I read with interest the article by David Fitchett and colleagues in CMAJ's series on the management of acute coronary syndromes.1 From a laboratory point of view, the reader should bear in mind several points, especially as troponins are now the arbiter par excellence of coronary syndrome diagnosis.2 The first is that a low-sensitivity test (CK MB [creatine kinase – MB isoenzyme activity or mass] level) should not be used to clarify the results of a high-sensitivity test (troponin).3,4 Laboratories are often asked for a CK MB level when a patient has an elevated troponin level in an unclear clinical situation; the results of the test for the CK MB level may be falsely negative. Secondly, the troponin I value considered “normal” is assay dependent and can differ among manufacturers. The clinician should be aware of the reference limits and the coefficient of variation at the lower limits of the troponin assay used at his or her institution. Both troponin and CK MB levels are proportional to myocardial damage, but the relationship between troponin and CK MB levels is more complex; one has to gain experience with each to know what to expect with, for example, a massive myocardial infarction. Lastly, risk stratification may become more complex and, one would hope, more exact with the use of additional markers such as C-reactive protein and homocysteine.