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Evaluation of Oxidative Stress in Biological Samples Using the Thiobarbituric Acid Reactive Substances Assay
Published on: May 12, 2020
Erythrocyte-rich thrombus aspirated from patients with ST-elevation myocardial infarction: association with oxidative
Kei Yunoki1, Takahiko Naruko, Kenichi Sugioka
1Department of Cardiology, Osaka City General Hospital, Osaka, Japan.
Erythrocyte-rich coronary thrombi in ST-elevation myocardial infarction (STEMI) patients are linked to increased oxidative stress and inflammation. This finding suggests a higher thrombus burden, leading to impaired myocardial reperfusion and adverse cardiac remodeling.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pathology
Background:
- Erythrocytes (red blood cells) are increasingly recognized as a component of atheromatous lesions and thrombi.
- Understanding the role of erythrocytes in ST-elevation myocardial infarction (STEMI) is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the association between the red blood cell (RBC) component of coronary thrombi and markers of oxidative stress and myocardial reperfusion in STEMI patients.
Main Methods:
- Immunohistochemical analysis of aspirated thrombi from 178 STEMI patients.
- Categorization of thrombi into tertiles based on glycophorin-A-positive area (RBC content).
- Measurement of plasma myeloperoxidase (MPO) levels as a marker of oxidative stress.
Main Results:
- Higher RBC content in thrombi correlated with significantly increased MPO-positive cells within the thrombus and higher plasma MPO levels.
- STEMI patients with high-RBC thrombi experienced more frequent distal embolization.
- Impaired myocardial reperfusion (incomplete ST-segment resolution, lower myocardial blush grades) and left ventricular remodeling were more common in the high-RBC group.
Conclusions:
- Erythrocyte-rich thrombi in STEMI are associated with greater inflammation and higher thrombus burden.
- Increased RBC content in coronary thrombi contributes to impaired myocardial reperfusion and adverse cardiac remodeling post-STEMI.
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