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Atherothrombotic stroke: clinical data and parameters of platelet haemostasis in patients in acute stage  [PDF]
Goldobin V.V.,Klocheva Е.G.,Asadullaeva P.M.,Vavilova T.V.
Saratov Journal of Medical Scientific Research , 2012,
Abstract: The aim of the study was the investigation of clinical data and platelet haemostasis parameters in patients with atherothrombotic stroke for secondary prophylaxis improvement. Materials and Methods. 41 patient: 26 (63,4%) males, 15 (36,6%) females, mean age 66,0±9,4 years and 18 healthy person were examined. Neurological examination was performed, patient condition was estimated with National Institute of Health Stroke Scale and Rankin scale. The set of investigation included clinical blood analysis, adenosinediphosphate-induced agregometry, flow-cytometry, molecular genetic analysis of gene Iba. Results. There was platelet activation in patients with atherothrombotic stroke according to flow-cytometry data. The conventional optic agregometry was not helpful for revealing of platelet activation. The expression of 1ba receptors correlated with the point of National Institute of Health Stroke Scale at discharge. The incidence of Iba gene mutation was higher in patients with atherothrombotic stroke comparing with control group. Conclusions. The revealed data predispose to the possibility of individual administration of antiagregant therapy in such patients.
Oral antiplatelet therapy for atherothrombotic disease: overview of current and emerging treatment options  [cached]
Fintel DJ
Vascular Health and Risk Management , 2012,
Abstract: Dan J FintelBluhm Cardiovascular Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL, USAAbstract: Clinical presentations of atherothrombotic vascular disease, such as acute coronary syndromes, ischemic stroke or transient ischemic attack, and symptomatic peripheral arterial disease, are major causes of morbidity and mortality worldwide. Platelet activation and aggregation play a seminal role in the arterial thrombus formation that precipitates acute manifestations of atherothrombotic disease. As a result, antiplatelet therapy has become the cornerstone of therapy for the prevention and treatment of atherothrombotic disease. Dual antiplatelet therapy with aspirin and a P2Y12 adenosine diphosphate (ADP) receptor inhibitor, such as clopidogrel or prasugrel, is the current standard-of-care antiplatelet therapy in patients with acute coronary syndromes managed with an early invasive strategy. However, these agents are associated with several important clinical limitations, including significant residual risk for ischemic events, bleeding risk, and variability in the degree of platelet inhibition. The residual risk can be attributed to the fact that aspirin and P2Y12 inhibitors block only the thromboxane A2 and ADP platelet activation pathways but do not affect the other pathways that lead to thrombosis, such as the protease-activated receptor-1 pathway stimulated by thrombin, the most potent platelet agonist. Bleeding risk associated with aspirin and P2Y12 inhibitors can be explained by their inhibitory effects on the thromboxane A2 and ADP pathways, which are critical for protective hemostasis. Interpatient variability in the degree of platelet inhibition in response to antiplatelet therapy may have a genetic component and contribute to poor clinical outcomes. These considerations underscore the clinical need for therapies with a novel mechanism of action that may reduce ischemic events without increasing the bleeding risk.Keywords: acute coronary syndromes, antiplatelet therapy, ADP, thromboxane A2, PAR-1, bleeding
Oral antiplatelet therapy for atherothrombotic disease: overview of current and emerging treatment options
Fintel DJ
Vascular Health and Risk Management , 2012, DOI: http://dx.doi.org/10.2147/VHRM.S26030
Abstract: al antiplatelet therapy for atherothrombotic disease: overview of current and emerging treatment options Review (5453) Total Article Views Authors: Fintel DJ Published Date February 2012 Volume 2012:8 Pages 77 - 89 DOI: http://dx.doi.org/10.2147/VHRM.S26030 Received: 09 September 2011 Accepted: 26 October 2011 Published: 16 February 2012 Dan J Fintel Bluhm Cardiovascular Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA Abstract: Clinical presentations of atherothrombotic vascular disease, such as acute coronary syndromes, ischemic stroke or transient ischemic attack, and symptomatic peripheral arterial disease, are major causes of morbidity and mortality worldwide. Platelet activation and aggregation play a seminal role in the arterial thrombus formation that precipitates acute manifestations of atherothrombotic disease. As a result, antiplatelet therapy has become the cornerstone of therapy for the prevention and treatment of atherothrombotic disease. Dual antiplatelet therapy with aspirin and a P2Y12 adenosine diphosphate (ADP) receptor inhibitor, such as clopidogrel or prasugrel, is the current standard-of-care antiplatelet therapy in patients with acute coronary syndromes managed with an early invasive strategy. However, these agents are associated with several important clinical limitations, including significant residual risk for ischemic events, bleeding risk, and variability in the degree of platelet inhibition. The residual risk can be attributed to the fact that aspirin and P2Y12 inhibitors block only the thromboxane A2 and ADP platelet activation pathways but do not affect the other pathways that lead to thrombosis, such as the protease-activated receptor-1 pathway stimulated by thrombin, the most potent platelet agonist. Bleeding risk associated with aspirin and P2Y12 inhibitors can be explained by their inhibitory effects on the thromboxane A2 and ADP pathways, which are critical for protective hemostasis. Interpatient variability in the degree of platelet inhibition in response to antiplatelet therapy may have a genetic component and contribute to poor clinical outcomes. These considerations underscore the clinical need for therapies with a novel mechanism of action that may reduce ischemic events without increasing the bleeding risk.
