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Updated: Jun 17, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Platelet activation and reactivity in the convalescent phase of ischaemic stroke
Maria Lukasik1, Marcin Rozalski, Boguslawa Luzak
1Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. mlukasik@ump.edu.pl
The study was aimed at the evaluation of blood platelet activation and reactivity in patients in the convalescent phase of stroke (n=58) and controls matched in respect to risk factors of vascular pathology (n=55). Both groups were treated daily with acetylsalicylic acid (ASA), 150 mg/day. Using flow cytometry, the expressions of P-selectin and the active GP IIb/IIIa receptor, as well as the fraction of platelet-derived microparticles (PMPs) and total platelet aggregates (Ag), were evaluated in non-stimulated platelets and in platelets stimulated in vitro by thrombin, thrombin receptor activating peptide (TRAP) or ADP. The expression of P-selectin in non-stimulated platelets was found to be significantly (p=0.04) lower in stroke patients. In parallel, these patients manifested a significantly (p=0.0008) higher proportion of PMPs and a lowered (p=0.003) proportion of Ag, as compared to the controls. In the stroke patients the increased expressions of P-selectin and active GP IIb/IIIa in TRAP- or ADP-activated cells were less pronounced (p<0.01), while the increments in PMP fraction remained higher (p<0.05). Our results may indicate that chronic platelet activation develops in patients in the convalescent phase of stroke and the process of PMP generation prevails over blood platelet degranulation and aggregation. This shift may be particularly unfavourable due to the procoagulative and proatherosclerotic properties of PMPs, accompanied by their decreased sensitivity to the action of antiplatelet drugs.
The study was aimed at the evaluation of blood platelet activation and reactivity in patients in the convalescent phase of stroke (n=58) and controls matched in respect to risk factors of vascular pathology (n=55). Both groups were treated daily with acetylsalicylic acid (ASA), 150 mg/day. Using flow cytometry, the expressions of P-selectin and the active GP IIb/IIIa receptor, as well as the fraction of platelet-derived microparticles (PMPs) and total platelet aggregates (Ag), were evaluated in non-stimulated platelets and in platelets stimulated in vitro by thrombin, thrombin receptor activating peptide (TRAP) or ADP. The expression of P-selectin in non-stimulated platelets was found to be significantly (p=0.04) lower in stroke patients. In parallel, these patients manifested a significantly (p=0.0008) higher proportion of PMPs and a lowered (p=0.003) proportion of Ag, as compared to the controls. In the stroke patients the increased expressions of P-selectin and active GP IIb/IIIa in TRAP- or ADP-activated cells were less pronounced (p<0.01), while the increments in PMP fraction remained higher (p<0.05). Our results may indicate that chronic platelet activation develops in patients in the convalescent phase of stroke and the process of PMP generation prevails over blood platelet degranulation and aggregation. This shift may be particularly unfavourable due to the procoagulative and proatherosclerotic properties of PMPs, accompanied by their decreased sensitivity to the action of antiplatelet drugs.
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