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Troponin I degradation in serum of patients with acute ischemic stroke
Jesper K Jensen1, Jonas Hallén, Terje Lund
1Department of Cardiology, Odense University Hospital, Denmark. jesperkjensen@dadlnet.dk
Insights
Troponin I degradation occurs in patients with acute ischemic stroke, similar to acute myocardial infarction. Further research is needed to understand the clinical impact of these troponin fragments.
Area of Science:
- Biochemistry
- Cardiology
- Neurology
Background:
- Troponin is a key biomarker for acute coronary syndrome.
- Troponin degradation post-release is known in acute coronary syndrome.
- Troponin degradation in non-acute coronary syndrome states is not well understood.
Purpose of the Study:
- To investigate troponin degradation in patients with acute ischemic stroke.
- To compare troponin degradation patterns in ischemic stroke with those in myocardial infarction.
Main Methods:
- Daily measurement of cardiac troponin I (cTnI) in 244 acute ischemic stroke patients over 5 days.
- Western blot analysis of cTnI using anti-cTnI antibodies.
- Comparison with serum cTnI concentrations and degradation patterns from myocardial infarction patients.
Main Results:
- Elevated troponin levels detected in 10% of patients.
- Both intact cTnI and up to seven degradation fragments were identified.
- Degradation patterns were similar to those observed in myocardial infarction.
Conclusions:
- Cardiac troponin I degradation patterns in acute ischemic stroke resemble those in acute myocardial infarction.
- The biological and clinical significance of troponin degradation in ischemic stroke requires further investigation.
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.
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