The impact of hyperglycemia and hyperlipidemia on plasma P-selectin and platelet markers after ischemic stroke

Platelet activation plays a key role in the pathogenesis of ischemic cerebrovascular diseases. Thus, it is very important to identify novel pharmacological targets for platelet inhibition to improve ischemic stroke treatment. The aim of the study was to assess the relationship between metabolic disorders and platelet activity markers in patients with acute ischemic stroke.

Ninety-four patients with acute ischemic stroke were divided into four groups with: normolipidemia and normoglycemia (NL/NG), n = 25; normolipidemia and hyperglycemia (NL/HG), n = 21; hyperlipidemia and normoglycemia (HL/NG), n = 27; hyperlipidemia and hyperglycemia (NL/NG), n = 21. Twenty-one healthy subjects served as controls. We assessed the CD62P expression on resting and thrombin-activated blood platelets using the flow cytometer and anti-CD61 and anti-CD62P monoclonal antibodies. CD61-positive microparticles were defined as platelet-derived microparticles. The level of sP-selectin in serum was measured by the ELISA method.

We observed a significant influence of hyperlipidemia and hyperglycemia on sP-selectin concentration. A strong correlation between higher sP-selectin concentration and enhanced LDL (p = 0.001), total cholesterol (p = 0.02), HbA_1c level (p < 0.001) was noticed. The level of sP-selectin and PDMPs (p < 0.001) were significantly higher in all groups of stroke patients compared with the controls. CD62P expression on resting and thrombin activated platelets were significantly lower in groups of patients with stroke.

Hyperlipidemia and hyperglycemia exert an equal stimulatory effect on tested platelet markers but with no synergistic action in stroke patients with both of the metabolic comorbidities. sP-selectin concentration in stroke patients best reflects the impact of hyperglycemia and hyperlipidemia on vascular lesions and platelet activation.