Abstract
INTRODUCTION: Beyond hemostasis and thrombosis, platelets are increasingly recognized as multifunctional cells involved in inflammation, vascular remodeling, and neurological diseases. Chronic cerebrovascular diseases impair cerebral blood flow and oxygen supply, leading to cognitive and motor dysfunction, where platelets may act as peripheral sensors reflecting neurovascular stress. This study investigated platelet activation profiles and platelet-leukocyte interactions in acute intracerebral hemorrhage (aICH), subacute intracerebral hemorrhage (sICH), and chronic cerebrovascular diseases (CCD). METHODS: Flow cytometry was used to assess platelet functions, including PAC-1 (activated GPIIb/IIIa) and P-selectin (CD62P), and platelet-leukocyte aggregates, including myeloid-platelet, lymphocyte-platelet, and monocyte-platelet in 20 CCD, 20 aICH, 30 sICH patients, and 48 healthy controls. RESULTS: PAC-1 expression was significantly reduced in aICH and sICH but elevated in CCD, indicating impaired integrin activation in acute and subacute stages and compensatory hyperreactivity in chronic disease. P-selectin expression was markedly decreased in CCD under both ADP and TRAP stimulation, suggesting persistent α-granule dysfunction in chronic conditions. Lymphocyte-platelet aggregates, especially T-cell interactions, were consistently diminished across all patient groups, reflecting disturbed platelet-immune communication with T lymphocytes. CONCLUSION: Patients with cerebrovascular disorders show distinct platelet activation patterns and impaired immune crosstalk. Reduced P-selectin expression and decreased lymphocyte-platelet aggregation, especially T-cell, indicate sustained platelet dysfunction and disrupted neuroinflammatory regulation. Flow cytometric assessment of these parameters provides valuable insight into neurovascular diseases at different stages and potential biomarkers for disease monitoring.