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Thrombosis and Haemostasis Jun 2022Cardiovascular disease, in particular due to arterial thrombosis, is a leading cause of mortality and morbidity, with crucial roles of platelets in thrombus formation....
Cardiovascular disease, in particular due to arterial thrombosis, is a leading cause of mortality and morbidity, with crucial roles of platelets in thrombus formation. For multiple plant-derived phytochemicals found in common dietary components, claims have been made regarding cardiovascular health and antiplatelet activities. Here we present a systematic overview of the published effects of common phytochemicals, applied in vitro or in nutritional intervention studies, on agonist-induced platelet activation properties and platelet signaling pathways. Comparing the phytochemical effects per structural class, we included general phenols: curcuminoids (e.g., curcumin), lignans (honokiol, silybin), phenolic acids (caffeic and chlorogenic acid), derivatives of these (shikimic acid), and stilbenoids (isorhapontigenin, resveratrol). Furthermore, we evaluated the flavonoid polyphenols, including anthocyanidins (delphinidin, malvidin), flavan-3-ols (catechins), flavanones (hesperidin), flavones (apigenin, nobiletin), flavonols (kaempferol, myricetin, quercetin), and isoflavones (daidzein, genistein); and terpenoids including carotenes and limonene; and finally miscellaneous compounds like betalains, indoles, organosulfides (diallyl trisulfide), and phytosterols. We furthermore discuss the implications for selected phytochemicals to interfere in thrombosis and hemostasis, indicating their possible clinical relevance. Lastly, we provide guidance on which compounds are of interest for further platelet-related research.
Topics: Blood Platelets; Flavonoids; Hemostasis; Humans; Phenols; Phytochemicals; Thrombosis
PubMed: 34715717
DOI: 10.1055/a-1683-5599 -
European Journal of Vascular and... Mar 2022The aim was to enhance understanding of the role of platelet biomarkers in the pathogenesis of vascular events and risk stratifying patients with asymptomatic or... (Review)
Review
OBJECTIVE
The aim was to enhance understanding of the role of platelet biomarkers in the pathogenesis of vascular events and risk stratifying patients with asymptomatic or symptomatic atherosclerotic carotid stenosis.
DATA SOURCES
Systematic review conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.
REVIEW METHODS
A systematic review collated data from 1975 to 2020 on ex vivo platelet activation and platelet function/reactivity in patients with atherosclerotic carotid stenosis.
RESULTS
Forty-three studies met the inclusion criteria; the majority included patients on antiplatelet therapy. Five studies showed increased platelet biomarkers in patients with ≥ 30% asymptomatic carotid stenosis (ACS) vs. controls, with one neutral study. Preliminary data from one study suggested that quantification of "coated platelets" in combination with stenosis severity may aid risk stratification in patients with ≥ 50% - 99% ACS. Platelets were excessively activated in patients with ≥ 30% symptomatic carotid stenosis (SCS) vs. controls (≥ 11 positive studies and one neutral study). Antiplatelet-High on Treatment Platelet Reactivity (HTPR), previously called "antiplatelet resistance", was observed in 23% - 57% of patients on aspirin, with clopidogrel-HTPR in 25% - 100% of patients with ≥ 50% - 99% ACS. Aspirin-HTPR was noted in 9.5% - 64% and clopidogrel-HTPR in 0 - 83% of patients with ≥ 50% SCS. However, the data do not currently support the use of ex vivo platelet function/reactivity testing to tailor antiplatelet therapy outside of a research setting. Platelets are excessively activated (n = 5), with increased platelet counts (n = 3) in recently symptomatic vs. asymptomatic patients, including those without micro-emboli on transcranial Doppler (TCD) monitoring (n = 2). Most available studies (n = 7) showed that platelets become more reactive or activated following carotid endarterectomy or stenting, either as an acute phase response to intervention or peri-procedural treatment.
CONCLUSION
Platelets are excessively activated in patients with carotid stenosis vs. controls, in recently symptomatic vs. asymptomatic patients, and may become activated/hyper-reactive following carotid interventions despite commonly prescribed antiplatelet regimens. Further prospective multicentre studies are required to determine whether models combining clinical, neurovascular imaging, and platelet biomarker data can facilitate optimised antiplatelet therapy in individual patients with carotid stenosis.
