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Abstract
Background. Although troponin is a cornerstone biomarker in the assessment and management of patients with acute coronary syndrome, much remains to be learned about the biology of this widely used biomarker, including its post-release modification. Degradation of troponin following release in patients with acute coronary syndrome has been described; however whether such post-release modification occurs in other non-acute coronary syndrome states remains unknown. The aim of this study was to define troponin degradation in patients with acute ischemic stroke. Materials and methods. Troponin I (cTnI) was measured daily during the first 5 days of admission in 244 patients with acute ischemic stroke. Western blot analysis was performed using anti-cTnI antibodies and compared with serum concentrations of cTnI in seven patients and one patient with myocardial infarction (positive control). Results. Elevated levels of troponin were detected in 25 (10 %) patients; in all, both intact cTnI and cTnI degradation products were detected, with up to seven degradation fragments found. Samples with the highest total cTnI levels gave the strongest and most numerous western-blotting bands. All fragments were comparable with the degradation pattern of the positive control in terms of position. Conclusions. Immunoblotting of blood samples from patients with acute ischemic stroke reveals similar degradation patterns of cTnI as has been described in patients with acute myocardial infarction. The biological ramification and potential clinical impact of this finding bears further scrutiny.
Acknowledgements and funding
Dr Jensen was supported by grants from the Danish Heart Foundation, Copenhagen, Denmark.
Dr Hallén was supported by grants from the South-Eastern Norway Regional Health Authority, Aker University Hospital Research Foundation and Center for Heart Failure Research, Oslo, Norway.
Dr Januzzi was supported by grants from Siemens, US and Roche, US.
Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the article.