June 2015 Br J Cardiol 2015;22:79 doi:10.5837/bjc.2015.022
Faheem A Ahmad, Stephen Dobbin, Allister D Hargreaves
Introduction Current evidence suggests there has been a marked proliferation of troponin testing within medical units as the troponin assay has become the cornerstone biomarker in the diagnosis of an acute myocardial infarction (AMI).1,2 Both troponin T (TnT) and troponin I (TnI) are cardio-specific structural subunits and highly sensitive and specific markers of myocardial injury.3,4 Newer generation high-sensitivity troponin (hs-Tn) assays can detect increasingly lower troponin concentrations within an earlier time window of up to three hours.5 Early implementation of first-generation assays were accompanied with poor patient selection; ava
May 2009 Br J Cardiol 2009;16:147–150
Gavin J Bryce, Christopher J Payne, Simon C Gibson, David B Kingsmore, Dominique S Byrne
Introduction Vascular disease is a systemic disorder, with 50–60% of patients undergoing peripheral vascular procedures having co-existent severe coronary artery disease and only 10% having normal coronary arteries.1,2 It is unsurprising, therefore, that vascular surgery is associated with a substantial risk of major adverse cardiovascular events (MACE) and death.2,3 Cardiac troponin I (cTnI) is a contractile protein that is released into the circulation after myocardial cell injury. Unlike other cardiac-related enzymes, cTnI is not found in skeletal muscle and is therefore a highly sensitive and specific marker of myocardial necrosis,4,5 a
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