Platelet activation [Neurosurgery Wiki]

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====== Platelet activation ======


[[Platelet]] activation is a key process in both protective [[hemostasis]] and pathological thrombosis through the activation of multiple pathways by the binding of several agonists (e.g., thromboxane A2 (TxA2), adenosine diphosphate (ADP), and thrombin) to their receptors.
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Platelet activation has been postulated to be involved in the pathogenesis of [[delayed cerebral ischemia]] (DCI) and [[cerebral vasospasm]] (CVS) after [[aneurysmal subarachnoid hemorrhage]] (aSAH).
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A study explains the activation of mechanoreceptor [[Piezo1]] under [[hypertension]] is the key to abnormal [[platelet activation]] and thrombosis while providing novel platelet intervention strategies to prevent [[thrombosis]]
((Zhao W, Wei Z, Xin G, Li Y, Yuan J, Ming Y, Ji C, Sun Q, Li S, Chen X, Fu W, Zhu Y, Niu H, Huang W. Piezo1 initiates platelet hyperreactivity and accelerates thrombosis in hypertension. J Thromb Haemost. 2021 Aug 19. doi: 10.1111/jth.15504. Epub ahead of print. PMID: 34411418.)).
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[[Prothrombotic state]]s of early brain injury (EBI) and [[delayed cerebral ischemia]] (DCI) after aSAH determine morbidity and mortality. To understand how [[platelet activation]] might contribute to such prothrombotic states, Ray et al. studied trends in [[coated platelets]] during EBI and DCI periods. Serial blood samples from a prospective cohort of aSAH patients were collected and assayed for coated-platelet levels. Patient's coated-platelet level during post-hospital discharge follow-up served as an estimate of baseline. Occurrence of DCI, Montreal cognitive assessment (MOCA) score of < 26, and modified Rankin scale (mRS) of 3-6 were considered poor clinical outcomes. Non-linear regression analysis detected a transition between periods of rising and declining coated-platelet levels at day 4. Additional regression analyses of coated-platelet trends before day 4 showed differences among patients with modified Fisher 3-4 [4.2% per day (95% CI 2.4, 6.1) vs. - 0.8% per day (95% CI - 3.4, 1.8); p = 0.0023] and those developing DCI [4.6% per day (95% CI 2.8, 6.5) vs. - 1.9% per day (95% CI - 4.5, 0.5); p < 0.001]. Differences between peak coated-platelet levels and baseline levels were larger, on average for those with DCI [18.1 ± 9.6 vs. 10.6 ± 8.0; p = 0.03], MOCA < 26 [17.0 ± 7.8 vs. 10.7 ± 7.4; p = 0.05] and mRS 3-6 [24.8 ± 10.5 vs. 11.9 ± 7.6; p = 0.01]. Coated-platelet trends after aSAH predict DCI and short-term clinical outcomes. The degree of rise in coated-platelets is also associated with adverse clinical outcomes
((Ray B, Pandav VM, Mathews EA, Thompson DM, Ford L, Yearout LK, Bohnstedt BN,
Chaudhary S, Dale GL, Prodan CI. Coated-Platelet Trends Predict Short-Term
Clinical OutcomeAfter Subarachnoid Hemorrhage. Transl Stroke Res. 2017 Dec 9.
doi: 10.1007/s12975-017-0594-7. [Epub ahead of print] PubMed PMID: 29224114.
)).