ADP-Induced Platelet Release Reaction in Acute Stroke

Mulley, Graham; Heptinstall, Stan; Taylor, Patricia M.; Mitchell, J R A

doi:10.1055/s-0038-1665245

Cited by 30 publications

(22 citation statements)

References 1 publication

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“…Bazı çalışmalarda İSK'nın nedeni olarak altta yatan trombosit fonksiyon bozukluğu suçlanmıştır (10)(11)(12). İSK'lı hastalarda trombosit fonksiyonlarını değerlendiren az sayıda çalışma olup bu çalışmaların sonuçları arasında çelişkiler bulunmaktadır (1,6,8).…”

Section: Discussionunclassified

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The Increase of The Mean Platelet Volume in Patients With Intracerebral Haemorrhage

Arıkanoğlu¹,

Çevik²,

Uzar³

et al. 2012

tnd

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ÖzetAmaç: Ortalama trombosit hacmi (OTH) trombosit fonksiyon ve aktivasyonunun bir göstergesidir. Trombosit fonksiyon bozukluğunun intraserebral kanama (İSK) etiyolojisi ve mortalite üzerindeki etkisi tam olarak anlaşılamamıştır. Bu çalışmanın amacı İSK'lı hastalarda OTH'deki değişimi ve mortalite üzer-ine etkisini retrospektif olarak araştırmaktır. Ge reç ve Yön tem: Çalışmaya intraserebral kanamalı 66 hasta (erkek/kadın: 32/34, ortalama yaş: 61,9± 16,9) alındı. İSK'lı hastalar ilk 10 günde ölenler ve yaşayanlar olarak 2 gruba ayrıldı. Gruplar arasında OTH ve hematom hacmi karşılaştırıldı. Ayrıca İSK'lı hastalar yaş ve cinsiyet yönünden benzer sağlıklı gönül-lülerin (erkek/kadın: 27/17, ortalama yaş: 59,9 ±3,2) OTH değeri ve trombosit sayısı ile karşılaştırıldı. Bulgular: İSK'lı hastaların ilk 24 saat içindeki OTH değerleri (8,33±1,27 fl) kontrol grubunun OTH değerlerine (7.76±1.14 fl) göre istatistiksel olarak yüksekti (p=0,018). İSK'lı hastaların ilk 24 saat içindeki trombosit değerleri (235,8±94,9 x10 3 /mL) kontrol grubunun trombosit değerlerine (279,1±94,9 x10 3 /mL) göre istatistiksel olarak düşüktü (p=0,022). İSK'lı hastalarda ilk 10 günde ölenler ile yaşayanlar arasındaki OTH ve trombosit değerleri arasında istatistiksel olarak anlamlı bir fark saptanmadı (p>0,05). İSK'lı hastalarda ilk 10 günde ölenlerin hematom volümü (31,1±33,7 ml) ile yaşayanların hematom volümü (8,7±13,4 ml) arasında istatistiksel olarak anlamlı fark bulundu (p<0,001). İSK hastaların hematom volümü ile OTH değeri arasında korelasyon bulunmadı. Sonuç: Ortalama trombosit hacmi İSK'lı hastalarda artmış olup bu durum trombosit fonksiyonlarındaki bozukluğa işaret edebilir. Bunun yanı sıra OTH artışı ile mortalite arasında bir ilişki bulmadık. (Türk Nöroloji Dergisi 2012; 18:54-6) Anah tar Ke li me ler: İntraserebral kanama, ortalama trombosit hacmi, mortalite Sum maryObjective: The mean platelet volume (MPV) is a biomarker of platelet function and activity. The influence of platelet function disorders on the aetiology of intracerebral haemorrhages (ICH) and mortality is not clear yet. The purpose of this study is to investigate the change in the MPV values in patients with ICH and to observe its influence on mortality in a retrospective manner. Ma te ri al and Met hod: Sixty-six patients with intracerebral haemorrhage (32 males, 34 females; mean age: 61.9±16.9) were enrolled in the study. Patients with ICH were divided into two groups as those who died within the first 10 days and those who survived. The MPV values and the haematoma volumes were compared between the groups. Also, the MPV values and platelet counts of the patients with ICH were compared with the values of healthy volunteers from similar age and sex groups (27 males, 17 females; mean age: 59.9±3.2). Re sults: The MPV values of the patients with ICH measured within 24 hours following the intracerebral haemorrhage (8.33±1.27 fl) were statistically significantly higher than the MPV values of the control group (7.76±1.14 fl) (p=0.018). The platelet counts of the patients with...

