Enhanced in vivo platelet activation in subtypes of ischemic stroke.

Abstract

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.

Effects of Anticoagulation Intensity on Hemostatic Markers in Patients With Non-Valvular Atrial Fibrillation

“…In contrast, Lip et al showed that there was a small but significant reduction in TG with conventional warfarin therapy (INR 1.5-2.5), although very low-dose warfarin or aspirin did not change the TG concentration. 4 Many studies have shown no significant changes in PF4 or TG with aspirin, [25][26][27] a consistent finding with the present results, but some studies have reported a significant reduction of TG with aspirin. 28,29 A possible explanation for the lack of significant decreases in PF4 and TG by antiplatelet treatment may be that different pathways activate the release of PF4 and TG and the inhibition of one pathway may not be enough to reduce the plasma concentrations of PF4 and TG.…”

Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation.

“…29 £-Thromboglobulin concentrations in both NVAF groups and platelet factor 4 concentration in the NVAF group with stroke were significantly increased, indicating platelet activation. Shah et al 30 studied groups of patients with thromboembolic and cardioembolic stroke and showed higher concentrations of /3-thromboglobulin in both groups but increased platelet factor 4 concentration only in thromboembolic stroke patients compared with matched controls.…”

Association of miR-34a, miR-130a, miR-150 and miR-155 polymorphisms with the risk of ischemic stroke

“…Blood vessel occlusion is primarily caused by thrombosis (53% of cases) or embolism (31% of cases) (5). Thrombus formation can be caused by excessive platelet generation (6), and the association between platelets and ischemic stroke has been widely studied (7)(8)(9). Platelets are involved in both normal hemostasis and thrombosis (10).…”