Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large clinical studies have demonstrated an unequivocal clinical benefit of antithrombotic therapy with inhibitors of the platelet surface-membrane glycoprotein (GP) IIb-IIIa receptor in a broad range of patients with ischemic heart disease. Potent antiplatelet effects of these agents, however, may increase the risk of bleeding complications, as occurred in the first large evaluation of this therapy, the Evaluation of c7E3 for Prevention of Ischemic Complications (EPIC) trial with abciximab (c7E3 Fab; ReoPro((R)); Centocor, Malvern, Pa). Although the incidence of bleeding events in subsequent studies has been reduced through the use of a low-dose, weight-adjusted heparin regimen and early removal of vascular sheaths in patients who have undergone percutaneous coronary interventions, hemorrhage continues to be the most common complication of GP IIb-IIIa inhibitor therapy. This review summarizes current experience related to bleeding complications with various GP IIb-IIIa inhibitors and suggests strategies for improved management of bleeding in patients receiving these agents.
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PMID:Bleeding complications of glycoprotein IIb-IIIa receptor inhibitors. 1050 34

Platelet-mediated coronary thrombosis is the primary pathophysiologic mechanism of acute coronary syndromes (ACS) and acute ischemic complications of percutaneous coronary intervention (PCI). The final common pathway of platelet aggregation that leads to thrombotic occlusion of coronary arteries involves cross-linking of receptor glycoprotein (GP) IIb-IIIa on adjacent platelets by adhesive plasma proteins, primarily fibrinogen. Clinical trials of several GP IIb-IIIa inhibitors have demonstrated an unequivocal clinical benefit of this potent antithrombotic therapy in patients with ACS as well as in those undergoing PCI. Nevertheless, a significant number of patients with ischemic heart disease may still be expected to require elective or emergency coronary artery bypass graft (CABG) after treatment with GP IIb-IIIa inhibitors. In the emergency CABG setting, complications and platelet blockade with GP IIb-IIIa inhibitors may further enhance the already heightened risk of bleeding as compared with elective procedures. This issue became apparent in the first large clinical trial of the GP IIb-IIIa inhibitor abciximab (c7E3 Fab, ReoPro((R)); Centocor, Malvern, Pa, and Eli Lilly and Co, Indianapolis, Ind) in patients undergoing high-risk PCI. In this study, mortality rates and bleeding complications were increased among patients undergoing emergency CABG after treatment with a bolus plus infusion of abciximab. Subsequent clinical experience also suggests that the potential for bleeding complications related to emergency CABG may be increased in patients treated with abciximab, particularly if the drug is discontinued within 6 hours of the operation. Higher bleeding risk with abciximab is a result of its prolonged antiplatelet effect, which is in contrast to the readily reversible platelet blockade provided by more recently developed small-molecule GP IIb-IIIa inhibitors such as the peptide eptifibatide (Integrilin((R)); COR Therapeutics, South San Francisco, Calif, and Key Pharmaceuticals, Kenilworth, NJ) and the nonpeptide tirofiban HCl (MK-383, Aggrastat((R)); Merck & Co, Whitehouse Station, NJ). Therefore, among patients requiring CABG after treatment with GP IIb-IIIa inhibitors, eptifibatide and tirofiban may be associated with fewer bleeding episodes than is abciximab. With recent approval of eptifibatide for patients with ACS and those scheduled for PCI and of tirofiban for patients with ACS, the number of patients receiving GP IIb-IIIa inhibitor therapy who subsequently undergo CABG is expected to increase significantly. Strategies for improved management of bleeding complications in these patients, including the choice of a GP IIb-IIIa inhibitor, are clearly needed and are discussed in detail.
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PMID:Safety of glycoprotein IIb-IIIa inhibitors: A heart surgeon's perspective. 1050 36

Acute coronary syndromes and percutaneous coronary interventions share a common pathophysiological mechanism of intimal disruption and platelet aggregation. Glycoprotein (GP) IIb/IIIa receptor antagonists, which interrupt the final common pathway of platelet activation and aggregation, have been shown to have clear clinical benefit as acute therapy. Treatment of 1000 patients with parenteral formulations prevents at least 1 death, 20 deaths or myocardial infarctions (MIs), and 30 deaths, MIs or revascularisation procedures over a 30-day period. These benefits are sustained at 6 months. Clinical trials of oral formulations are underway. The challenges of dose, haemorrhage and thrombocytopenia must be surmounted before oral antagonists can be incorporated into clinical practice. Despite enrolment of thousands of patients in randomised trials of GPIIb/IIIa antagonists, much additional information is needed to refine the use of this therapy in practice. Application of this drug class will advance a new therapeutic standard for ischaemic heart disease.
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PMID:Glycoprotein IIb/IIIa receptor antagonists in non-ST elevation acute coronary syndromes and percutaneous revascularisation: a review of trial reports. 1055 33