Topics: Aspirin; Biomarkers; Blood Platelets; Carotid Stenosis; Humans; Platelet Aggregation Inhibitors; Stroke
PubMed: 35181225
DOI: 10.1016/j.ejvs.2021.10.045 -
Seminars in Thrombosis and Hemostasis Jul 2023Pathogen reduction technologies (PRTs) such as Mirasol and Intercept were developed to eliminate transfusion-transmitted infections. The impact of PRTs on platelet...
Pathogen reduction technologies (PRTs) such as Mirasol and Intercept were developed to eliminate transfusion-transmitted infections. The impact of PRTs on platelet function during the storage period, their effect on platelet storage lesions, and the optimal storage duration following PRTs have not been clearly defined. The aim of this study was to systematically review the existing literature and investigate the impact of PRTs on functional alterations of PRT-treated platelets during the storage period. The authors identified 68 studies suitable to be included in this review. Despite the high heterogeneity in the literature, the results of the published studies indicate that PRTs may increase platelet metabolic activity, accelerate cell apoptosis, and enhance platelet activation, which can subsequently lead to a late exhaustion of activation potential and reduced aggregation response. However, these effects have a minor impact on platelet function during the early storage period and become more prominent beyond the fifth day of the storage period. Large in vivo trials are required to evaluate the effectiveness of PRT-treated platelets during the storage period and investigate whether their storage can be safely extended to more than 5 days, and up to the traditional 7-day storage period.
Topics: Humans; Blood Platelets; Platelet Activation; Blood Preservation; Platelet Transfusion
PubMed: 36252605
DOI: 10.1055/s-0042-1757897 -
Sports Medicine (Auckland, N.Z.) Apr 2018Cocoa flavanols (CFs) have antioxidant and anti-inflammatory capacities and can improve vascular function. It has recently been suggested that CF intake may improve... (Review)
Review
BACKGROUND
Cocoa flavanols (CFs) have antioxidant and anti-inflammatory capacities and can improve vascular function. It has recently been suggested that CF intake may improve exercise performance and recovery. This systematic review aimed to evaluate the literature on the effects of CF intake on exercise performance and recovery and exercise-induced changes in vascular function, cognitive function, oxidative stress, inflammation, and metabolic parameters.
METHODS
Two electronic databases (Pubmed and Web of Science) were searched for studies examining the combination of CF intake and exercise in humans (up to 28 March 2017). Articles were included if the exact amount of CFs was mentioned. The methodological quality and level of bias of the 13 included studies was assessed according to the checklist for randomized controlled trials from the Dutch Cochrane center.
RESULTS
Acute, sub-chronic (2 weeks) and chronic (3 months) CF intake reduced exercise-induced oxidative stress. Evidence on the effect of CF on exercise-induced inflammation and platelet activation was scarce. Acute CF intake reduced and tempered the exercise-induced increase in blood pressure in obese participants. Acute and sub-chronic CF intake altered fat and carbohydrate metabolism during exercise. Acute and sub-chronic CF intake did not have ergogenic effects in athletes, while chronic CF intake improved mitochondrial efficiency in untrained participants. While combining sub-chronic CF intake and exercise training improved cardiovascular risk factors and vascular function, evidence on the synergistic effects of CF and exercise training on oxidative stress, inflammation, and fat and glucose metabolism was lacking.
CONCLUSION
CF intake may improve vascular function, reduce exercise-induced oxidative stress, and alter fat and carbohydrate utilization during exercise, but without affecting exercise performance. There is a strong need for future studies examining the synergetic effect of chronic CF intake and exercise training.
