Cardiovascular diseases are leading cause of morbidity in the world. Measurement of the level of biochemical markers in the serum is one of World Health Organisation (WHO) criteria in diagnosing acute myocardial infarction (AMI). Non-specific clinical state of patients and insufficiently sensitive electrocardiographic (ECG) diagnostics, at patient's hospital admission time, point out the importance of biochemical markers in acute myocardial infarction diagnosis. Technology development and new diagnostic methods lead to the invention of highly sensitive and specific marker as myocardial damage evidence. Cardiac Troponin I (cTnI) is specific marker for myocardial damage1. Its elevation in the serum within myocardial ischemia symptomatology is important in diagnosis of myocardial infarction.

/pdf/cardiac-troponin-i-the-gold-standard-in-acute-myocardial-3o4v32drns.pdf

Cardiac troponin I: the gold standard in acute myocardial infarction diagnosis

This article describes the molecular biology of troponin in heart disease. Prospective uses for this biomarker are mentioned, with a particular emphasis on cardiac troponin fragments that could be associated with distinct clinical entities. The article explores the topic of specific cardiac troponin fragments resulting from modification or degradation, linked with different pathological processes, as indications of novel potential uses for this biomarker in heart disease. In addition, it addresses some implications that could have an impact on several circumstances that confront physicians within clinical practice. Heart Metab. 2009;43:5‐8.

The biological basis of troponin in heart disease: possible uses for troponin fragmentology

Elucidation of African elephant beta casein phosphorylation state and casein micelle structure

This review briefly synthesizes the molecular biology of troponin, which is currently the best biochemical marker for the detection of cardiac injury and, thus, acute myocardial infarction as well. Potential new uses for the marker based on these insights, with a specific interest in cardiac troponin fragments that potentially could be linked to distinct clinical conditions, are described. Some of the clinical problems clinicians are faced with including how to use the markers in renal failure and the difficulties associated with the heterogeneity of current troponin assays are also discussed. Finally, we present the possibility of specific cardiac troponin fragments resulting from modification or degradation, associated with distinct pathological processes, as new potential uses for this biomarker.

New potential uses for cardiac troponins

The present invention relates to methods and kits for the prediction of risk for heart failure using post-translation modified forms of cardiac troponin T as a biomarker.

Post-translation modified cardiac troponin T as a biomarker of a risk for heart failure

Introduction: Cardiac troponin I and T (cTnI and cTnT) are specific biochemical serum markers for acute myocardial infarction (AMI). However, cTnI diagnostic assays are plagued by difficulties, resulting in >20-fold differences in measured values. These discrepancies may result from the release of the numerous cTnI modification products that are present in ischaemic myocardium. The resolution of these discrepancies requires an investigation of the exact forms of the troponins present in the bloodstream of patients after myocardial injury. Material and methods: A Westernblot direct serum analysis protocol was developed that allowed us to detect intact cTnI and a spectrum of up to 11 modified products in the serum from patients with AMI. Results: We document both a cTnI degradation pattern and the existence of phosphorylated cTnI in serum. The number and extent of these modifications reflect patterns similar to the time profiles of the routine clinical serum markers of total creatine kinase, creatine kinase-MB, and cTnI (determined by ELISA). Data from in vitro experiments, which were undertaken to study the degradation of human recombinant cTnI and cTnT when spiked in serum, indicate that some modification products present in patient serum existed in the myocardium. Discussion: This pilot study defines, for the first time, what forms of cTnI and cTnT appear in the bloodstream of AMI patients, and it clarifies the lack of standardization between different cTnI diagnostic assays.

Molekylære forandringer af troponin I og T påvist i serum hos patienter med akut myokardieinfarkt

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Molekylære forandringer af troponin I og T påvist i serum hos patienter med akut myokardieinfarkt