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Section: Discussionunclassified

“…Mulley ve ark. tromboembolik inmeli hastalarda trombosit reaktivitesinde artış bulurken İSK'lı hastalarda ise trombosit reaktivitesinde azalmayı belirtmişlerdir (11). Mayda ve ark.…”

Section: Discussionunclassified

The Increase of The Mean Platelet Volume in Patients With Intracerebral Haemorrhage

Arıkanoğlu¹,

Çevik²,

Uzar³

et al. 2012

tnd

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“…Others have recently reported that the ADP-induced platelet release reaction is reduced in persons with primary intracerebral hemorrhage -a disease strongly related to hypertension and involving the same vascular territory as lacunar infarction. 13 Nearly normal /3-TG values have also been noted in patients with hemorrhagic cerebrovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Enhanced in vivo platelet activation in subtypes of ischemic stroke.

Shah

Beamer

Coull

1985

Stroke

116

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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.

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“…Several studies, including important early work by Mulley, Heptinstall and colleagues on ADP-induced platelet reactivity, have shown that platelets are excessively activated or hyper-reactive in the early [9][10][11][12][13][14], subacute [12] or late phases [10,11,13,14] after TIA or ischaemic stroke.…”

Section: Introductionmentioning

confidence: 99%

Platelet function testing in transient ischaemic attack and ischaemic stroke: A comprehensive systematic review of the literature

et al. 2015

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The majority of patients with ischaemic cerebrovascular disease (CVD) are not protected from further vascular events with antiplatelet therapy. Measurement of inhibition of platelet function ex vivo on antiplatelet therapy, using laboratory tests that correlate with the clinical effectiveness of these agents, would potentially enable physicians to tailor antiplatelet therapy to suit individuals. A systematic review of the literature was performed to collate all available data on ex vivo platelet function/reactivity in CVD patients, especially those treated with aspirin, dipyridamole or clopidogrel. Particular emphasis was paid to information from commonly available whole blood platelet function analysers (PFA-100 Õ , VerifyNow Õ and Multiplate Õ ). Data on pharmacogenetic mechanisms potentially influencing high on-treatment platelet reactivity (HTPR) on antiplatelet therapy in CVD were reviewed. Two-hundred forty-nine potentially relevant articles were identified; 93 manuscripts met criteria for inclusion. The prevalence of ex vivo HTPR in CVD varies between 3-62% with aspirin monotherapy, 8-61% with clopidogrel monotherapy and 56-59% when dipyridamole is added to aspirin in the early, subacute or late phases after TIA/stroke onset. The prevalence of HTPR on aspirin was higher on the PFA-100 than on the VerifyNow in one study (p50.001). Furthermore, the prevalence of HTPR on aspirin was lower when one used 'novel longitudinal' rather than 'cross-sectional, case-control' definitions of HTPR on the PFA early after TIA or stroke (p ¼ 0.003; 1 study). Studies assessing the influence of genetic polymorphisms on HTPR in CVD patients are limited, and need validation in large multicentre studies. Available data illustrate that an important proportion of CVD patients have ex vivo HTPR on their prescribed antiplatelet regimen, and that the prevalence varies depending on the definition and assay used. Large, adequately-sized, prospective multicentre collaborative studies are urgently needed to determine whether comprehensive assessment of HTPR at high and low shear stress with a range of user-friendly whole blood platelet function testing platforms, in conjunction with pharmacogenetic data, improves our ability to predict the risk of recurrent vascular events in CVD patients, and thus enhance secondary prevention following TIA or ischaemic stroke.

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ADP-Induced Platelet Release Reaction in Acute Stroke

Cited by 30 publications

References 1 publication

The Increase of The Mean Platelet Volume in Patients With Intracerebral Haemorrhage

The Increase of The Mean Platelet Volume in Patients With Intracerebral Haemorrhage

Enhanced in vivo platelet activation in subtypes of ischemic stroke.

Platelet function testing in transient ischaemic attack and ischaemic stroke: A comprehensive systematic review of the literature

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