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Updated: Jun 8, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Activation of platelets and cellular coagulation in cerebral small-vessel disease
Tom Oberheiden1, Christian Blahak, Xuan Duc Nguyen
11st Department of Medicine, Germany.
Insights
Platelet and monocyte activation, indicated by elevated CD40L, CD62P, and aggregates, is present in cerebral small-vessel disease (cSVD). This activation may contribute to cSVD development, though not correlating with disease severity.
Area of Science:
- Cardiovascular Research
- Neurology
- Hematology
Background:
- Platelets and monocytes are crucial in large-vessel atherosclerosis.
- Platelet and coagulation activation markers are elevated in cardiovascular diseases and acute cerebral ischemia.
Purpose of the Study:
- To investigate the role of platelets and cellular coagulation activation in cerebral small-vessel disease (cSVD).
Main Methods:
- Assessed platelet and monocyte activation markers (CD40L, CD62P, tissue factor) and platelet-monocyte aggregates via flow cytometry in 24 cSVD patients.
- Measured plasma levels of soluble CD40L, IL-6, and IL-7 using ELISA.
- Compared findings to 10 healthy controls.
Main Results:
- cSVD patients exhibited significantly higher platelet CD40L and CD62P expression, increased platelet-monocyte aggregates, and enhanced monocyte tissue factor exposure compared to controls.
- Significantly lower plasma IL-7 levels were observed in cSVD patients.
- Platelet and monocyte activation did not correlate with cSVD severity (Fazekas scores).
Conclusions:
- Patients with cSVD demonstrate an upregulation of the platelet CD40L and CD62P system.
- Cellular coagulation activation is evident in cSVD patients.
- This activation may play a role in the initiation and progression of cSVD.
Abstract:
Platelets and monocytes play a pivotal role in the initiation and progression of large-vessel atherosclerosis. An up-regulation of various platelet and coagulation activation markers has been described in cardiovascular diseases and in patients with acute cerebral ischemia. In the present study the role of platelets and cellular coagulation activation in cerebral small-vessel disease (cSVD) was assessed. In 24 patients with cSVD but without established large-vessel disease, whole blood samples were obtained. Patients were divided into three subgroups (Fazekas 1, 2 and 3) according to extent of cSVD based on morphological magnetic resonance imaging criteria. Surface expression of CD40L and CD62P on platelets, tissue-factor exposition on monocytes and platelet-monocyte aggregates were measured with flow cytometry. Plasma levels of soluble CD40L, interleukin (IL)-6 and IL-7 were assessed by ELISA. Patients with cSVD show a significantly elevated expression of platelet CD40L (P < 0.001) and CD62P (P < 0.023), significantly elevated amounts of platelet-monocyte aggregates (P < 0.004), a significantly enhanced tissue-factor exposition on monocytes (P < 0.019) and significantly lower plasma levels of IL-7 compared to 10 healthy controls. However, this platelet and monocyte activation did not correlate with the severity of cSVD. Patients with cSVD show an up-regulation of the platelet CD40L and CD62P system and an activation of cellular coagulation which might contribute to the initiation and progression of cSVD.
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