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The original WHO definition of myocardial infarction (MI) in 1971 was based on epidemiological rather than clinical principles and biomarkers of myocardial injury were not required for the diagnosis of MI according to this description.1 Because this definition lacked sensitivity and specificity, a multinational task force was convened, which ultimately led to the creation of the clinically oriented first and second universal definitions of MI in 2000 and 2007,2 ,3 respectively. Thereafter, biomarkers of myocardial injury assumed a central role in the diagnosis of MI.
Creatine phospokinase myocardial band fraction (CK-MB) had an important impact on the diagnosis of patients with coronary events in the past.4 While the development of mass assays improved both the clinical sensitivity and specificity for myocardial injury compared with the measurement of enzyme activity, an increased frequency of CK-MB elevations due to skeletal muscle injury, and a failure to detect all myonecrosis, made it clear that cardiac biomarkers with even better specificity and sensitivity were needed.4 Cardiac troponins (I or T) are structural proteins unique to the heart, and have become an integral part of the most recent universal definition of MI.3 Elevated troponin levels were found to provide superior prognostic value than CK-MB in patients presenting with MI.5 In addition, advances in assay technology have led to the development of high-sensitivity cardiac troponin assays, which enable the detection of cardiac troponin concentrations that are lower by a factor of 10 than those measureable using conventional assays.6
Peri-procedural myocardial infarction and the troponin versus CK-MB debate
Peri-procedural MI (PMI) may result from side-branch occlusion, abrupt vessel closure, coronary dissection or compromise of the microvascular circulation following distal embolisation or the no-reflow phenomenon …
Linked article 302211.
Funding COS is the recipient of a research grant from the European Association of Percutaneous Coronary Intervention of the European Society of Cardiology. This work was supported in part by a grant to SW from the Swiss National Science Foundation (33CM30-140336).
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.