Topics: Antioxidants; Athletic Performance; Biomarkers; Blood Pressure; Cacao; Cerebrovascular Circulation; Chocolate; Exercise; Flavonoids; Humans
PubMed: 29299877
DOI: 10.1007/s40279-017-0849-1 -
Brain and Nerve = Shinkei Kenkyu No... Nov 2008Aspirin inhibits platelet activation through the permanent inactivation of the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (referred to as COX-1), and... (Review)
Review
Aspirin inhibits platelet activation through the permanent inactivation of the cyclooxygenase (COX) activity of prostaglandin H synthase-1 (referred to as COX-1), and consequently inhibits the biosynthesis of thromboxane A2 (TXA2), a platelet agonist. Recent meta-analysis has revealed that long-term aspirin administration has clear benefits for the secondary prevention of cardiovascular diseases with an odds reduction of 23% and an absolute risk reduction of 3.1% over 2 years. However, this indicates that not all individuals respond equally to aspirin therapy and cardiovascular events may occur during aspirin therapy, this is often denoted as "clinical aspirin resistance". Several reports have, indeed, suggested that the effect of aspirin administration varies considerably among the patients at high risk for cardiovascular events. Approximately one forth of the patients showed persistent platelet reactivity in vitro despite the use of aspirin (denoted "laboratory aspirin resistance"), this was determined by laboratory tests including the test for arachidonic acid-induced platelet aggregation and the assays using point-of-care devices. Recent clinical studies have proposed that resistance to aspirin (laboratory aspirin resistance) can relate to the cardiovascular outcomes in patients treated with aspirin (clinical aspirin resistance). A systematic review and meta-analysis on aspirin resistance have indicated that patients who are resistant to aspirin are at a greater risk (odds ratio: 3.85) of clinically important cardiovascular morbidity than patients who are sensitive to aspirin. However, many issues are yet to be resolved in order to apply the concept of "aspirin resistance" to actual clinical practice. The relevance of the various ex vivo functional indexes of platelet capacity to in vivo platelet activation and the precise mechanisms underlying aspirin resistance are still largely unknown. To assess what kind of laboratory assays is the best predictor for cardiovascular events and the risk factors of aspirin resistance, including non-compliance, concurrent intake of other drugs such as nonsteroid anti-inflammatory drugs, and polymorphism of COX-1, we have conducted a multicenter, prospective cohort study (ProGEAR study). We hope that these results will contribute to an individualized antiplatelet therapy through the identification of aspirin nonresponders as a high-risk group for cardiovascular events.
Topics: Aspirin; Cardiovascular Diseases; Cyclooxygenase 1; Cyclooxygenase Inhibitors; Drug Resistance; Humans; Pharmacogenetics; Platelet Activation; Platelet Aggregation Inhibitors
PubMed: 19069170
DOI: No ID Found -
Inflammation Research : Official... Mar 2024The availability of robust biomarkers of endothelial activation might enhance the identification of subclinical atherosclerosis in rheumatoid arthritis (RA). We... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The availability of robust biomarkers of endothelial activation might enhance the identification of subclinical atherosclerosis in rheumatoid arthritis (RA). We investigated this issue by conducting a systematic review and meta-analysis of cell adhesion molecules in RA patients.
METHODS
We searched electronic databases from inception to 31 July 2023 for case-control studies assessing the circulating concentrations of immunoglobulin-like adhesion molecules (vascular cell, VCAM-1, intercellular, ICAM-1, and platelet endothelial cell, PECAM-1, adhesion molecule-1) and selectins (E, L, and P selectin) in RA patients and healthy controls. Risk of bias and certainty of evidence were assessed using the JBI checklist and GRADE, respectively.
RESULTS
In 39 studies, compared to controls, RA patients had significantly higher concentrations of ICAM-1 (standard mean difference, SMD = 0.81, 95% CI 0.62-1.00, p < 0.001; I = 83.0%, p < 0.001), VCAM-1 (SMD = 1.17, 95% CI 0.73-1.61, p < 0.001; I = 95.8%, p < 0.001), PECAM-1 (SMD = 0.82, 95% CI 0.57-1.08, p < 0.001; I = 0.0%, p = 0.90), E-selectin (SMD = 0.64, 95% CI 0.42-0.86, p < 0.001; I = 75.0%, p < 0.001), and P-selectin (SMD = 1.06, 95% CI 0.50-1.60, p < 0.001; I = 84.8%, p < 0.001), but not L-selectin. In meta-regression and subgroup analysis, significant associations were observed between the effect size and use of glucocorticoids (ICAM-1), erythrocyte sedimentation rate (VCAM-1), study continent (VCAM-1, E-selectin, and P-selectin), and matrix assessed (P-selectin).
