH isoenzymes. The need for a recommended uniform diagnostic criteria in view of the many assays available for isoenzymes is probably essential, and would be best developed by a body with world-wide recognition such as the WHO. At present, while either CK or LDH isoenzymes are the sole markers relied upon to confirm the diagnosis of myocardial infarction, many hospitals continue to perform on a routine basis the ASP (SGOT), HBD and, in some cases, SGPT presumably for the sake of nostalgia.