thienopyridine and Arteriosclerosis

thienopyridine has been researched along with Arteriosclerosis* in 6 studies

Reviews

6 review(s) available for thienopyridine and Arteriosclerosis

ArticleYear
[Thienopyridines in the treatment and prevention of cardiovascular diseases. Part V. Combination of clopidogrel and acetylsalicylic acid in the treatment of stable patients with atherothrombotic cardiovascular diseases].
    Kardiologiia, 2010, Volume: 50, Issue:5

    In a series of articles the authors consider clinical pharmacology and experience of clinical application of blockers of platelet P2Y12 receptors, most well known representatives of which ticlopidine and clopidogrel according to chemical structure belong to thienopyridine derivatives. In the fifth communication we consider data of two randomized studies in which efficacy and safety of clopidogrel in combination with acetylsalicylic acid (ASA) has been assessed in comparison with ASA in stable patients with atherothrombotic cardiovascular disease. It has been shown in both studies that in stable patients with atherothrombotic cardiovascular disease long-term therapy with combination of clopidogrel and ASA was no more effective than monotherapy with ASA or clopidogrel but was associated with high risk of hemorrhagic complications. Thus contrary to acute coronary syndromes and percutaneous interventions with stenting combinations of clopidogrel and ASA is not indicated to patients with stable course cardiovascular diseases.

    Topics: Acute Coronary Syndrome; Angioplasty, Balloon, Coronary; Arteriosclerosis; Aspirin; Cardiovascular Diseases; Clopidogrel; Coronary Circulation; Death, Sudden, Cardiac; Drug Therapy, Combination; Fibrinolytic Agents; Hemorrhage; Humans; Middle Aged; Myocardial Infarction; Platelet Aggregation Inhibitors; Pyridines; Randomized Controlled Trials as Topic; Risk Factors; Sex Factors; Streptokinase; Stroke; Thrombosis; Ticlopidine; Time Factors

2010
[Update on antithrombotic treatments in arterial diseases].
    Revue medicale suisse, 2007, Feb-07, Volume: 3, Issue:97

    In most cases, arterial diseases are characterized by atherothrombosis causing organ or limb ischemia. Antithrombotic agents are a cornerstone in the therapeutic management of this pathology. Present approaches include anticoagulants and four types of antiplatelet drugs: aspirin, thienopyridines, dipyridamole and the anti-GPIIbIIIa molecules. Several questions are still pending, in particular concerning treatment tailoring according to clinical presentation and the duration of the antiplatelet treatment. This review focuses on the indications of the currently available antithrombotic agents in arterial diseases of atherothrombotic origin.

    Topics: Abciximab; Antibodies, Monoclonal; Anticoagulants; Arteriosclerosis; Aspirin; Dipyridamole; Eptifibatide; Humans; Immunoglobulin Fab Fragments; Peptides; Platelet Aggregation Inhibitors; Pyridines; Thrombosis; Tirofiban; Treatment Outcome; Tyrosine

2007
Clopidogrel and ticlopidine: P2Y12 adenosine diphosphate-receptor antagonists for the prevention of atherothrombosis.
    Seminars in thrombosis and hemostasis, 2005, Volume: 31, Issue:2

    Ticlopidine and clopidogrel belong to the same chemical family of thienopyridine adenosine diphosphate (ADP)-receptor antagonists. They have shown their efficacy as platelet antiaggregant and antithrombotic agents in many animal models, both ex vivo and in vivo. Although ticlopidine was discovered more than 30 years ago, it was only recently that the mechanism of action of ADP-receptor antagonists was characterized in detail. Ticlopidine and clopidogrel both behave in vivo as specific antagonists of P2Y (12), one of the ADP receptors on platelets. Metabolic steps that involve cytochrome P450-dependent pathways are required to generate the active metabolite responsible for this in vivo activity. The active moiety is a reactive thiol derivative that targets P2Y (12) on platelets. The interaction is irreversible, accounting for the observation that platelets are definitely antiaggregated, even if no active metabolite is detectable in plasma. The interaction is specific for P2Y (12); other purinoceptors such as P2Y (1) and P2Y (13) are spared. This results in inhibition of the binding of the P2Y (12) agonist 2-methylthio-ADP and the ADP-induced downregulation of adenylyl cyclase. Platelet aggregation is affected not only when triggered by ADP but also by aggregation inducers when used at concentrations requiring released ADP as an amplifier. The efficacy and safety of clopidogrel has been established in several large, randomized, controlled trials. The clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE) trial demonstrated the superiority of clopidogrel over acetylsalicylic acid (ASA) in patients at risk of ischemic events, including ischemic stroke, myocardial infarction (MI), and peripheral arterial disease. The clopidogrel in unstable angina to prevent recurrent ischemic events (CURE) trial showed a sustained, incremental benefit when clopidogrel was added to standard therapy (including ASA) in patients with unstable angina and non-Q-wave MI. The clopidogrel for the reduction of events during observation (CREDO) trial demonstrated the benefit of continuing clopidogrel (plus ASA) for 12 months, as opposed to 1 month, after percutaneous coronary intervention. The proven efficacy of clopidogrel, coupled with its favorable safety and tolerability profile, has prompted its evaluation in an extensive, ongoing clinical trial program that will help to further characterize the benefit of clopidogrel in patients with a range of atherothromboti

