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Proteins Involved in Platelet Signaling Are Differentially Regulated in Acute Coronary Syndrome: A Proteomic Study  [PDF]
Andrés Fernández Pargui?a,Lilian Grigorian-Shamajian,Rosa M. Agra,Elvis Teijeira-Fernández,Isaac Rosa,Jana Alonso,Juan E. Vi?uela-Roldán,Ana Seoane,José Ramón González-Juanatey,ángel García
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013404
Abstract: Platelets play a fundamental role in pathological events underlying acute coronary syndrome (ACS). Because platelets do not have a nucleus, proteomics constitutes an optimal approach to follow platelet molecular events associated with the onset of the acute episode.
Platelet GP IIb/IIIa Receptor Inhibition by Eptifibatide in non ST-elevation MI-Acute Coronary Syndrome
M Momtahen,S Abdi,F Javadzadeh,BF Farsad
Iranian Cardiovascular Research Journal , 2009,
Abstract: Background: Recent trials of platelet glycoprotein IIb/IIIa receptor inhibitors have improved our understandingto best use these powerful antiplatelet drugs in acute coronary syndrome. We tested the hypothesis that inhibitionof GPIIb/IIIa platelet receptor with Eptifibatide is effective as an empiric therapy in patients with acute coronarysyndrome who do not necessarily undergo immediate revascularization.Methods: Since Feb 2006 one hundred and ninety-six patients who had presented with non ST-elevation acutecoronary syndrome (NSTE-ACS) were randomly assigned to receive Eptifibatide in addition to standard therapy,for up to 72 hours or routine standard therapy. The primary end point was composite of death and non-fatalmyocardial infarction (MI) or urgent target vessel revascularization (TVR) in 30 days.Results: The incidence of composite end point of death, non fatal MI and urgent TVR was significantly lower inEptifibatide group than standard group (16% vs. 0% - P value <0.01),particularly in troponin positive subgroupof patients (27.8% vs. 0% - P value <0.01).Any major adverse reaction such as major bleeding, stroke, or thrombocytopenia was not seen.Conclusion: Early administration of GP IIb/IIIa receptor inhibitor is recommended in patients with high-riskacute coronary syndrome.
IL-17A Facilitates Platelet Function through the ERK2 Signaling Pathway in Patients with Acute Coronary Syndrome  [PDF]
Shuang Zhang, Jing Yuan, Miao Yu, Hong Fan, Zhang-Qiang Guo, Rui Yang, He-Ping Guo, Yu-Hua Liao, Min Wang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040641
Abstract: Background Platelet aggregation mediated by inflammation played a critical role in the development of coronary heart diseases (CHD). Our previous clinical researches showed that Th17 cells and their characteristic cytokine IL-17A were associated with the plaque destabilization in patients with acute coronary syndrome (ACS). However, the potent effect of IL-17A on platelets-induced atherothrombosis remains unknown. Methods and Results In this study, we detected the plasma IL-17A levels and platelet aggregation in patients with stable angina (SA), unstable angina (UA), acute myocardial infarction (AMI) and chest pain syndrome (CPS). In addition, the markers of platelet activation (CD62P/PAC-1) and the mitogen-activated protein kinases (MAPKs) pathway were detected in platelets from ACS patients. We found that plasma IL-17A levels and platelet aggregation in patients with ACS (UA and AMI) were significantly higher than patients with SA and CPS, and the plasma IL-17A levels were positively correlated with the platelet aggregation (R = 0.47, P<0.01). In addition, in patients with ACS, the platelet aggregation, CD62P/PAC-1 and the phosphorylation of ERK2 signaling pathway were obviously elevated in platelets pre-stimulated with IL-17A in vitro. Furthermore, the specific inhibitor of ERK2 could attenuate platelet aggregation and activation triggered by IL-17A. Conclusion Our experiment firstly proved that IL-17A could promote platelet function in patients with ACS via activating platelets ERK2 signaling pathway and may provide a novel target for antiplatelet therapies in CHD.
Balancing Potency of Platelet Inhibition with Bleeding Risk in the Early Treatment of Acute Coronary Syndrome  [cached]
Slattery, David E,Pollack, Charles V
Western Journal of Emergency Medicine : Integrating Emergency Care with Population Health , 2009,
Abstract: Objective: To review available evidence and examine issues surrounding the use of advanced antiplatelet therapy in an effort to provide a practical guide for emergency physicians caring for patients with acute coronary syndromes (ACS).Data Sources: American College of Cardiology/American Heart Association (ACC/AHA) 2007 guidelines for the management of patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI), AHA/ACC 2007 focused update for the management of patients with STEMI, selected clinical articles identified through the PubMed database (1965-February 2008), and manual searches for relevant articles identified from those retrieved.Study Selection: English-language controlled studies and randomized clinical trials that assessed the efficacy and safety of antiplatelet therapy in treating patients with all ACS manifestations.Data Extraction and Synthesis: Clinical data, including treatment regimens and patient demographics and outcomes, were extracted and critically analyzed from the selected studies and clinical trials. Pertinent data from relevant patient registries were also evaluated to assess current clinical practice.Conclusions: As platelet activation and aggregation are central to ACS pathology, antiplatelet agents are critical to early treatment. A widely accepted first-line treatment is aspirin, which acts to decrease platelet activation via inhibition of thromboxane A2 synthesis. Thienopyridines, which inhibit ADP-induced platelet activation, and glycoprotein (GP) receptor antagonists, which bind to platelet GP IIb/IIIa receptors and hinder their role in platelet aggregation and thrombus formation, provide complementary mechanisms of platelet inhibition and are often employed in combination with aspirin. While the higher levels of platelet inhibition that accompany combination therapy improve protection against ischemic and peri-procedural events, the risk of bleeding is also increased. Thus, the challenge in choosing appropriate therapy in the emergency department lies in balancing the need for potent platelet inhibition with the potential for increased risk of bleeding and future interventions the patient is likely to receive during the index hospitalization.[WestJEM. 2009;10:163-175.]
