Coated‐platelets in ischemic stroke: differences between lacunar and cortical stroke

Prodan, Călin I.; Joseph, Peter M.; Vincent, Andrea S.; Dale, George L.

doi:10.1111/j.1538-7836.2008.02890.x

Cited by 60 publications

(84 citation statements)

References 24 publications

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“…1,10 The phenotypic differences between coated-and noncoated-platelets center on the presence of bound Figure 1 were subdivided according to coated-platelet levels at time of initial stroke. Recurrence incidence (%) is plotted as a function of follow-up time for lowest coated-platelet tertile group ( Á Á Á Á Á Á Á Á Á Á Á ; coated-platelet levels from 9.6% to 34.0%); middle tertile group (----; 34.1% to 46.0%); and highest tertile group ( Á -Á -Á -Á -Á ; 46.1% to 69.7%).…”

Section: Discussionmentioning

confidence: 99%

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Higher Coated-Platelet Levels are Associated with Stroke Recurrence following Nonlacunar Brain Infarction

Prodan

Stoner

Cowan

et al. 2012

J Cereb Blood Flow Metab

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Coated-platelets are procoagulant platelets observed upon dual-agonist stimulation with collagen and thrombin. Coated-platelet levels are elevated in patients with nonlacunar (large-vessel) ischemic stroke and decreased in patients with spontaneous intracerebral hemorrhage as compared with controls. The purpose of this study was to investigate a possible relationship between coated-platelet levels and stroke recurrence in patients with nonlacunar ischemic stroke. We assayed coated-platelet levels in 190 consecutive patients with nonlacunar stroke who were followed for up to 12 months; 20 subjects experienced recurrent stroke. Subjects were categorized into tertiles of coated-platelet levels. The distributions of time-to-recurrent stroke were estimated for each tertile using cumulative incidence curves and compared statistically using a log-rank test. The cumulative incidence of recurrent stroke at 12 months differed among the coated-platelet tertiles: 2% for the first tertile (lowest coated-platelet levels), 18% for the second tertile, and 17% for the third tertile (overall log-rank test, P ¼ 0.019). These data suggest that higher levels of coated-platelets, measured shortly after a nonlacunar stroke, are associated with an increased incidence of stroke recurrence. This observation offers an additional tool for identifying patients at highest risk for stroke recurrence following a nonlacunar (large-vessel) infarct.

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Section: Discussionmentioning

confidence: 99%

“…The event rate estimates were based on our previously published research data on coated-platelet levels in ischemic stroke. 10,11 Sample size calculations were performed using PASS software (NCSS, LLC, Kaysville, UT, USA). 26 …”

Section: Statistical Analysesmentioning

confidence: 99%

Higher Coated-Platelet Levels are Associated with Stroke Recurrence following Nonlacunar Brain Infarction

Prodan

Stoner

Cowan

et al. 2012

J Cereb Blood Flow Metab

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“…32 In addition, recent studies showed abnormal coated-platelet synthesis in patients with cerebrovascular disease, with elevated coated-platelet levels in patients with nonlacunar ischemic stroke and decreased coated-platelet levels in patients with spontaneous intracerebral hemorrhage. 15,16,33,34 Finally, limited studies have indicated that coated-platelets are potentiated by inflammation. 35 Perhaps coated-platelet synthesis represents a sensitive biomarker of the disease process that includes APP abnormalities, cerebrovascular disease, and inflammatory components and may produce insight into the multifaceted pathways associated with AD.…”

Section: Discussionmentioning

confidence: 99%

Coated-platelet levels and progression from mild cognitive impairment to Alzheimer disease