The purpose of this manuscript is to review the available antagonists of platelet glycoprotein (GP) IIb/IIIa. The critical role of platelet aggregation in the pathogenesis of acute coronary syndromes of unstable angina and non-Q-wave myocardial infarction, as well as in mediating abrupt vessel closure and periprocedural infarction after percutaneous coronary interventions, has been recognised recently. Platelet aggregation is mediated through expression of activated GP IIb/IIIa and its subsequent binding to circulating fibrinogen. Inhibition of this interaction with one of 3 commercially available agents has been demonstrated to reduce ischaemic complications of coronary intervention and to reduce the rates of death and myocardial infarction in patients with acute coronary syndromes. Differential pharmacological characteristics of the drugs abciximab, tirofiban and eptifibatide are described and the trials which have defined their role in the management of ischaemic heart disease are reviewed.
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PMID:GP IIb/IIIa antagonists. Clinical experience and potential uses in cardiology. 1056 65

Ischemic mechanisms in pa2000Mar;58(1)1-10 studied for more than 150 years. Antiplatelet agents did show benefit in secondary prevention. Aspirin is the most common antiaggregant in clinical use today. However, the benefit produced by the "best" antiplatelet regimen in stroke prevention is lower than 40%. The adherence of circulating platelets to the subendothelium is mediated by glycoprotein (GP) residing on the cell's surface. GPIIb/IIIa is the most important platelet membrane receptor that mediates the process of platelet aggregation, and thrombus formation. Thus, new drugs that block the GPIIb/IIIa receptor have recently emerged. Clinical trials using these agents have shown effectiveness in acute coronary syndromes. However, the absence of studies in cerebrovascular disease and the potential hemorrhagic complications questioned their use in stroke prevention. We review the clinical trials using the new GPIIb/IIIa agents in myocardial ischemia, and consider the potential implications for cerebrovascular disease.
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PMID:Arteriosclerosis and the promise of GPIIb/IIIa inhibitors in stroke. 1077 Aug 59

Because anticoagulant and GP IIb/IIIa inhibitors reduce mortality, myocardial ischemia, AMI, and reintervention, these agents are now becoming the standard of care for patients with USA and NQWMI. Unanswered questions remain about the best treatment regimen, appropriate dosing, long-term benefit, and cost-effectiveness of these agents, however, and many additional trials are ongoing or planned. As nurses administer these drugs, assess the patients' responses to therapy, and educate patients and families about these agents, they contribute to recent advances in preventing ischemic heart disease.
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PMID:New adjunctive therapy for ischemic syndromes. 1078 82

Blockage of platelet glycoprotein IIb/IIIa receptor by Reopro (c7E3 Fab-abciximab) has been shown to reduce markedly ischemic complications during and following elective and high-risk coronary intervention (CI). Between July '96 and February '98, 120 consecutive patients (85 men and 34 women, aged 34-90--mean 62) received Reopro (20 mg bolus, followed by 10 micrograms/min for 12-48 hours). 100 were treated with Reopro in the catheterization laboratory, in 76 as prophylactic treatment preceding high-risk CI and in 24 as bailout treatment for acute complications during CI. 20 additional patients were treated in the CCU for acute coronary syndromes, 17 of whom underwent CI 6-48 hours later. Coronary angiography demonstrated multivessel disease in 66 (56%), and the target lesions were LAD--77, RCA--41, LCX--22, SVG--6, and 2 unprotected LMCA (total: 148 lesions dilated in 117 patients). Of the 117 CI, 44 were PTCA alone, and 73 included stenting. Indications for prophylactic Reopro for high risk CI were: acute MI (< or = 48 hours), early post-MI angina, unstable AP, and/or complex anatomy with visible thrombus. In this high-risk population the overall success rate (open artery, no MI, discharged alive, no need for urgent re-vascularization) was 97% when Reopro was given prophylactically prior to CI. The success rate was lower (87.5%) when Reopro was given in bailout situations. In 20 patients with acute coronary syndromes treated in the CCU while receiving maximal combined conventional therapy (including full-dose heparin), all symptoms and dynamic ischemic ECG changes disappeared within minutes following Reopro. 17 underwent successful CI during hospitalization and 3 were treated medically. Reopro given prior to high risk CI was associated with a very low rate of complications. In a few cases with acute coronary syndromes, Reopro given in the CCU cases immediate relief of myocardial ischemia and reduced the need for urgent coronary intervention.
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PMID:[Use of abciximab (Reopro) in the catheterization laboratory and in unstable coronary syndromes]. 1091 55