    Topics: Adenosine Diphosphate; Animals; Arteriosclerosis; Aspirin; Clinical Trials as Topic; Clopidogrel; Cohort Studies; Double-Blind Method; Drug Resistance; Fibrinolytic Agents; Forecasting; Humans; Membrane Proteins; Meta-Analysis as Topic; Platelet Aggregation; Platelet Aggregation Inhibitors; Purinergic P2 Receptor Antagonists; Pyridines; Randomized Controlled Trials as Topic; Rats; Receptors, Purinergic P2; Receptors, Purinergic P2Y12; Thrombophilia; Thrombosis; Ticlopidine

2005
Platelet ADP receptor antagonists: ticlopidine and clopidogrel.
    Best practice & research. Clinical haematology, 2004, Volume: 17, Issue:1

    The central role of platelets in the 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 gold standard of therapy and is effective in cerebral, coronary and peripheral arterial disease with a 25% reduction in myocardial infarction, stroke and vascular death. The platelet ADP receptor antagonists were developed to further improve the clinical results of therapy. Ticlopidine provides an additional 10% relative risk reduction over aspirin alone in stroke prevention and coronary stent placement. However, ticlopidine is accompanied by occasional life-threatening adverse hematological events. The action of clopidogrel is similar to that of ticlopidine, and it is comparably effective. However, the side-effect profile of clopidogrel is much more favorable.

    Topics: Arteriosclerosis; Clopidogrel; Humans; Platelet Aggregation Inhibitors; Purinergic P2 Receptor Antagonists; Pyridines; Ticlopidine; Treatment Outcome

2004
Clopidogrel's role in the management of atherosclerotic disease: a focus on acute coronary syndromes.
    Expert review of cardiovascular therapy, 2003, Volume: 1, Issue:4

    Recent advances in our understanding of the role of the platelet in the atherosclerotic process beyond the acute formation of arterial blood clots, such as inflammation, have highlighted the role of antiplatelet agents as being much more than just 'blood thinners.' Some of the most important cardiovascular trials performed in the last 20 years have studied antiplatelet therapies. However, despite their long history, current global health implications and proven benefit, there remain substantial gaps in our understanding as to how to best utilize the limited number of antiplatelet agents available. This article will discuss the mechanism of action of the antiplatelet class known as thienopyridines, the pharmacodynamics and pharmacokinetics of the thienopyridine agent clopidogrel (Plavix, Bristol-Myers Squibb and Sanofi Pharmaceuticals) as well as the literature supporting its clinical benefits and areas of ongoing research that will help clarify the optimal utilization of clopidogrel for the treatment of cardiovascular disease.

    Topics: Angina, Unstable; Angioplasty, Balloon, Coronary; Arteriosclerosis; Aspirin; Clinical Trials as Topic; Clopidogrel; Humans; Myocardial Infarction; Platelet Aggregation Inhibitors; Pyridines; Stents; Ticlopidine; Treatment Outcome; Vascular Diseases

2003
Platelets: is aspirin sufficient or must we know how to pronounce abciximab?
    Seminars in vascular surgery, 2002, Volume: 15, Issue:4

    Although vascular disease may present with symptoms that are representative of a focal exacerbation of atherosclerosis, it is inherently a systemic disease. Consequently, vascular surgeons must be capable of recommending to their patients pharmacologic approaches that will decrease future risk of cardiovascular-related morbidity and death. Antiplatelet treatments, in particular, have been shown to reduce future cerebrovascular and coronary events. Moreover, these medications have utility in maintaining peripheral vessel and graft patency after surgical bypass, endarterectomy, or percutaneous translumenal angioplasty. The future of optimal antiplatelet therapy will consist of strategies that block multiple platelet activation pathways simultaneously. Moreover, the use of directed antiplatelet medications promises more effective control of platelet physiology with a concomitant increase in safety. The authors review herein current recommendations for the use of aspirin, thienopyridines, and GP IIb/IIIa inhibitors in patients with peripheral vascular disease.

    Topics: Abciximab; Antibodies, Monoclonal; Arteriosclerosis; Aspirin; Blood Platelets; Clopidogrel; Endarterectomy, Carotid; Humans; Immunoglobulin Fab Fragments; Platelet Aggregation Inhibitors; Platelet Glycoprotein GPIIb-IIIa Complex; Pyridines; Ticlopidine; Tirofiban; Tyrosine

2002