Prodan¹,

Ross²,

Stoner³

et al. 2011

Neurology

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Objectives: Coated-platelets are a subset of platelets produced by dual-agonist activation with collagen and thrombin. These platelets retain full-length amyloid precursor protein on their surface, are elevated in patients with amnestic as compared to nonamnestic mild cognitive impairment (MCI), and correlate with disease progression in Alzheimer disease (AD). Prompted by these findings, we investigated the association between coated-platelet production in amnestic MCI and rate of progression to AD.Methods: Coated-platelet levels were assayed in 74 patients with amnestic MCI who were subsequently followed longitudinally for up to 36 months in an outpatient dementia clinic. Levels are reported as percent of cells converted into coated-platelets. Subjects were categorized into tertiles of coated-platelet levels. The distributions of time to progression to AD were estimated for each tertile using cumulative incidence curves and compared statistically using a log-rank test. Cox proportional hazards regression was used to adjust for potential confounders.Results: The 24-month cumulative incidence of progression to AD was different among tertiles:4% for the first tertile (lowest coated-platelet levels), 13% for the second tertile, and 37% for the third tertile (overall log-rank test, p ϭ 0.02). The hazard rate of progression to AD for patients in the highest coated-platelet tertile was 5.1 times that for patients in the lowest tertile (p ϭ 0.04), whereas the hazard rate for the middle tertile was similar to that for the lowest tertile (hazard rate ratio ϭ 1.5, p ϭ 0.7). Conclusions:

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“…A logical extension of our first report on coated-platelets in ischemic stroke 11 is whether these activated platelets also have a role in hemorrhagic stroke. While it is accepted that a bleeding diathesis is not the primary cause of hemorrhagic strokes, it is logical that a bleeding tendency might well contribute to the pathophysiology of this stroke subtype.…”

Section: Coated-platelets and Hemorrhagic Strokementioning

confidence: 99%

Coated–platelets in Ischemic Stroke

Prodan¹,

Dale²

2010

US Neurology

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Stroke is the third leading cause of death and the number one cause of disability in the US, with an estimated incidence of 780,000 strokes/ year.1 Approximately 10% of all strokes are hemorrhagic, with the remainder being ischemic. Within the ischemic category, two major sub-classes are recognized. Ischemic strokes occurring within large blood vessels of the brain account for approximately 80% of the total and are thought to be the result of thromboembolic events originating in the heart or diseased large arteries. Lacunar strokes are the second major classification of ischemic stroke, occurring in small (200-300µm) penetrating arteries of the brain. The etiology of lacunar strokes is not considered to be embolic but rather represents endogenously generated clots, perhaps as a result of endothelial abnormalities. Largevessel strokes, subsequently referred to as cortical (or non-lacunar) strokes, have a worse prognosis for 30-day mortality, residual disability, and recurrence than do lacunar strokes. 2,3 Modifiable risk factors for ischemic stroke include hypertension, diabetes, smoking, and hyperlipidemia, 1 all factors that similarly contribute to atherosclerotic disease. While platelet participation is recognized as integral to the thrombotic process associated with ischemic strokes, there has been limited evidence to suggest that variations in platelet reactivity may also be a risk factor. This paucity of data is at least partially due to technical limitations in quantitating platelet reactivity, and also possibly due to the numerous platelet parameters that could affect thrombotic potential. Coated-plateletsOur interest in the platelet's role in ischemic stroke resulted from studies with coated-platelets, a subset of activated platelets with pro-thrombotic characteristics first described in 2000 by Alberio et al. Willebrand factor, and thrombospondin, were also retained on the surface of these dual activated cells.Dissection of the synthetic processes associated with coated-platelet formation indicated that serotonin was covalently attached to platelet pro-coagulant proteins via a transglutaminase reaction 5 and that serotonin derivatization was responsible for the tight binding of these proteins to the coated-platelet surface. 6 A proposed model for the structure of coated-platelets is shown in Figure 1. 7A recent study examining 70 normal controls found the average coatedplatelet level was 31.6±13.2% (mean ± SD); however, the range was 7-59%. 8 This is an exceptionally large range for a potential prothrombotic marker. We therefore sought to determine factors affecting coated-platelet levels and observed several relevant medications and behaviors. 8 For example, individuals who smoke have elevated coatedplatelet levels, while individuals on aspirin have lower coated-platelet levels. 8 Patients using selective serotonin re-uptake inhibitors (SSRIs) also had decreased levels of coated-platelets, 8 an observation likely associated with the role of serotonin in coated-platelet formation. 5 In addition, infl...

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Coated‐platelets in ischemic stroke: differences between lacunar and cortical stroke

Cited by 60 publications

References 24 publications

Higher Coated-Platelet Levels are Associated with Stroke Recurrence following Nonlacunar Brain Infarction

Higher Coated-Platelet Levels are Associated with Stroke Recurrence following Nonlacunar Brain Infarction

Coated-platelet levels and progression from mild cognitive impairment to Alzheimer disease

Coated–platelets in Ischemic Stroke

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