THIENOPYRIDINES: PLATELET ADP RECEPTOR ANTAGONIST  [cached]
Dangi Girija,Bele Dheeraj Singh,Sharma Komal
Journal of Drug Delivery and Therapeutics , 2011,
Abstract: Atherothrombosis results from atherosclerosis progression, and its clinical manifestations [acute coronary syndromes (ACS), stroke, etc]. These events are secondary to atherosclerotic plaque disruption and subsequent thrombus formation. Atherosclerosis prevention focuses mainly on the management of cardiovascular risk factors whereas thrombosis-related complications use antithrombotic therapies. The central role played by platelets in pathophysiology of arterial vascular disease has focused attention on the development of effective platelet inhibitor modalities to mitigate the clinical consequences of atherothrombotic disease. Aspirin has been the mainstay; the thienopyridines provide new opportunities for those patients who are intolerant, resistant or have failed to respond to aspirin, and for those who can derive greater bene t from combined therapy. Thienopyridines (ticlopidine, clopidogrel etc.) are a class of ADP receptor/P2Y12 inhibitors used for their anti-platelet activity. The co-administration of aspirin-clopidogrel results in enhancement of platelet inhibition as they act via different platelet receptors. This article reviews the current antiplatelet agents in ACSs and role of thienopyridines as antiplatelet agents in management.
Is elevated SUA associated with a worse outcome in young Chinese patients with acute cerebral ischemic stroke?
Bin Zhang, Cong Gao, Ning Yang, WeiZhi Zhang, XingWang Song, JianRui Yin, ShuXiang Pu, YongHong Yi, QingChun Gao
BMC Neurology , 2010, DOI: 10.1186/1471-2377-10-82
Abstract: We analyzed the relationship between SUA and clinical prognosis of 585 young Chinese adults with acute ischemic stroke as determined by the modified Rankin Scale at discharge. Using multivariate logistic regression modeling, we explore the relationship between SUA levels and patient's clinical prognosis.Lower SUA levels at time of admission were observed more frequently in the lowest quintile for patients with severe stroke (P = 0.02). Patients with cerebral infarction patients caused by small-vessel blockage had higher SUA concentrations (P = 0.01) and the lower mRS scores (P < 0.01) were observed in, while the lowest SUA concentrations and the highest mRS scores were seen in patients with cardiogenic cerebral infarction patients. Logistic regression analysis adjusted for confounders confirmed the following independent predictors for young cerebral infarction: uric acid (-0.003: 95%CI 0.994 to 0.999) and platelet (0.004, 95%CI 0.993 to 0.996).Elevated SUA is an independent predictor for good clinical outcome of acute cerebral infarction among young adults.Stroke in young adults is an important cause of lifelong disability. Thus it is very important to study the pathogenesis and prognosis of young patients with cerebral infarction. Conventional risk factors for arterial thrombosis at young age, such as gender, smoking, diabetes mellitus, obesity and hypercholesterolemia do not fully explain the cerebrovascular risk, Therefore additional factors may exist which contribute to the likelihood of developing arterial thrombosis in young adults. Studies have shown that elevated SUA can increase the risk of hypertension, diabetes, dyslipidemia, obesity, and renal failure [1-3].More recent researchers have established a relationship between elevated SUA and vascular events (mainly cardiovascular disease), and it is believed that elevated serum uric acid levels could increase the morbidity and mortality from cerebral infarction [4-7]. However, other large-scale studies have f
Assessment of prolactin associated platelet activation in ischemic stroke  [PDF]
Ay?egül Akagündüz Ege,?ule Bilen,Fikri Ak
Journal of Clinical and Experimental Investigations , 2012,
Abstract: Objectives: We aimed to investigate whether there wereany relations between prolactin levels, prolactin associatedplatelet activation and ischemic stroke, and whetherthey had role in etiology of ischemic stroke.Materials and methods: Totally 57 patients with thediagnosis of acute ischemic stroke and 43 age and sexmatched controls with no history of ischemic vascular diseaseswere included in the study. Prolactin levels, meanplatelet volume (MPV) a marker of platelet activation, andplatelet count, of the patients, after 12 hours of fasting,compared with the measurements of control group.Results: Patients had significantly higher prolactin levels.A correlation between prolactin levels and early measurementsof MPV was not detected. While there was no differencein terms of MPV, the platelet count was significantlyhigher in the patient group.Conclusions: In the present study, the existence of aneffect of prolactin on the mean platelet volume, or a relationshipbetween early ischemic stroke and MPV couldnot be shown. However, in ischemic stroke patients, inearly phase, presence of higher levels of prolactin andplatelet count may be meaningful in etiology of ischemicevents. Besides, presence of higher prolactin levels inearly phase of ischemic stroke may lead to consider thepotential role of prolactin elevation in ischemic strokepathogenesis. J Clin Exp Invest 2012; 3(1): 1-6
