From King’s College London BHF Centre, Rayne Institute, St Thomas’ Hospital, London, UK (T.K., J.M., N.I., M.M.); Department of Cardiology and Cardiovascular Research Institute Basel, University Hospital Basel, Switzerland (R.T., C.P., J.B., T.N., P.B., Z.S., M.R.G., K.W., P.H., K.G., S.L., S.S., D.F.W., J.C., N.K., J.L., W.K., S.O., T.R., C.M.); Department of General and Interventional Cardiology, University Heart Center Hamburg, Germany (R.T., M.R.G.); Emergency Department, Centre for Biomedical Network Research on Rare Diseases Instituto de Salud Carlos III, Hospital del Mar–IMIM, Barcelona, Spain (K.W.); Emergency Department, Hospital Clinic, Barcelona, Spain (O.M.); Global Research in Acute Conditions Network (O.M., F.J.M.S., B.M., C.M.); Emergency Department, Hospital Clinico San Carlos, Madrid, Spain (F.J.M.S.); 2nd Cardiology Department, Zabrze, University Silesia, Katowice, Poland (B.M.); Laboratory Medicine, University Hospital Basel, Switzerland (K.R.); and Institute of Physiological Chemistry, Martin Luther University Halle-Wittenberg, Germany (E.W.).
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Background:Cardiac myosin-binding protein C (cMyC) is a cardiac-restricted protein that is more abundant than cardiac troponins (cTn) and is released more rapidly after acute myocardial infarction (AMI). We evaluated cMyC as an adjunct or alternative to cTn in the early diagnosis of AMI.Methods:Unselected patients (N=1954) presenting to the emergency department with symptoms suggestive of AMI, concentrations of cMyC, and high-sensitivity (hs) and standard-sensitivity cTn were measured at presentation. The final diagnosis of AMI was independently adjudicated using all available clinical and biochemical information without knowledge of cMyC. The prognostic end point was long-term mortality.Results:Final diagnosis was AMI in 340 patients (17%). Concentrations of cMyC at presentation were significantly higher in those with versus without AMI (median, 237 ng/L versus 13 ng/L, P<0.001). Discriminatory power for AMI, as quantified by the area under the receiver-operating characteristic curve (AUC), was comparable for cMyC (AUC, 0.924), hs-cTnT (AUC, 0.927), and hs-cTnI (AUC, 0.922) and superior to cTnI measured by a contemporary sensitivity assay (AUC, 0.909). The combination of cMyC with hs-cTnT or standard-sensitivity cTnI (but not hs-cTnI) led to an increase in AUC to 0.931 (P<0.0001) and 0.926 (P=0.003), respectively. Use of cMyC more accurately classified patients with a single blood test into rule-out or rule-in categories: Net Reclassification Improvement +0.149 versus hs-cTnT, +0.235 versus hs-cTnI (P<0.001). In early presenters (chest pain <3 h), the improvement in rule-in/rule-out classification with cMyC was larger compared with hs-cTnT (Net Reclassification Improvement +0.256) and hs-cTnI (Net Reclassification Improvement +0.308; both P<0.001). Comparing the C statistics, cMyC was superior to hs-cTnI and standard sensitivity cTnI (P<0.05 for both) and similar to hs-cTnT at predicting death at 3 years.Conclusions:cMyC at presentation provides discriminatory power comparable to hs-cTnT and hs-cTnI in the diagnosis of AMI and may perform favorably in patients presenting early after symptom onset.Clinical Trial Registration:URL: https://www.clinicaltrials.gov. Unique identifier: NCT00470587.