Course of Platelet Activation Markers After Ischemic Stroke

Marquardt, Lars; Ruf, Andreas; Mansmann, Ulrich; Winter, R.; Schüler, Matthias; Buggle, Florian; Mayer, H.; Grau, Armin J.

doi:10.1161/01.str.0000034398.34938.20

Cited by 152 publications

(135 citation statements)

References 38 publications

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“…One possibility could be that glutamate is increased in blood as a result of impaired clearance of the amino acid from the bloodstream, because our data showed impaired platelet uptake in patients until three months after stroke. These data are in agreement with recent findings by Marquardt et al (2002), showing increased markers of platelet activation up to 3 months after stroke. Since platelet life span is limited to 8 to 10 days, these authors conclude that ongoing platelet stimulation must be present in stroke patients, and propose that inflammatory mediators such as cytokines might be involved in this process.…”

Section: Discussionsupporting

confidence: 94%

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Aliprandi

Longoni

Stanzani

et al. 2005

J Cereb Blood Flow Metab

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Experimental studies have shown the role of excitotoxicity in the pathogenesis of ischemic brain lesions, and glutamate levels have been found to be elevated in CSF and plasma from patients, early after stroke. In this study, we investigated whether platelets could be involved in the mechanism of altered plasma glutamate levels after stroke. Forty four patients, from 6 hours to 9 months after ischemic stroke, 15 age-related healthy controls and 15 controls with stroke risk factors or previous transient ischemic attack were enrolled. Glutamate plasma levels, platelet glutamate release after aggregation and platelet glutamate uptake were assessed. Plasma glutamate levels were increased up to 15 days after the ischemic event in stroke patients, and the levels at day 3 were inversely correlated with the neurologic improvement between day 3 and 15. Ex vivo platelet glutamate release was decreased by 70% in stroke patients, suggesting previous in vivo platelet activation. Moreover, platelet glutamate uptake in these patients was decreased by 75% up to 15 days and was still reduced 90 days after stroke. Our data show a prolonged increase of glutamate in plasma after stroke, which might presumably be linked to altered platelet functions, such as excessive release of the amino acid or impaired uptake.

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Section: Discussionsupporting

confidence: 94%

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Aliprandi

Longoni

Stanzani

et al. 2005

J Cereb Blood Flow Metab

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“…Platelet activation and increased platelet-monocyte interaction have been described in patients with stroke (Htun et al, 2006;Marquardt et al, 2002), and they have been related to worse outcome (Zeller et al, 2005). Platelet-monocyte interaction occurs through P-selectin and P-selectin glycoprotein ligand-1 (Yang et al, 1999).…”

Section: Figurementioning

confidence: 99%

Monocyte Subtypes Predict Clinical Course and Prognosis in Human Stroke

Urra

Villamor

Amaro

et al. 2009

J Cereb Blood Flow Metab

179

164

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The number of circulating monocytes increases after stroke. In this study, we assessed the time course and phenotype of monocyte subsets and their relationship with the clinical course and outcome in 46 consecutive stroke patients and 13 age-matched controls. The proportion of the most abundant 'classical' CD14 high CD16À monocytes did not change after stroke, whereas that of CD14 high CD16 + monocytes increased and CD14 dim CD16 + monocytes decreased. CD14 high CD16 + monocytes had the highest expression of TLR2, HLA-DR and the angiogenic marker, Tie-2; CD14 dim CD16 + monocytes had the highest expression of costimulatory CD86 and adhesion molecule CD49d. Platelet-monocyte interactions were highest in CD14 high CD16À monocytes and lowest in CD14 dim CD16 + monocytes. In adjusted models, 1/CD14 high CD16À monocytes were associated with poor outcome (OR: 1.38), higher mortality (OR: 1.40) and early clinical worsening (OR: 1.29); 2/CD14 high CD16 + monocytes were inversely related to mortality (OR: 0.32); and 3/CD14 dim CD16 + monocytes were inversely related to poor outcome (OR: 0.74) and infarction size (r = À0.45; P = 0.02). These results illustrate that the predominant monocyte subtype conveys harmful effects after stroke, which include stronger interaction with platelets. Alternatively, rarer subpopulations of monocytes are beneficial with a phenotype that could promote tissue repair and angiogenesis. Therefore, monitoring of monocyte subtypes may emerge as a useful tool at the bedside for stroke patients.

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“…In addition, platelets with a more reactive state play an important role in stroke events. [1][2][3] In particular, patients with atherosclerotic plaque rupture show an enhanced platelet activation and have increased amounts of platelet-leukocyte aggregates. 3 In the last years, studies have investigated the role that genetic alterations which increase platelet reactivity play in the risk of thrombosis, while the role of genetic changes leading to platelet hyporeactivity in the development of hemorrhagic disorders has been rarely surveyed.…”

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confidence: 99%