Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We identified 1,369 consecutive patients who received glycoprotein IIb/IIIa inhibitors during 1,461 stenting procedures (2,382 lesions); of these, 240 (17.5%) were aged > or =75 years (253 procedures, 430 lesions). Very elderly patients (> or =75 years) had similar in-hospital outcomes but a higher hemorrhagic stroke rate than patients aged <75 years.
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PMID:Comparison of frequency of hemorrhagic stroke in patients <75 years versus > or =75 years of age among patients receiving glycoprotein IIb/IIIa inhibitors during percutaneous coronary interventions. 1475 88

Platelet activation and aggregation have become increasingly recognized as the primary processes involved in the cascade that leads to thrombus formation in atherosclerotic vascular disease. Glycoprotein IIb/IIIa receptor inhibitors (GPI) favorably impact thrombus formation and distal embolization by inhibiting the final common pathway of platelet aggregation. Glycoprotein IIb/IIIa inhibitors have been used effectively in a wide variety of clinical scenarios including unstable angina, non-ST segment elevation myocardial infarction, ST segment elevation myocardial infarction, and low and high risk percutaneous coronary interventions with and without intracoronary stenting, however there is limited data regarding the use of these potent antiplatelet agents in the setting of extracardiac vascular disease. This article will review the non-cardiac applications of glycoprotein IIb/IIIa inhibitors in the setting of acute ischemic stroke, carotid and vertebral angioplasty and stenting, acute critical limb ischemia, and percutaneous interventions in peripheral arterial occlusive disease.
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PMID:Noncardiac applications of glycoprotein IIb/IIIa inhibitors. 1527 67

The benefits of aspirin use in the emergent care of MI and stroke have been well established. Recent studies have further demonstrated the importance of antiplatelet therapy in the acute setting, primarily with the use of intravenous glycoprotein IIb/IIIa receptor inhibitors. Aspirin and the thienopyridines (ticlopidine and clopidogrel) are oral antiplatelet agents that interfere with platelet activation in complementary, but separate pathways. Combination therapy of clopidogrel and aspirin has demonstrated benefit for the management of acute coronary syndromes, ischemic cerebrovascular disease and peripheral vascular disease in several large trials. This article reviews the pathophysiology of platelet activation, landmark trials on oral antiplatelet agents, and the current recommendation for the use of oral antiplatelet agents in the emergency department.
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PMID:Facilitating optimal care of acute coronary, cerebrovascular and peripheral vascular syndromes in the emergency department: the role of oral antiplatelet therapy. 1527 85

Platelet aggregation plays an important role in pathological situations such as myocardial infarction, unstable angina, peripheral artery disease, and stroke. Thus, pharmacological agents that specifically inhibit platelet aggregation are of great interest in the treatment and prevention of these cardiovascular diseases. Since binding of activated glycoprotein IIb/IIIa complex, a platelet surface integrin, to fibrinogen is the final step leading to platelet aggregation regardless of the initial stimulus, many researches have focused on the development of drugs that could antagonize this integrin. Three intravenous glycoprotein IIb/IIIa antagonists are currently marketed for the prevention of myocardial infarction in patients undergoing percutaneous intervention: Abciximab, Eptifibatide and Tirofiban. To further test the clinical efficacy of these agents, oral glycoprotein IIb/IIIa antagonists have been developed but only led to disappointing clinical results. Nevertheless, due to recognized usefulness of oral agents for the prevention and treatment of cardiovascular diseases, a great number of new orally active compounds are under clinical or preclinical evaluation. The aim of this review is to describe the chemical, pharmacological and clinical properties of existing and forthcoming glycoprotein IIb/IIIa antagonists.
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PMID:Progress in the field of GPIIb/IIIa antagonists. 1532 Jul 98

