Discordant diagnoses of acute myocardial infarction due to the different use of assays and cut-off points of cardiac troponins.

OBJECTIVES: Several assays for the measurement of cardiac troponin (cTn) are available, but differences in their analytical performances may affect the diagnosis of acute myocardial infarction (MI). METHODS: A survey was conducted at all Danish departments of clinical biochemistry at hospitals receiving patients with suspected acute MI to gather information about the assay and cut-off value used. cTn was measured in blood samples from 574 patients enrolled into the Odense Chest Pain Biobank with 3 different assays: the 4th generation cTnT (cTnT(4th)), high-sensitivity cTnT (cTnT(hs); Roche Diagnostics) and cTnI (Abbott Diagnostics). To evaluate concordance, patients were dichotomised according to the 99th percentile value for each assay. Additionally, a cut-off at 50 ng/l for cTnT(hs) was used, as this is the currently employed cut-off point in Denmark. RESULTS: Using a cTnT(4th) cut-off value of >0.03 µg/l, 130 patients (23%) had potential MI. With the cTnT(hs) assay and cut-off values at 50 versus 14 ng/l, respectively, 136 (24%) versus 301 (52%) patients had potential MI. With the cTnI cut-off point, 205 patients (36%) should be considered as having had an acute MI. CONCLUSIONS: The use of different cTn assays and cut-off values may result in a discordant frequency of MI diagnoses. This makes efforts to harmonize cTn assays and cut-off levels mandatory.

A critical appraisal of the phenomenon of aspirin resistance.

Aspirin is the mainstay antiplatelet treatment in patients with high risk of cardiovascular atherothrombotic events, and its beneficial effect is documented in several clinical trials. Nevertheless, the effectiveness of aspirin has been questioned by the emergence of the concept of 'aspirin resistance' (AR). This phenomenon, although lacking a precise definition, covers the fact that some patients do not exhibit the expected platelet inhibition by use of various techniques for measuring platelet function. In this critical review, we evaluate the methods used for measuring AR. We will discuss the available data regarding the prevalence and the clinical importance of the phenomenon. Finally, the potential mechanisms underlying AR are considered.