CONCLUSIONS
The results of our study support a significant role of cell adhesion molecules in mediating the interplay between RA and atherosclerosis. Further studies are warranted to determine whether the routine use of these biomarkers can facilitate the detection and management of early atherosclerosis in this patient group. PROSPERO Registration Number: CRD42023466662.
Topics: Humans; Intercellular Adhesion Molecule-1; Vascular Cell Adhesion Molecule-1; Platelet Endothelial Cell Adhesion Molecule-1; E-Selectin; P-Selectin; Cell Adhesion Molecules; Arthritis, Rheumatoid; Biomarkers; Atherosclerosis
PubMed: 38240792
DOI: 10.1007/s00011-023-01837-6 -
Intensive Care Medicine Jun 2020Despite increasing improvement in extracorporeal membrane oxygenation (ECMO) technology and knowledge, thrombocytopenia and impaired platelet function are usual findings... (Meta-Analysis)
Meta-Analysis Review
Despite increasing improvement in extracorporeal membrane oxygenation (ECMO) technology and knowledge, thrombocytopenia and impaired platelet function are usual findings in ECMO patients and the underlying mechanisms are only partially elucidated. The purpose of this meta-analysis and systematic review was to thoroughly summarize and discuss the existing knowledge of platelet profile in adult ECMO population. All studies meeting the inclusion criteria (detailed data about platelet count and function) were selected, after screening literature from July 1975 to August 2019. Twenty-one studies from 1.742 abstracts were selected. The pooled prevalence of thrombocytopenia in ECMO patients was 21% (95% CI 12.9-29.0; 14 studies). Thrombocytopenia prevalence was 25.4% (95% CI 10.6-61.4; 4 studies) in veno-venous ECMO, whereas it was 23.2% (95% CI 11.8-34.5; 6 studies) in veno-arterial ECMO. Heparin-induced thrombocytopenia prevalence was 3.7% (95% CI 1.8-5.5; 12 studies). Meta-regression revealed no significant association between ECMO duration and thrombocytopenia. Platelet function impairment was described in 7 studies. Impaired aggregation was shown in 5 studies, whereas loss of platelet receptors was found in one trial, and platelet activation was described in 2 studies. Platelet transfusions were needed in up to 50% of the patients. Red blood cell transfusions were administered from 46 to 100% of the ECMO patients. Bleeding events varied from 16.6 to 50.7%, although the cause and type of haemorrhage was not consistently reported. Thrombocytopenia and platelet dysfunction are common in ECMO patients, regardless the type of ECMO mode. The underlying mechanisms are multifactorial, and understanding and management are still limited. Further research to design appropriate strategies and protocols for its monitoring, management, or prevention should be matter of thorough investigations.
Topics: Adult; Blood Platelets; Extracorporeal Membrane Oxygenation; Hemorrhage; Humans; Platelet Count; Thrombocytopenia
PubMed: 32328725
DOI: 10.1007/s00134-020-06031-4 -
Chinese Journal of Integrative Medicine Nov 2021To investigate the correlation of platelet and coagulation function with blood stasis syndrome (BSS) in coronary heart disease (CHD). (Meta-Analysis)
Meta-Analysis
OBJECTIVE
To investigate the correlation of platelet and coagulation function with blood stasis syndrome (BSS) in coronary heart disease (CHD).
METHODS
The protocol for this meta-analysis was registered on PROSPERO (CRD42019129452). PubMed, Excerpta Medica Database (Embase), the Cochrane Library, and China National Knowledge Infrastructure (CNKI) were searched from inception to 1st June, 2020. Trials were considered eligible if they enrolled BSS and non-BSS (NBSS) patients with CHD and provided information on platelet and coagulation function. The platelet function, coagulation function, and fibrinolytic activity were compared between the BSS and NBSS groups. Forest plots were generated to show the SMDs or ESs with corresponding 95% CIs for each study. Subgroup analysis and sensitivity analysis were performed to explore potential sources of heterogeneity.
