Evaluation of Platelet Activation, Coagulation, and Fibrinolytic Activation in Patients With Symptomatic Lacunar Stroke

Ilhan, Demet; Özbabalık, Demet; Gülcan, Erim; Özdemir, Özhan; Gülbaçs, Zafer

doi:10.1097/nrl.0b013e318198d8bc

Cited by 19 publications

(11 citation statements)

References 33 publications

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“…A total of 7 studies were included [24,25,26,27,28,29,30] (336 lacunar strokes) but available data did not permit meta-analysis. Jood et al [26] report levels of PAI significantly higher in lacunar stroke versus non-stroke controls acutely and chronically.…”

Section: Plasma Markersmentioning

confidence: 99%

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Blood Markers of Coagulation, Fibrinolysis, Endothelial Dysfunction and Inflammation in Lacunar Stroke versus Non-Lacunar Stroke and Non-Stroke: Systematic Review and Meta-Analysis

et al. 2013

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Background: The cause of cerebral small vessel disease is not fully understood, yet it is important, accounting for about 25% of all strokes. It also increases the risk of having another stroke and contributes to about 40% of dementias. Various processes have been implicated, including microatheroma, endothelial dysfunction and inflammation. A previous review investigated endothelial dysfunction in lacunar stroke versus mostly non-stroke controls while another looked at markers of inflammation and endothelial damage in ischaemic stroke in general. We have focused on blood markers between clinically evident lacunar stroke and other subtypes of ischaemic stroke, thereby controlling for stroke in general. Summary: We systematically assessed the literature for studies comparing blood markers of coagulation, fibrinolysis, endothelial dysfunction and inflammation in lacunar stroke versus non-stroke controls or other ischaemic stroke subtypes. We assessed the quality of included papers and meta-analysed results. We split the analysis on time of blood draw in relation to the stroke. We identified 1,468 full papers of which 42 were eligible for inclusion, including 4,816 ischaemic strokes, of which 2,196 were lacunar and 2,500 non-stroke controls. Most studies subtyped stroke using TOAST. The definition of lacunar stroke varied between studies. Markers of coagulation/fibrinolysis (tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), fibrinogen, D-dimer) were higher in lacunar stroke versus non-stroke although fibrinogen was no different to non-stroke in the acute phase. tPA and PAI were no different between lacunar and non-lacunar stroke. Fibrinogen and D-dimer were significantly lower in lacunar stroke compared to other ischaemic strokes, both acutely and chronically. Markers of endothelial dysfunction (homocysteine, von Willebrand Factor (vWF), E-selectin, P-selectin, intercellular adhesion molecule-1 (ICAM), vascular cellular adhesion molecule-1 (VCAM)) were higher or had insufficient or conflicting data (P-selectin, VCAM) in lacunar stroke versus non-stroke. Compared to other ischaemic stroke subtypes, homocysteine did not differ in lacunar stroke while vWF was significantly lower in lacunar stroke acutely [atherothrombotic standardized mean difference, SMD, -0.34 (-0.61, -0.08); cardioembolic SMD -0.38 (-0.62, -0.14)], with insufficient data chronically. Markers of inflammation (C-reactive protein (CRP), tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6)) were higher in lacunar stroke versus non-stroke, although there were no studies measuring TNF-α chronically and the sole study measuring IL-6 chronically showed no difference between lacunar stroke and non-stroke. Compared to other ischaemic stroke subtypes, there was no difference (CRP) or insufficient or conflicting data (TNF-α) to lacunar stroke. IL-6 was significantly lower [atherothrombotic SMD -0.37 (-0.63, -0.10); cardioembolic SMD -0.52 (-0.82, -0.22)] in lacunar stroke acutely, with insufficient data chronically. Key Messages: ...

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Section: Plasma Markersmentioning

confidence: 99%

“…Here, 9 studies were included [25,30,32,34,37,38,39,40,41] (364 lacunar strokes) of which 4 could be meta-analysed (fig. 2).…”

Section: Plasma Markersmentioning

confidence: 99%

Blood Markers of Coagulation, Fibrinolysis, Endothelial Dysfunction and Inflammation in Lacunar Stroke versus Non-Lacunar Stroke and Non-Stroke: Systematic Review and Meta-Analysis

et al. 2013

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“…Slavka et al (16) concluded that patients with increased MPV values (≥11.01 fL) were at a higher risk of ischemic heart disease. Ilhan et al (17) found a significant difference in MPV levels between patients with symptomatic lacunar stroke infarcts and controls (p<0.01). Mayda-Domac et al (18) observed that MPV was an independent risk factor for ischemic stroke (p=0.007) and hemorrhagic stroke (p=0.001).…”

Section: Discussionmentioning

confidence: 95%

The Acute Effect of Erythropoietin on Mean Platelet Volume Levels during Hypoxia Reoxygenation Injury in Rats

