Differences in platelet–leukocyte aggregates among subtypes of acute cerebral ischemia

Turgut, Burhan; Turgut, Nilda; Çelik, Yahya; Tekgündüz, Emre; Pamuk, Gülsüm Emel; Demir, Muzaffer

doi:10.1016/j.jns.2011.02.026

Cited by 19 publications

(15 citation statements)

References 31 publications

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“…An increase in intermediate CD14 ++ CD16 + monocytes and their binding to platelets 7 days post percutaneous coronary intervention after myocardial infarction is further associated with an increased risk for ischemic stroke besides other adverse cardiovascular events (86). Of note, one study reported that changes in PLA levels occur mainly in large and small vessel disease, but not in cardioembolic disease (87). …”

Section: Platelet-leukocyte Interactions In Pathologic Conditionsmentioning

confidence: 99%

Measuring and interpreting platelet-leukocyte aggregates

et al. 2018

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Platelets, besides their specialised role in haemostasis and atherothrombosis, actively modulate innate and adaptive immune responses with crucial roles in immune surveillance, inflammation and host defence during infection. An important prerequisite for platelet-mediated changes of immune functions involves direct engagement with different types of leukocytes. Indeed, increased platelet-leukocyte aggregates (PLAs) within the circulation and/or locally at the site of inflammation represent markers of many thrombo-inflammatory diseases, such as cardiovascular diseases, acute lung injury, renal and cerebral inflammation. Therefore, measurement of PLAs could provide an attractive and easily accessible prognostic and/or diagnostic tool for many diseases. To measure PLAs in different (patho-)physiological settings in human and animal models flow cytometric and microscopic approaches have been applied. These techniques represent complementary tools to study different aspects relating to the involvement of leukocyte subtypes and molecules, as well as location of PLAs within tissues, dynamics of their interactions and/or dynamic changes in leukocyte and platelet behaviour. This review summarises various approaches to measure and interpret PLAs and discusses potential experimental factors influencing platelet binding to leukocytes. Furthermore, we summarise insights gained from studies regarding the underlying mechanism of platelet-leukocyte interactions and discuss implications of these interactions in health and disease.

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Section: Platelet-leukocyte Interactions In Pathologic Conditionsmentioning

confidence: 99%

Measuring and interpreting platelet-leukocyte aggregates

et al. 2018

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“…A total of 7 studies were included [27,28,30,31,46,48,49] (227 lacunar strokes) but available data did not permit meta-analysis. P-selectin was significantly higher in lacunar versus non-stroke acutely in 2 studies [46,49] but 1 study [30] found no difference. Another study [48] found P-selectin significantly lower in lacunar versus atherothrombotic stroke acutely but all other studies found no difference or did not report significance levels.…”

Section: Plasma Markersmentioning

confidence: 99%

“…We included 8 studies [29,34,35,39,47,49,52,53] (490 lacunar strokes) but available data did not permit meta-analysis; 2 studies [39,52] provided just over 50% of the data. CRP was higher in lacunar stroke versus non-stroke acutely in 3 studies [34,49,52], significantly so in 2, and the other [34] did not report if the higher value was significant. CRP was significantly lower in lacunar versus atherothrombotic stroke in 1 study [34] acutely; all other studies reported no difference (or did not state significance) between lacunar and non-lacunar stroke, acutely and chronically.…”

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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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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“…Álvarez-Perez and colleagues showed a higher CRP in LAA when compared with SVD (p=0.010) and undetermined (p=0.003) strokes, but not with CE ones [52]. Adding more controversy to the role of CRP as etiologic biomarker, some authors detected no differences in CRP serum levels between etiology groups [53, 54]. Alternative approaches, such as meta-analysis or studies including greater cohorts of patients, are necessary to clarify the relation between CRP levels and different stroke etiologies.…”

Section: Stroke Etiology and Circulating Proteinsmentioning

confidence: 99%

Cardioembolic Stroke Diagnosis Using Blood Biomarkers

Llombart¹,

García‐Berrocoso²,

Bustamante³

et al. 2014

CCR

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Stroke is one of the main causes of death and disability in the world. Cardioembolic etiology accounts for approximately one fifth of all ischemic strokes whereas 25-30% remains undetermined even after an advanced diagnostic workup. Despite there is not any biomarker currently approved to distinguish cardioembolic stroke among other etiologies in clinical practice the use of biomarkers represents a promising valuable complement to determine stroke etiology reducing the number of cryptogenic strokes and aiding in the prescription of the most appropriated primary and secondary treatments in order to minimize therapeutic risks and to avoid recurrences. In this review we present an update about specific cardioembolic stroke-related biomarkers at a protein, transcriptomic and genetic level. Finally, we also focused on reported biomarkers associated with atrial fibrillation (a cardiac illness strongly related with cardioembolic stroke subtype) thus with a potential to become biomarkers to detect cardioembolic stroke in the future.

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Differences in platelet–leukocyte aggregates among subtypes of acute cerebral ischemia

Cited by 19 publications

References 31 publications

Measuring and interpreting platelet-leukocyte aggregates

Measuring and interpreting platelet-leukocyte aggregates

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

Cardioembolic Stroke Diagnosis Using Blood Biomarkers

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