Is Any Correlation between Platelet Indices with Extent of Coronary Artery Involvement in Ischemic Heart Diseases?  [PDF]
Mohammad Hassan Adel, Masood Seyedian, Marjan Jafarsalehi, Mohammad Hossein Najafi, Mohammad Nourizadeh, Mehdi Mohebi, Sara Nourizadeh
Health (Health) , 2016, DOI: 10.4236/health.2016.812129
Abstract: Ischemic heart disease (IHD) is the most common cause of death around the world. Nowadays Platelet counts (PC) and volumetric platelet indices are available routinely in most laboratories and reflect the level of mobility and production of platelets. It seems that the excessive flexibility and size of the platelets and their local activation have correlation with extent of ischemic heart disease. So our objective is the study of platelet indices in ischemic heart disease. This non-randomized prospective study was performed on 245 patients with ischemic heart disease, who underwent the coronary angiography. The patients were divided into four groups: stable angina, unstable angina, acute myocardial infarction and control group; and then platelet indices, including the platelet counts (PC), the average platelet volume (MPV), the Platelet Distribution Width (PDW) and plateletcrit (PCT) in each group with the extent of coronary disease were compared based on an Syntax Score system and observational methods. The average ages of the patients were 57 years and 65% of them were male and the rest were female. A significant difference is exists between indices in all three groups compared to the control that this difference was related to gender and the type of the coronary artery involvement. However, only in infarction group, PDW in different disease intensities was significantly different. In this study, unlike many of the previous studies no relationship was found between the MPV with the extent of coronary disease.
急性冠脉综合征患者血清miRNA-208与血小板功能的关系*
Relationship between serum miRNA-208 and platelet function in patients with acute coronary syndrome
 [PDF]

,,,,张丽华,简立国,孙利强,牛少辉
- , 2017, DOI: 10.13705/j.issn.1671-6825.2017.02.020
Abstract: 目的:探讨急性冠脉综合征(ACS)患者血清miRNA-208与血小板功能的关系。方法:选取2014年1月至2015年9月郑州大学第二附属医院收治的ACS患者60例(ACS组)和非ACS患者20例(对照组),根据诊断结果将ACS组进一步分为心肌梗死组(n=32)和不稳定心绞痛组(n=28)。入院即刻对3组患者进行静脉血液采集,测定血小板计数(PLT)、血小板分布宽度(PDW)及平均血小板体积(MPV); 利用实时荧光定量PCR法测定血清miRNA-208。结果:与对照组比较,心肌梗死组和不稳定心绞痛组血清miRNA-208、PDW、MPV升高,差异有统计学意义(P<0.05)。与不稳定心绞痛组比较,心肌梗死组血清miRNA-208、PDW、MPV升高,差异有统计学意义(P<0.05)。ACS患者血清miRNA-208与PDW和MPV呈正相关(r=0.828、0.766,P<0.05)。结论:ACS患者血清miRNA-208与血小板活化密切相关, miRNA-208参与了血小板活化的调控。
Aim: To investigate the relationship between serum miRNA-208 and platelet function in patients with acute coronary syndrome(ACS).Methods: A total of 60 cases of ACS(ACS group)and 20 cases of non-ACS(control group)were collected,and the ACS group was further allocated into myocardial infarction group(AMI group, n=32)and unstable angina pectoris group(UA group, n=28). Platelet(PLT), platelet distribution width(PDW)and mean platelet volume(MPV)were measured. The serum miRNA-208 was measured by real-time fluorescence quantitative PCR method.Results: Compared with control group, the serum level of miRNA-208, PDW and MPV were significantly higher in the AMI group and the UA group(P<0.05).Compared with the UA group, the serum level of miRNA-208, PDW, MPV were significantly higher in the AMI group(P<0.05). In patients with ACS, the serum level of miRNA-208 was correlated with PDW and MPV(r=0.828,0.766,P<0.05).Conclusion: miRNA-208 is closely related to platelet activation and involves in the regulation of platelet activation in patients with ACS
Anticoagulants in acute coronary syndrome  [cached]
I.A. Latfullin,A.A. Podolskaya
Rational Pharmacotherapy in Cardiology , 2009,
Abstract: Clinical efficacy of unfractionated and low molecular heparins in acute coronary syndrome is discussed. New synthetic heparin derivative fondaparinux (Arixtra) is focused. Author’s brief experience of fondaparinux clinical implementation is presented.