Platelet Function in Patients with Diabetes Mellitus: From a Theoretical to a Practical Perspective  [PDF]
Nicholaos Kakouros,Jeffrey J. Rade,Antonios Kourliouros,Jon R. Resar
International Journal of Endocrinology , 2011, DOI: 10.1155/2011/742719
Abstract: Patients with diabetes mellitus have an increased prevalence of vascular disease. Pathologic thrombosis associated with atherosclerotic plaque rupture is a major cause of morbidity and mortality. Platelets are intimately involved in the initiation and propagation of thrombosis. Evidence suggests that platelets from patients with type 2 diabetes have increased reactivity and baseline activation compared to healthy controls. We review the pathophysiology of platelet hyperreactivity in DM patients and its implications in clinical practice, with particular focus on acute coronary syndromes, percutaneous coronary intervention, and novel antiplatelet agents. 1. Introduction Diabetes mellitus, that affects over 25 million people in the US and an estimated 285 million worldwide, is associated with a significant burden of cardiovascular disease [1, 2]. Patients with type 2 diabetes mellitus (DM2) have a 2- to 4-fold increased risk of premature cerebral, coronary, and peripheral vascular disease that together constitute the leading cause of death in these patients [3, 4]. Unlike the diabetes-specific microvasculopathy, neuropathy, nephropathy, and retinopathy, the macroangiopathic process in patients with diabetes represents an accelerated but pathophysiologically similar process to atherosclerosis in nondiabetic subjects. Thrombotic events of these vascular lesions, particularly in the cerebral and coronary vasculature, can be life threatening. Normal blood flow and thromboresistance is dependent on vasomotion, blood corpuscular elements, plasma components, and their interaction with the endothelial surface. Rupture of an atherosclerotic plaque exposes subendothelial material that promotes platelet activation and the local initiation of the coagulation cascade that can lead to thrombus formation at the site of endothelial disruption. Acute vascular events, such as myocardial infarction and stroke, are due to such atherothrombotic events rather than gradual progression of luminal stenosis caused by atheromatous plaque. Patients with DM not only have a greater atheromatous plaque burden but also a thrombotic diathesis that is in part due to changes in the coagulation system with increased levels of plasma fibrinogen, increased intravascular thrombin generation, and reduced fibrinolytic potential [5, 6]. Equally importantly, however, platelets from patients with diabetes mellitus have dysregulated signaling pathways that lead to an increased tendency to activate and aggregate in response to a given stimulus (platelet hyperreactivity). Platelet activation
A combined genome-wide linkage and association approach to find susceptibility loci for platelet function phenotypes in European American and African American families with coronary artery disease
Rasika A Mathias, Yoonhee Kim, Heejong Sung, Lisa R Yanek, VJ Mantese, J Enrique Hererra-Galeano, Ingo Ruczinski, Alexander F Wilson, Nauder Faraday, Lewis C Becker, Diane M Becker
BMC Medical Genomics , 2010, DOI: 10.1186/1755-8794-3-22
Abstract: Clinical data on 37 agonist-induced platelet function phenotypes were evaluated before and after a 2-week trial of ASA (81 mg/day) in 1231 European American and 846 African American healthy subjects with a family history of premature CAD. Principal component analysis was performed to minimize the number of independent factors underlying the covariance of these various phenotypes. Multi-point sib-pair based linkage analysis was performed using a microsatellite marker set, and single-SNP association tests were performed using markers from the Illumina 1 M genotyping chip from deCODE Genetics, Inc. All analyses were performed separately within each ethnic group.Several genomic regions appear to be linked to ASA response factors: a 10 cM region in African Americans on chromosome 5q11.2 had several STRs with suggestive (p-value < 7 × 10-4) and significant (p-value < 2 × 10-5) linkage to post aspirin platelet response to ADP, and ten additional factors had suggestive evidence for linkage (p-value < 7 × 10-4) to thirteen genomic regions. All but one of these factors were aspirin response variables. While the strength of genome-wide SNP association signals for factors showing evidence for linkage is limited, especially at the strict thresholds of genome-wide criteria (N = 9 SNPs for 11 factors), more signals were considered significant when the association signal was weighted by evidence for linkage (N = 30 SNPs).Our study supports the hypothesis that platelet phenotypes in response to ASA likely have genetic control and the combined approach of linkage and association offers an alternative approach to prioritizing regions of interest for subsequent follow-up.Platelet activation plays a critical role in atherothrombotic diseases such as acute myocardial infarction (MI) and stroke. Aspirin (acetylsalicylic acid [ASA]) is a mainstay of both primary and secondary prevention of MI and stroke [1]. ASA inhibits cyclooxygenase-1 (COX-1) and thromboxane-dependent platelet activatio
Mean Platelet Volume and Peripheral Blood Count Response in Acute Ischemic Stroke
Baburhan Guldiken,Hulya Ozkan,Levent Kabayel
Trakya Universitesi Tip Fakultesi Dergisi , 2008,
Abstract: Objectives: Mean platelet volume (MPV) is a marker of the platelet activity and is reported to increase in vascular diseases. The aim of the study is to investigate the relationship between MPV and the subtypes of acute ischemic stroke.Patients and Methods: The patient group consisted of 102 acute ischemic stroke patients who were divided into the large vessel (n=43) and the small vessel (n=59) disease subgroups. Their MPV values were compared with those of 48 age/sex-matched healthy individuals. The relationship of MPV with the subtypes and severity of stroke, and other hematological parameters (platelet count, platecrit, hemoglobin, hematocrit, erythrocyte count, mean corpuscular volume, leukocyte, neutrophil, lymphocyte, monocyte) was further investigated.Results: No difference was found in terms of MPV values between the patient subgroups and control group, and no relation was found between MPV and stroke severity and other hematological parameters (p>0.05). A significant increase in the leukocyte and neutrophil count was seen in patients of the large vessel disease group when compared with the small vessel disease and control group (p<0.005). Neutrophil count is found to be a risk factor for the stroke severity (β=0.362, p=0.01, OR=1.437, CI %95 0.02-0.08).Conclusion: No significant change in MPV was seen in acute ischemic stroke. High leukocyte and neutrophil levels are markers for the large vessel disease subtype and severity of ischemic stroke.
Predictive value of routine hematological and biochemical parameters on 30-day fatality in acute stroke  [cached]
Bhatia R,Garg R,Gaur S,Kar A
Neurology India , 2004,
Abstract: OBJECTIVE: This prospective study was planned to study the prognostic value of routine clinical, hematological and biochemical parameters, including platelet aggregation in patients of acute stroke, on fatality occurring during the first 30 days. MATERIAL AND METHODS: In this study 116 consecutive patients (77 males and 39 females) of stroke (within 72 hours of onset) were included. After clinical evaluation and neuroimaging, blood investigations, hemoglobin, total leukocyte count, platelet count, platelet aggregation, erythrocyte sedimentation rate (ESR), blood sugar, urea, creatinine, sodium, potassium, serum cholesterol, serum bilirubin, aspartate aminotransferase (SGOT), alanine aminotransferase (SGPT), albumin, and globulin estimations were performed. The patients were followed up for a maximum period of 30 days from the onset of stroke, and patients who expired were grouped as ′expired′ and the rest as ′survivors′. Logistic regression analysis was carried out among the significant parameters to identify independent predictors of 30-day fatality. RESULTS: Univariate analysis demonstrated that among hematological parameters, high total leukocyte count and ESR, at admission, correlated significantly with an undesirable outcome during the initial 30 days. Among biochemical parameters, elevated urea, creatinine, serum transaminases (SGOT and SGPT) and globulin levels correlated significantly with death. Logistic regression analysis demonstrated that a low Glasgow Coma Scale (GCS) score along with biochemical parameters such as high serum creatinine, SGPT, ESR and total leukocyte count correlated with death. CONCLUSION: Impaired consciousness, high total leukocyte count, raised ESR, elevated creatinine and SGPT levels, estimated within 24 hours of hospitalization, are the most important indicators of 30-day mortality in patients with first-time ischemic stroke.
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