Abstract 15758: Direct Comparison of Cardiac Myosin Binding Protein C to Cardiac Troponins for the Early Diagnosis of Acute Myocardial Infarction
Introduction: Cardiac myosin binding protein C (cMyC) is a cardiac-restricted protein that is more abundant than cardiac Troponin (cTn) and is released rapidly following AMI. These characteristics provide the rationale to evaluate cMyC as an adjunct or even alternative to cTn in the early diagnosis of acute myocardial infarction (AMI).
Hypothesis: cMyC is a useful diagnostic tool to assess patients with possible AMI and the biomarker’s specificity and sensitivity are comparable or superior to the current gold standard: hs-cTn.
Methods: In 1954 unselected patients presenting to the emergency department with symptoms suggestive of AMI, concentrations of cMyC and (h)s-cTn were measured at presentation. The final diagnosis of AMI was adjudicated by 2 independent cardiologists using all available clinical information including serial measurements of hs-cTnT. Long-term mortality was the prognostic end point.
Results: The adjudicated final diagnosis was AMI in 340 patients (17%). Concentrations of cMyC at presentation were significantly higher in those with AMI as compared to other diagnoses (median 237ng/L vs. 13ng/L, p <0.001). The diagnostic accuracy of cMyC as quantified by the area under the receiver-operating characteristic curve (AUC; 0.924 (95% CI, 0.908-0.937) was comparable to that of hs-cTn (hs-cTnT 0.927 (95% CI, 0.913-0.942), hs-cTnI Architect 0.922 (95% CI, 0.908-0.937) and superior to s-cTnI 0.909 (95% CI, 0.889-0.929) Centaur cTnI Ultra. The combination of cMyC with hs-cTnT or s-cTnI (but not hs-cTnI) lead to a statistically significant albeit numerically small increase in AUC to 0.935 (p<0.0001) and 0.928 (p<0.0001), respectively. cMyC was superior to hs-cTnI and s-cTnI ultra (p=0.01 and p<0.001, respectively) and similar to hs-cTnT at predicting death at 2 years.
Conclusions: cMyC has high diagnostic and prognostic utility as either an alternative or adjunct to (h)s-cTn.
Author Disclosures: T.E. Kaier: Research Grant; Significant; British Heart Foundation Clinical Research Fellowship. R. Twerenbold: Honoraria; Modest; Speaker honoraria from Roche. Consultant/Advisory Board; Modest; Roche. T. Reichlin: Research Grant; Modest; Swiss National Science Foundation, the Swiss Heart Foundation, the University of Basel, the Professor Max Cloetta Foundation and the Department of Internal Medicine (University Hospital Basel). Honoraria; Modest; Brahms and Roche. J. Marjot: None. J. Boeddinghaus: None. T. Nestelberger: None. K. Wildi: None. M. Rubini Gimenez: Honoraria; Modest; Speaker honoraria from Abbott. M.S. Marber: Ownership Interest; Modest; Marber is named as an inventor on a patent held by King’s College London for the detection of cardiac myosin binding protein-C as a biomarker of myocardial injury. C. Mueller: Research Grant; Significant; Swiss National Science Foundation and the Swiss Heart Foundation, the Cardiovascular Research Foundation Basel, 8sense, Abbott, ALERE, Brahms, Critical Diagnostics, Nanosphere, Roche, Siemens, USB. Honoraria; Modest; Abbott, ALERE, Brahms, Novartis, Roche, and Siemens.
- © 2016 by American Heart Association, Inc.