Prasugrel for the treatment of patients with acute coronary syndrome
Filippo Marzot, Vittorio Pengo
Vascular Health and Risk Management , 2009, DOI: http://dx.doi.org/10.2147/VHRM.S3428
Abstract: asugrel for the treatment of patients with acute coronary syndrome Review (5032) Total Article Views Authors: Filippo Marzot, Vittorio Pengo Published Date April 2009 Volume 2009:5 Pages 321 - 324 DOI: http://dx.doi.org/10.2147/VHRM.S3428 Filippo Marzot, Vittorio Pengo Clinical Cardiology, Thrombosis Centre, University of Padua, Italy Abstract: Prasugrel (CS-747, LY640315) is a novel member of the thienopyridine class of oral anti-platelet agents (also including ticlopidine and clopidogrel). Like other thienopyridines, prasugrel is a prodrug that is inactive in vitro. Prasugrel’s conversion to its active metabolite is more rapid and efficient than that of other thienopyridines, with a less strict dependence on specific cytochrome P-450 enzymes. Prasugrel’s active metabolite (R-138727) binds specifically and irreversibly to the platelet P2Y12 purinergic receptor, thus inhibiting ADP-mediated platelet activation and aggregation. Preclinical data and early clinical data in healthy subjects showed greater platelet inhibition and consistency with prasugrel as opposed to clopidogrel. Clinical studies in patients with cardiovascular disease confirmed the greater efficacy of prasugrel compared with clopidogrel. Collectively, these phase 1/1b studies and a phase 2 study (JUMBO-TIMI 26) aided in dose selection for the phase 3 trial (TRITONTIMI 38) in patients with acute coronary syndrome undergoing percutaneous coronary intervention. This trial once again confirmed the greater anti-platelet effect of prasugrel, but also highlighted a higher risk of bleeding, even fatal. Another phase 2 trial (PRINCIPLE-TIMI 44) compared prasugrel and high-dose clopidogrel in patients undergoing cardiac catheterization for planned PCI.
Prasugrel for the treatment of patients with acute coronary syndrome  [cached]
Filippo Marzot,Vittorio Pengo
Vascular Health and Risk Management , 2009,
Abstract: Filippo Marzot, Vittorio PengoClinical Cardiology, Thrombosis Centre, University of Padua, ItalyAbstract: Prasugrel (CS-747, LY640315) is a novel member of the thienopyridine class of oral anti-platelet agents (also including ticlopidine and clopidogrel). Like other thienopyridines, prasugrel is a prodrug that is inactive in vitro. Prasugrel’s conversion to its active metabolite is more rapid and efficient than that of other thienopyridines, with a less strict dependence on specific cytochrome P-450 enzymes. Prasugrel’s active metabolite (R-138727) binds specifically and irreversibly to the platelet P2Y12 purinergic receptor, thus inhibiting ADP-mediated platelet activation and aggregation. Preclinical data and early clinical data in healthy subjects showed greater platelet inhibition and consistency with prasugrel as opposed to clopidogrel. Clinical studies in patients with cardiovascular disease confirmed the greater efficacy of prasugrel compared with clopidogrel. Collectively, these phase 1/1b studies and a phase 2 study (JUMBO-TIMI 26) aided in dose selection for the phase 3 trial (TRITONTIMI 38) in patients with acute coronary syndrome undergoing percutaneous coronary intervention. This trial once again confirmed the greater anti-platelet effect of prasugrel, but also highlighted a higher risk of bleeding, even fatal. Another phase 2 trial (PRINCIPLE-TIMI 44) compared prasugrel and high-dose clopidogrel in patients undergoing cardiac catheterization for planned PCI.Keywords: prasugrel, oral antiplatelet agents, acute coronary syndrome
Percutaneous coronary intervention in patients with acute coronary syndrome: focus on bivalirudin  [cached]
Ravi K Ramana,Bruce E Lewis
Vascular Health and Risk Management , 2008,
Abstract: Ravi K Ramana, Bruce E LewisDivision of Cardiology, Loyola University Medical Center, Maywood, Illinois, USAAbstract: Previously, indirect thrombin inhibitors such as unfractionated heparin or low-molecular-weight heparin were used as a standard anticoagulation during percutaneous coronary intervention to prevent procedural thrombotic complications but at a risk of hemorrhagic complications. More recently, bivalirudin, a member of the direct thrombin inhibitor class, has been shown to have 1) predictable pharmacokinetics, 2) ability to inhibit free- and clot-bound thrombin, 3) no properties of platelet activation, 4) avoidance of heparin-induced thrombocytopenia, and 5) a significant reduction of bleeding without a reduction in thrombotic or ischemic endpoints compared to heparin and glycoprotein IIbIIIa inhibitors when used in patients presenting with acute coronary syndrome who are planned for an invasive treatment strategy.Keywords: bivalirudin, coronary intervention, direct thrombin inhibitor, acute coronary syndrome
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