Key result
High-sensitivity troponin assays are recommended for early rule-out of acute myocardial infarction, though their slow rise and late peak limit their utility for very early diagnosis.
While high-sensitivity troponin assays are currently recommended for early rule-out of AMI, their limitations suggest a need for novel biomarkers with faster kinetics and higher specificity.
Chest pain is a common presenting symptom; however, the majority of emergency chest pain admissions are not due to acute myocardial infarction (AMI). AMI can be life threatening and early diagnosis or rule out of AMI might potentially improve morbidity and mortality, as well as reduce time to decision and therefore overall treatment costs. High-sensitivity troponin (hs-troponin) assays have been developed that enable precise quantification of extremely low troponin concentrations. Such hs-troponin assays are recommended in early rule-out protocols for AMI, when measured at presentation and again at 3-6 h. However, troponin is less than ideally suited for early diagnosis of acute myocardial injury because of its slow rise, late peak and low specificity for coronary plaque rupture. A new biomarker with a more rapid elevation to peak concentration than hs-troponin and lower background levels in patients with chronic cardiovascular conditions would be a preferred diagnostic test. This review discusses the development of hs-troponin assays and other biomarkers, evaluates their place in the early diagnosis of AMI, discusses troponin elevation without AMI and discusses current guideline recommendations.
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Maznyczka et al. (2015) conducted a review in acute myocardial infarction. High-sensitivity troponin assays and other biomarkers was evaluated. High-sensitivity troponin assays are recommended for early rule-out of acute myocardial infarction, though their slow rise and late peak limit their utility for very early diagnosis.
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