We compared the antithrombotic efficacy of FK419 [(S)-2-acetylamino-3-[(R)-[1-[3-(piperidin-4-yl)propionyl]piperidin-3-ylcarbonyl]amino] propionic acid trihydrate], a novel nonpeptide glycoprotein IIb/IIIa antagonist, with recombinant tissue plasminogen activator (rt-PA) and other antithrombotic agents (aspirin, ozagrel, argatroban and heparin). FK419 not only inhibited ADP- and collagen-induced guinea pig platelet aggregation, but also induced disaggregation for ADP-induced aggregated platelets in vitro. In the photochemically induced middle cerebral artery thrombosis model in guinea pigs, FK419 dose-dependently shortened the time to first reperfusion and the total middle cerebral artery occlusion time and reduced ischemic brain damage and ameliorated neurological deficits measured 24 h after middle cerebral artery occlusion. Rt-PA similarly improved the middle cerebral artery patency, brain damage and neurological deficits. Neither aspirin, ozagrel, argatroban nor heparin restored the middle cerebral artery blood flow and improved the brain damage or neurological deficits. These results demonstrated that novel glycoprotein IIb/IIIa antagonist FK419 could disperse thrombus and ameliorated ischemic brain damage, suggesting that FK419 would be an attractive intervention for stroke patients.
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PMID:Restoration of middle cerebral artery thrombosis by novel glycoprotein IIb/IIIa antagonist FK419 in guinea pig. 1536 93

The European Stroke Prevention Study showed greater stroke prevention for Aggrenox than either for aspirin or dipyridamole alone. To test whether Aggrenox has superior antiplatelet properties to aspirin alone we conducted the AGgrenox versus Aspirin Therapy Evaluation (AGATE) trial. Forty patients with prior ischemic stroke not taking aspirin for at least 30 days were randomized to Aggrenox (2 pills/daily) or aspirin (81 mg plus matching placebo/daily) for 30 days. Platelet function was assessed at baseline, 24 h, and days 3, 7, 15, and 30 by aggregometry, flow cytometry and cartridge-based analyzers. Both Aggrenox and aspirin provided fast and sustained platelet inhibition. Aggrenox(R), however, especially after 15 days, showed significant prolongation of the closure time (P=0.04), diminished expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1) (P=0.01), glycoprotein IIb (GPIIb) antigen (P=0.02), and GPIIb/IIIa activity (P=0.01) by PAC-1 C antibody, CD63 (P=0.03), as well as inhibition of Protease Activated Receptors (PAR-1) associated with intact (SPAN12, P=0.01) and cleaved (WEDE15, P=0.01) thrombin receptors as compared with aspirin. Surprisingly, GPIb expression increased, especially after aspirin. In the randomized trial of small sample size, aspirin and Aggrenox produced fast and sustained platelet inhibition. In 25 of 90 direct comparisons, Aggrenox was superior to aspirin, whereas in 4 of 90, aspirin was superior to Aggrenox. In 61 of 90 direct comparisons, aspirin and Aggrenox were equivalent. Aggrenox was associated with a profound reduction of PAR-1 receptors, an observation that may be related to the greater clinical benefit of Aggrenox compared with Aspirin in preventing recurrent stroke.
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PMID:Magnitude and time course of platelet inhibition with Aggrenox and Aspirin in patients after ischemic stroke: the AGgrenox versus Aspirin Therapy Evaluation (AGATE) trial. 1538 Oct 54

The acute coronary syndromes (ACS), consisting of ST-segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), and unstable angina, remain a leading cause of death in the United States. Through the process of atherothrombosis, underlying atherosclerosis can progress to an acute ischemic coronary event. This disease mechanism is also common to ischemic stroke and peripheral arterial disease. As ACS is a heterogeneous disease, accurate patient diagnosis and risk categorization is essential. Treatment approaches for both STEMI and NSTEMI ACS consist of a combination of surgical intervention and pharmacotherapy, with antiplatelet agents such as clopidogrel, aspirin and glycoprotein IIb/IIIa receptor antagonists playing an essential role.
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PMID:Role of antiplatelet therapy in cardiovascular disease I: Acute coronary syndromes. 1553 83

