The validation of cMyBP-C as a new diagnostic marker of myocardial infarction

Lead Research Organisation: King's College London
Department Name: Cardiovascular

Abstract

Only a small proportion of patients with chest pain have acute myocardial infarction (MI). Although the ECG provides a very useful immediate test often patients have to be admitted in order to be sure they are not having an MI. The diagnosis of MI is made by the release of cardiac proteins known as troponins. These proteins are released slowly into the blood and also disapear slowly from the blood. The consequence is that patients need to be kept in hospital for at least 12 hours to make sure troponins do not appear in their blood. Furthermore once they do appear, and a diagnosis of MI is made, it can be difficult to know if patients are having further MIs because the troponins stay elevated after the first MI. The purpose of this application is to determine if another cardiac protein, known as cardiac myosin binding protein C, is released more quickly and/or cleared more quickly than troponin.

Technical Summary

Acute myocardial infarction (AMI) is the most common cause for death and effective treatments are available providing diagnosis is rapid. The current diagnostic gold standard is the appearance in the serum of cardiac troponin I or T. However, their slow release delays diagnosis, their persistence limits their utility in the identification of reinfarction and they have low specificity when used at their population-defined lower limit of normality. Our aim is to qualify and validate a potential new biomarker of AMI known as cardiac myosin binding protein C (cMyBP-C) that we have identified through our research and is the intellectual property of KCL. The validation will comprise 2 steps. The first is to use our current test on blood samples taken at frequent intervals from 20 patients with suspected AMI to compare the temporal profile of the troponins with our new marker. The second is to further develop and test methods to detect post-translational modifications of cMyBP-C which may better define the cardiac pathology responsible for release.

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