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Endothelial markers and adhesion molecules in acute ischemic stroke--sequential change and differences in stroke
Kazuko Kozuka1, Tatsuo Kohriyama, Eiichi Nomura
1Third Department of Internal Medicine, Hiroshima University School of Medicine, 1-2-3, Kasumi, Minami-Ku, Hiroshima City 734-8551, Japan.
Atherosclerosis
|March 8, 2002
Summary
Endothelial and platelet activation markers are elevated in acute ischemic stroke patients. These markers, including von Willebrand factor and soluble P-selectin, persist into the subacute phase, indicating ongoing endothelial damage, particularly in atherothrombotic infarction.
Area of Science:
- Biomedical science
- Neurology
- Vascular biology
Background:
- Stroke involves endothelial cell and platelet activation.
- Biomarkers can indicate stroke pathophysiology.
Purpose of the Study:
- To measure endothelial markers and adhesion molecules in acute ischemic stroke patients.
- To differentiate between atherothrombotic and lacunar infarction based on these markers.
Main Methods:
- Measured plasma von Willebrand factor (vWf), soluble thrombomodulin (sTM), soluble P-selectin (sP-selectin), and soluble E-selectin (sE-selectin).
- Assessed markers during acute (within 48h) and subacute (after 1 month) phases.
- Compared 52 stroke patients with 86 age-matched controls.
Main Results:
- Stroke patients showed elevated vWf, sP-selectin, and sE-selectin in both phases.
- sTM was elevated only in the subacute phase.
- Atherothrombotic infarction had sustained vWf and sP-selectin elevation and increased sTM in the subacute phase.
- Lacunar infarction showed higher sTM and sE-selectin only in the acute phase.
Conclusions:
- Endothelial damage may persist into the subacute phase in atherothrombotic infarction.
- Endothelial injury is more pronounced in the acute phase of lacunar infarction.
- Evaluating these markers aids understanding stroke pathophysiology and potential treatments.