Tsompos¹,

Panoulis²,

Toutouzas³

et al. 2016

Haseki

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Ad dressforCor res pon den ce/Ya z›fl maAd re si:Constantinos Tsompos Mesologi County Hospital, Clinic of Obstetrics and Gynecology, Mesologi, Greece E-mail: tsomposconstantinos@gmail.com Received/GeliflTarihi:14 August 2016 Ac cep ted/Ka bulTa ri hi: 16 November 2016 Aim: This biomedical study tested the effect of erythropoietin (Epo) in rat model, especially in a hypoxia-reoxygenation one. The trend of this factor was evaluated hematologically using serum mean platelets volume (MPV) values. Methods:Forty rats with a mean mass 247.7 g were used. MPV values were evaluated at 60 min (for groups A and C) and at 120 min (for groups B and D) of reoxygenation. Epo was provided only in groups C and D.Results:Epo administration non-significantly lowered the MPV levels by 0.12% +2.13% (p=0.9513). Reoxygenation time non-significantly augmented the MPV levels by 1.37%+2.11% (p=0.4873). However, Epo administration together with reoxygenation time non-significantly reduced the MPV levels by 0.27%+0.92% (p=0.7585). Conclusion:Epo administration had a non-significant short-time decline effect on MPV levels. Keywords: Hypoxia, erythropoietin, reoxygenation, mean platelets volumeGiriş:Bu deneysel çalışmada, eritropoietinin (Epo) etkisi fare modelinde, özellikle bir hipoksi-reoksijenasyon protokolü dahilinde incelendi. Bu molekülün etkisi, kan ortalama trombosit düzeyleri (MPV) kullanılarak hematolojik olarak incelendi.Yöntemler:Ortalama 247,7 gr ağırlığa sahip 40 adet fare çalışmada kullanıldı. MPV düzeyleri 60 dakikalık (A ve C grupları) ve 120 dakikalık (B ve D grupları) reoksijenasyonlarla ölçüldü. Sadece C ve D gruplarına Epo verildi. Bulgular: Epo uygulanması MPV düzeylerini kayda değer olmayan bir şekilde %0,12±%2,13 (p=0,9513) oranında yükseltirken reoksijenasyon süresi MPV düzeylerini kayda değer olmayan bir şekilde %1,37±%2,11 (p=0,4873) arttırdı. Ancak, Epo verilmesi ile reoksijenasyon süresi bir araya geldiğinde MPV değerlerini %0,27±%0,92 (p=0,7585) oranında düşürerek ortak bir etki yarattı.Sonuç: Epo uygulamasının MPV düzeyleri üzerinde kayda değer olmayan bir kısa vadeli azalma etkisi olduğu görüldü.

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“…In contrast, other authors claim that the mean platelet volume is unrelated to stroke severity and subtype [27]. From the literature it also appears that lacunar strokes are associated with increased platelet activity [25] and that circulating P-selectin increases in large-vessel infarctions [28].…”

Section: Introductionmentioning

confidence: 96%

“…In acute stroke, concentrations of the protein appear to increase [6]. Still, other scientists have been unable to demonstrate soluble P-selectin alterations in stroke [25]. Even fewer studies have been devoted to platelet alterations in different stroke subsets.…”

Section: Introductionmentioning

confidence: 99%

Platelets and acute cerebral infarction

et al. 2012

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Stroke is worldwide a leading cause of death and disability. Its etiology is regarded as heterogeneous. Platelets are implicated in its pathophysiology, but our understanding of their specific role is incomplete. Only sparse and conflicting information exists about platelet reactivity and activity in acute stroke. Some scientists take the view that platelets activate in conjunction with acute cerebral infarctions. Others put forward evidence corroborating the contrary notion. Increased soluble P-selectin as a sign of platelet and/or endothelial activity seems to be a feature of the disease. The latter point of view is opposed by other researchers. Due to these conflicting opinions, this study is devoted to platelet characteristics in acute cerebral infarctions. We studied subjects (n ¼ 72; age 74 AE 10(SD) years; 31 females) having acute stroke. As controls served atrial fibrillation (AF) patients (n ¼ 58; age 69 AE 7(SD) years; 12 females) subject to electrical cardioversion, a flow cytometer was put to use for measuring platelet reactivity and activity. After agonist provocation, both platelet bound P-selectin and fibrinogen were employed as estimates of platelet reactivity. Dilutions of a thrombin-receptor-activating peptide (TRAP-6) (74 and 57 mmol/l) (P-selectin and fibrinogen) and ADP (8.5 and 1.7 mmol/l) (fibrinogen only) were put to use as platelet agonists. Membrane-bound P-selectin without agonist stimulation served as a measure of in vivo platelet activation. Soluble P-selectin, as determined from a commercial ELISA, was used to assess platelet and/or endothelial activity. In acute stroke neither platelet-bound P-selectin nor fibrinogen after stimulation, i.e. reactivity, differed from AF controls. In contrast, lower platelet activity as judged from surface attached and circulating P-selectin without agonist stimulation proved to be a feature of cerebral infarctions. The p-values were p < 0.001 and p < 0.01, respectively. It is concluded that acute stroke is not associated with platelet reactivity platelets circulate less activated during the disease. It is evident that the mechanisms reflecting platelet reactivity and activity being investigated in this study play minor roles in stroke pathophysiology. New powerful platelet inhibitory drugs are currently introduced. To avoid major bleeding studies on platelet, behavior in acute stroke are necessary before including these medications in stroke treatment protocols.

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Evaluation of Platelet Activation, Coagulation, and Fibrinolytic Activation in Patients With Symptomatic Lacunar Stroke

Abstract: Different hemostatic factors may play a role in the pathogenesis of lacunar stroke. Evaluating the role of hemostatic factors on different types of strokes may help us identify new therapeutic strategies and different prognostic stratifications for ischemic stroke.

Cited by 19 publications

References 33 publications

Blood Markers of Coagulation, Fibrinolysis, Endothelial Dysfunction and Inflammation in Lacunar Stroke versus Non-Lacunar Stroke and Non-Stroke: Systematic Review and Meta-Analysis

Blood Markers of Coagulation, Fibrinolysis, Endothelial Dysfunction and Inflammation in Lacunar Stroke versus Non-Lacunar Stroke and Non-Stroke: Systematic Review and Meta-Analysis

The Acute Effect of Erythropoietin on Mean Platelet Volume Levels during Hypoxia Reoxygenation Injury in Rats

Platelets and acute cerebral infarction

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