Abstract
Chest pain is responsible for 6–10% of all presentations to acute healthcare providers. Triage is inherently difficult and heavily reliant on the quantification of cardiac Troponin (cTn), as a minority of patients with an ultimate diagnosis of acute myocardial infarction (AMI) present with clear diagnostic features such as ST-elevation on the electrocardiogram. Owing to slow release and disappearance of cTn, many patients require repeat blood testing or present with stable but elevated concentrations of the best available biomarker and are thus caught at the interplay of sensitivity and specificity.We identified cardiac myosin-binding protein C (cMyC) in coronary venous effluent and developed a high-sensitivity assay by producing an array of monoclonal antibodies and choosing an ideal pair based on affinity and epitope maps. Compared to high-sensitivity cardiac Troponin (hs-cTn), we demonstrated that cMyC appears earlier and rises faster following myocardial necrosis. In this review, we discuss discovery and structure of cMyC, as well as the migration from a comparably insensitive to a high-sensitivity assay facilitating first clinical studies. This assay was subsequently used to describe relative abundance of the protein, compare sensitivity to two high-sensitivity cTn assays and test diagnostic performance in over 1900 patients presenting with chest pain and suspected AMI. A standout feature was cMyC’s ability to more effectively triage patients. This distinction is likely related to the documented greater abundance and more rapid release profile, which could significantly improve the early triage of patients with suspected AMI.
Highlights
Despite it being a frequent occurrence in emergency departments (ED) around the world, chest pain triage remains a challenge for patients and physicians alike
Technological advances result in many more patients being tested ‘Troponin-positive’, without necessarily being ‘acute myocardial infarction (AMI)-positive’—while impressive with respect to assay development, cardiac Troponin (cTn) was inherently unsuited for early diagnosis of acute myocardial injury and this has not been mitigated by moving detection limits to ever-lower levels
Our group has identified cardiac myosin-binding protein C as a candidate marker [20], a cardiac sarcomeric protein which is at least twice as abundant in the heart as cTnI or cTnT [21]. We have shown it is released into the serum after myocardial infarction in the mouse [20] and in patients [22], findings which have been confirmed by others [23]
Summary
Despite it being a frequent occurrence in emergency departments (ED) around the world, chest pain triage remains a challenge for patients and physicians alike. Responsible for 6–10% of all presentations to acute healthcare providers [1,2,3,4], the presenting complaint of chest pain results in a high rate of admissions (1:3, according to data from the UK [5]), but a paradoxically low probability (10%) of a final diagnosis of acute myocardial infarction (AMI) [6]. The inability to make a rapid and accurate diagnosis causes financial and medical, psychological and social burden to the
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