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Acute Coronary Syndrom

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Imaging Coronary Anatomy and Reducing Myocardial Infarction Cardiac monocytes and macrophages after myocardial infarction Heart Regeneration by Endogenous Stem Cells and Cardiomyocyte Proliferation: Controversy, Fallacy, and Progress Application of High-Sensitivity Troponin in Suspected Myocardial Infarction Incidence, predictors, and outcomes of DAPT disruption due to non-compliance vs. bleeding after PCI: insights from the PARIS Registry Multivessel PCI Guided by FFR or Angiography for Myocardial Infarction Association Between Collateral Circulation and Myocardial Viability Evaluated by Cardiac Magnetic Resonance Imaging in Patients With Coronary Artery Chronic Total Occlusion Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest Ticagrelor versus Clopidogrel in Patients with STEMI Treated with Fibrinolytic Therapy: TREAT Trial Early Versus Standard Care Invasive Examination and Treatment of Patients with Non-ST-Segment Elevation Acute Coronary Syndrome: The VERDICT (Very EaRly vs Deferred Invasive evaluation using Computerized Tomography) - Randomized Controlled Trial

Clinical Trial2017 Oct 17;136(16):1495-1508.

JOURNAL:Circulation. Article Link

Direct comparison of cardiac myosin-binding protein C with cardiac troponins for the early diagnosis of acute myocardial infarction

Kaier TE, Twerenbold R, Marber M et al. Keywords: cMyC; cardiac myosin-binding protein C; myocardial infarction, APACE; troponin I; troponin T

ABSTRACT


BACKGROUNDCardiac 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.


METHODSUnselected 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.

RESULTSFinal 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.

CONCLUSIONScMyC 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 REGISTRATIONURL: https://www.clinicaltrials.gov. Unique identifier: NCT00470587.

© 2017 The Authors.