Coronary heart disease is the number one cause of death in the world and acute coronary syndromes (ACS) continue to be associated with high rates of morbidity. ACS refers to the spectrum of acute myocardial ischemia, including unstable angina, ST segment elevation myocardial infarction (STEMI), and acute MI without ST segment elevation (NSTEMI). Current guidelines indicate both aspirin and glycoprotein IIb/IIIa receptor antagonists (if catheterization/revascularization are planned) as class IA recommendations in ACS. Anticoagulant therapy, in the form of heparin, is a class IA recommendation for the acute hospital phase of ACS. The risk of recurrent thrombotic events following ACS remains high in the post-hospital phase, creating a rationale for the use of oral direct thrombin inhibitors such as ximelagatran, in both the acute and long-term settings. The Efficacy and Safety of the Oral Direct Thrombin Inhibitor Ximelagatran in Patients with Recent and Myocardial Damage (ESTEEM) trial, a placebo-controlled, double-blind study of post-MI patients, evaluated 4 dosing regimens of ximelagatran versus placebo in the initial months following an ACS and found an encouraging reduction in the end points of death, MI, and stroke with the use of an oral direct thrombin inhibitor.
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PMID:Reducing cardiac events after acute coronary syndromes. 1561 14

The optimal reperfusion strategy in elderly patients with ST-segment elevation myocardial infarction (STEMI) remains a topic of debate. This lack of consensus stems from the exclusion or under-representation of the elderly in clinical trials. This review evaluates the available literature pertaining to reperfusion therapy for the treatment of STEMI in the elderly. We identified all published studies evaluating the effectiveness of thrombolytic therapy, primary percutaneous coronary intervention (PCI), or adjunctive therapies to reperfusion by conducting an electronic search of MEDLINE through December 2003. Meta-analysis of clinical trials suggests a survival benefit of thrombolytic therapy in the elderly with STEMI, whereas some observational studies have raised concerns about the lack of short-term benefit or possibility of harm with thrombolysis. However, most observational studies demonstrate improved intermediate-term survival with thrombolysis. In contrast, multiple clinical trials and observational studies indicate improved survival and low risk of stroke with primary PCI compared with thrombolysis in elderly patients with STEMI. Information on the efficacy of newer antithrombotic agents as adjunct to thrombolysis or primary PCI is scarce. Available data suggest an increased risk of intracerebral bleeding with the combination of a fibrin-specific agent and a glycoprotein IIb/IIIa receptor antagonist in patients >75 years of age. Clearly targeted large-scale clinical trials are needed to evaluate the relative merits of available reperfusion strategies as well as newer antithrombotic adjunctive therapies in the elderly with STEMI.
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PMID:Reperfusion strategies for acute myocardial infarction in the elderly: benefits and risks. 1570 88

Distal embolization is the main potential risk of carotid stenting, and techniques to minimize this risk are evolving. Between July 1998 and March 2002, 305 consecutive patients who underwent elective or urgent percutaneous carotid intervention at The Cleveland Clinic were prospectively followed. During this period, the clinical practice of carotid stenting evolved from the routine use of glycoprotein IIb/IIIa inhibitors (GPIs) to routine emboli-prevention device (EPD) placement. A total of 199 patients received adjunctive GPIs (91% abciximab), and 106 patients underwent the procedure with an EPD (85% filter design, 15% occlusive balloon). At 30 days, the composite end point of neurologic death, nonfatal stroke, and major bleeding, including intracranial hemorrhage, was significantly lower among patients treated with EPDs compared with those treated with GPIs (0% vs 5.1%, p = 0.02). EPDs may provide an overall safer and more effective means of neuroprotection during carotid stenting than GPIs.
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PMID:Comparison of the safety and efficacy of emboli prevention devices versus platelet glycoprotein IIb/IIIa inhibition during carotid stenting. 1575 16


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