In the past, an acute myocardial infarction (AMI) was primarily diagnosed by evaluating symptoms during the patient presentation. ECG measurement and enzyme assays were the only tools available. The enzymes creatine kinase (CK), lactate dehydrogenase (LD), and aspartate aminotransferase (AST) were assayed several times a day and often for several days to observe peak concentrations and they would then return to normal. By observing these rise and fall kinetics, an AMI could be diagnosed (even if somewhat retroactively). Some increased specificity was achieved with the development of isoenzyme assays for LD and CK. However, even these more specific tests were less than ideal. This is because the three enzymes named above (and even, to a lesser extent, their more specific isoenzymes), are still found in other tissues. This makes them non-specific markers compared to newer troponin-based assays.
In the 1980s, the most specific cardiac isoenzyme was CK-MB, an isoform of creatine kinase. Although CK-MB is not completely cardiac-specific, it is more specific than the other enzymes available at the time. Because of this, CK-MB quickly became the benchmark test for acute cardiac workups.
Today, the diagnosis and monitoring for heart disease has evolved further still and is based almost entirely on troponin measurement for myocardial injury (although CK-MB testing is still performed for acute cardiac workups in many hospitals) and BNP or NTpro-BNP for cardiac overload or congestive heart failure (CHF). Lipoproteins and cholesterol are still used for screening and risk assessment.
