Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. Determining the level of cardiac troponins (cTn), structural proteins unique to the heart, is a cornerstone of AMI diagnosis. One important limitation of standard cTn assays is a sensitivity deficit at presentation due to a delayed increase of circulating cTn levels. Recent multicentre studies have shown that novel, more sensitive and more precise cTn assays improve the early diagnosis of AMI. cTn must be interpreted as a quantitative variable. ├óÔé¼´åİDetectable™ levels will become the standard and must be clearly differentiated from ├óÔé¼´åİelevated™ levels. The differential diagnosis of a small amount of cardiomyocyte necrosis and, therefore, mild elevation of cTn, is broad and includes acute and chronic disorders. The differential diagnosis of more extensive cardiomyocyte necrosis, and therefore substantial elevation of cTn, is much smaller and largely restricted to AMI, myocarditis and Tako-Tsubo cardiomyopathy.
Acute myocardial infarction, cardiac troponins, diagnosis, cardiomyocyte necrosis, myocarditis, Tako-Tsubo cardiomyopathy
Disclosure: The authors have no conflicts of interest to declare.
Received: 15 October 2010 Accepted: 5 January 2011 Citation: European Cardiology, 2011;7(1):18├óÔé¼ÔÇ£20
Correspondence: Christian Mueller, Department of Internal Medicine, University Hospital Basel, Petersgraben 4, Basel CH-4031, Switzerland. E: firstname.lastname@example.org
Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. Accordingly, prompt identification of patients with AMI is critical, as established therapies exist that are of proven benefit.1,2 More than 15 million patients per year present to emergency departments with symptoms compatible with acute myocardial ischaemia in the US and Europe; only 20├óÔé¼ÔÇ£30%, however, are eventually proven to have acute ischaemic heart disease due to AMI in half of these patients.1 Crowding in emergency departments, in part due to delays in evaluating this large number of patients, is a major problem.
Electrocardiography and cardiac troponin (cTn) now form the diagnostic cornerstones of clinical assessment.1,2 Often, an electrocardiogram (ECG) alone is insufficient to diagnose AMI: first, because significant ECG changes are absent in many AMI patients and, second, because S-T segment deviation is observed in many other conditions.1├óÔé¼ÔÇ£3 cTns, structural proteins unique to the heart, are sensitive and specific biochemical markers of myocardial damage.1,2,4 Fully automated, rapidly available contemporary assays for cTn are superior to other available biomarkers for the diagnosis of AMI.5 In addition, elevated cTns identify patients with acute coronary syndrome at high risk because of adverse anatomy and pro-coagulant activity.6 These patients benefit from aggressive anticoagulation, an early invasive strategy and glycoprotein IIb/IIIa blockade.1,2,4 One limitation of contemporary cTn assays is that circulating levels may not become detectable for three to four hours.1,2,7 At times, diagnosis requires serial sampling for six to 12 hours. Delays in diagnosing disease (├óÔé¼´åİruling in™) hold back prompt treatment, while delays in excluding disease (├óÔé¼´åİruling out™) interfere with evaluation of alternative diagnoses ├óÔé¼ÔÇ£ both of which contribute to overcrowding in emergency departments and costs exceeding several billion US dollars per year.8
Most standard cTn assays are unable to measure cTn in healthy persons.9 Thus the true upper normal limit, the 99th percentile, is defined by the assay and not by biology. Recently, improvements in cTn assay technology have allowed manufacturers to provide automated assays that meet the quality specifications set out by the International Federation of Clinical Chemistry.2 These assays have a lower limit of detection below the 99th percentile of a normal reference population and a low level of imprecision (coefficient of variation <10%) at that value.10 This feature is critical, since cTn values above the 99th percentile of a normal reference population are, at present, a conditio sine qua non for the diagnosis of AMI.
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