This paper up-dates the Clinical Guidelines for Unstable Angina/Non Q wave Myocardial Infarction of the Spanish Society of Cardiology. Due to the increased efficacy of adequate management in the early phases, it has been considered necessary to include recommendations for the pre Hospital and Emergency department phase. Prehospital management. Patients with thoracic pain compatible with myocardial ischemia should be transferred to Hospital as quickly as possible and an ECG tracing performed. Initial management includes rest, sublingual nitroglycerin and aspirin. In the Emergency department. Immediate clinical attention and accessibility to a defibrillator should be available. If ECG tracing discloses ST elevation reperfusion strategy is to be implemented immediately. If no ST elevation is present, the probability of myocardial ischemia and risk factor evaluation is essential for adequate management. A simplified risk stratification classification is presented, that also determines the most adequate site for admission: Coronary Care Unit if high risk factors are present, Cardiology ward for the intermediate risk patient and ambulatory treatment if low risk. Management in Coronary Care Unit. Includes routine ECG monitoring and analgesia. Antithrombotic and anti ischemic treatment include new indication for GP IIb-IIIa and Low molecular weight heparins. Coronary arteriography and revascularisation are recommended, if refractory or recurrent angina, left ventricles dysfunction or other complications are present. Management in the ward is based on adequate chronic medical treatment, risk stratification, and secondary prevention strategy. Coronary arteriography before discharge must be considered in the light of the result of non-invasive tests.
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PMID:[Clinical practice guidelines of the Spanish Society of Cardiology on unstable angina/infarction without ST elevation]. 1094 76

Advances in the understanding of acute coronary syndromes have occurred rapidly in the last 5 years and have dramatically changed the way patients are evaluated, diagnosed, and managed. Medical advances, such as antiplatelet and antithrombin agents and growing databases on interventional outcomes have created a new world of therapeutic options for the spectrum of ischemic heart disease. As more options become available, nurses are under increasing pressure to stay abreast of what these options have to offer patients, and which patients benefit most from each therapeutic approach. The purpose of this article is to review the newest therapies for acute coronary syndromes, including GP IIb/IIIa inhibitors, low molecular weight heparins, and direct thrombin inhibitors, and discuss indications and contraindications for each of these therapies. Changes in diagnostic approach using troponin T and I are also presented.
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PMID:New strategies in the management of acute coronary syndromes. 1107 76

Platelet fibrinogen receptor (GPIIb/IIIa) antagonists clinically improve the effectiveness of thrombolysis or PTCA in treatment of acute myocardial infarction. 7E3Fab, the chimeric Fab fragment of a monoclonal GPIIb/IIIa antibody, reduces the incidence of death, reinfarction or restenosis in patients and may improve blood flow and regional wall motion in reperfused myocardium. Besides inhibition of platelet aggregation, 7E3Fab may block fibrinogen bridging between the polymorphonuclear neutrophil (PMN) adhesion molecule MAC-1 and platelet GP IIb/IIIa, thus attenuating interaction of platelets with PMN. Experimentally, the interaction of platelets with PMN exacerbated postischemic myocardial stunning. In our own studies in isolated guinea pig hearts, human PMN, platelets and fibrinogen where simultaneously infused during the initial reperfusion period after 15 min of global ischemia. FACS analysis of cells in the coronary effluant revealed that 7E3Fab reduced platelet GP IIb/IIIa expression to 10% of baseline. PMN-platelet aggregate formation in the coronary effluate was markedly reduced by 7E3Fab, parallel to a decrease of PMN-platelet aggregates found by in situ double fluorescence microscopy in the postischemic coronary vasculature. The inhibition of PMN-platelet aggregate formation by 7E3Fab treatment coincided with a significant improvement of external heart work, which suffered a 50% reduction after ischemia, reperfusion, and exposure to PMN, platelets and fibrinogen. Obviously, application of 7E3Fab inhibits formation and coronary retention of PMN-platelet aggregates in the postischemic, reperfused myocardium. This effect may contribute to the clinically observed beneficial effects of this adjuvant treatment after myocardial ischemia.
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PMID:Effects of endothelium/leukocytes/platelet interaction on myocardial ischemia--reperfusion injury. 1115 4


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