RESULTS
The systematic search identified 1,583 articles. Thirty trials involving 10,323 patients were included in the meta-analysis. The results showed that mean platelet volume, platelet distribution width, platelet aggregation rate, platelet P selectin, fibrinogen, plasminogen activator inhibitor-1 (PAI-1), thromboxane B2 (TXB2), 6-keto-prostaglandin F1alpha (6-keto-PGF1 α), and TXB2/6-keto-PGF1 α were higher in the BSS group than in the NBSS group (P<0.05 or P<0.01). Activated partial thromboplastin time was lower in the BSS group than in the NBSS group in the acute phase of CHD (P<0.01). The R and K values in thromboelastography and tissue plasminogen activator (t-PA) and t-PA/PAI-1 were lower in the BSS group than in the NBSS group (all P<0.01). No difference was found in the results of platelet count, plateletcrit, maximum amplitude, von Willebrand factor, prothrombin time, thrombin time, international normalized ratio, etc. between groups.
CONCLUSIONS
Increased platelet function, hypercoagulability, and decreased fibrinolytic activity were found among CHD patients with BSS.
Topics: Blood Coagulation; Blood Platelets; Coronary Disease; Humans; Platelet Aggregation; Tissue Plasminogen Activator
PubMed: 34532747
DOI: 10.1007/s11655-021-2871-2 -
The World Journal of Biological... Jun 2020Neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR) and monocyte/lymphocyte ratio (MLR) are inexpensive and reproducible biomarkers of inflammation. This... (Meta-Analysis)
Meta-Analysis
Neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR) and monocyte/lymphocyte ratio (MLR) are inexpensive and reproducible biomarkers of inflammation. This is the first meta-analysis exploring the role of NLR, MLR and PLR in non-affective psychosis. Eight studies have been identified from the main electronic databases. Meta-analyses based on random-effects models have been carried out generating pooled standardised mean differences (SMDs) between non-affective psychotic patients and healthy controls (HCs). Subjects with non-affective psychosis had a significant higher NLR and MLR as compared with HC (respectively SMD = 0.715; < 0.001; =57.565% and SMD = 0.417; = 0.001; =65.754%), confirmed by heterogeneity-based sensitivity analysis. Subgroup analyses showed no differences in effect size across different study characteristics, including drug treatment status, diagnosis, and setting. Meta-regression showed that age influenced the relationship between non-affective psychosis and MLR. A trend of significance, not confirmed by heterogeneity-based sensitivity analysis, was observed in PLR with patients showing higher PLR than HC. Our meta-analysis supports the hypothesis that an inflammatory activation occurs in non-affective psychosis and inflammatory ratios, especially NLR and MLR, may be useful to detect this activation.
Topics: Blood Platelets; Humans; Lymphocytes; Monocytes; Neutrophils; Psychotic Disorders
PubMed: 30806142
DOI: 10.1080/15622975.2019.1583371 -
Seminars in Thrombosis and Hemostasis Jul 2022The microtubule inhibitor and anti-inflammatory agent colchicine is used to treat a range of conditions involving inflammasome activation in monocytes and neutrophils,...
The microtubule inhibitor and anti-inflammatory agent colchicine is used to treat a range of conditions involving inflammasome activation in monocytes and neutrophils, and is now known to prevent coronary and cerebrovascular events. In vitro studies dating back more than 50 years showed a direct effect of colchicine on platelets, but as little contemporary attention has been paid to this area, we have critically reviewed the effects of colchicine on diverse aspects of platelet biology in vitro and in vivo. In this systematic review we searched Embase, Medline, and PubMed for articles testing platelets after incubation with colchicine and/or reporting a clinical effect of colchicine treatment on platelet function, including only papers available in English and excluding reviews and conference abstracts. We identified 98 relevant articles and grouped their findings based on the type of study and platelet function test. In vitro, colchicine inhibits traditional platelet functions, including aggregation, clotting, degranulation, and platelet-derived extracellular vesicle formation, although many of these effects were reported at apparently supraphysiological concentrations. Physiological concentrations of colchicine inhibit collagen- and calcium ionophore-induced platelet aggregation and internal signaling. There have been limited studies of in vivo effects on platelets. The colchicine-platelet interaction has the potential to contribute to colchicine-mediated reduction in cardiovascular events, but there is a pressing need for high quality clinical research in this area.
Topics: Blood Platelets; Colchicine; Hemostasis; Humans; Platelet Aggregation; Platelet Function Tests
PubMed: 35882248
DOI: 10.1055/s-0042-1749660