Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The era of platelet glycoprotein (GP) IIb/IIIa receptor inhibition in cardiology was inaugurated in 1994 with the publication of the Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC) trial results. EPIC demonstrated that the GP IIb/IIIa blocker abciximab, administered as a bolus and 12-hour infusion, afforded protection against ischemic complications in high-risk patients undergoing angioplasty and atherectomy, including those with unstable angina or evolving myocardial infarction (MI). A significant reduction in the incidence of death, acute MI, or revascularization was apparent at 30 days and also sustained at 6-month and 3-year follow-up. The subsequent Evaluation in PTCA to Improve Long-Term Outcome with Abciximab GP IIb/IIIa Blockade (EPILOG) study extended these findings to the full spectrum of coronary intervention patients, confirming that abciximab provided similar benefits in low-risk patients as well. The EPILOG trial also proved that any excess bleeding risk associated with potent antiplatelet therapy could be brought down to placebo levels through the use of a low-dose, weight-adjusted heparin regimen, early vascular sheath removal, and elimination of routine postprocedural heparinization. The potential for an advantage of GP IIb/IIIa blockade in patients with refractory unstable angina/non-Q-wave MI was demonstrated in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial, which showed that a 24-hour preprocedural abciximab infusion effectively stabilized these patients, thereby enhancing the safety of intervention and reducing the 30-day incidence of ischemic events. A similar pattern of benefit has emerged from clinical trials of such other GP IIb/IIIa inhibitors as eptifibatide, lamifiban, and tirofiban. Trials are currently underway to clarify the benefits of GP IIb/IIIa blockers in patients undergoing stenting and as an adjunct to thrombolytic therapy or primary angioplasty in patients with acute MI (ST-segment elevation).
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PMID:An overview of the results of clinical trials with glycoprotein IIb/IIIa inhibitors. 959 18

Myocardial infarction results from a platelet-rich occlusive coronary thrombus. Platelet membrane glycoprotein IIb/IIIa plays an important role in platelet adhesion and aggregation. Two polymorphisms of the gene encoding the IIIa subunit. PLA1 and PLA2, have been identified. We investigated the frequency of these polymorphisms in 114 consecutive patients with a history of angina-like chest pain admitted for coronary arteriography. Forty-three of these patients had previously suffered a myocardial infarction. The PLA2 polymorphism was found in 21% of the patients with previous myocardial infarction and in 27% of the patients with angina-like chest pain but no previous myocardial infarction (p = 0.634). There was also no significant association with the extent of coronary disease. There is no evidence, therefore, from this study of an association between the PLA polymorphisms and the occurrence of myocardial infarction.
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PMID:Coronary thrombosis and the platelet glycoprotein IIIA gene PLA2 polymorphism. 971 40

In the management of unstable angina and non-Q-wave acute myocardial infarction (AMI), there is considerable debate regarding the use of invasive strategy versus conservative strategy. The Thrombolysis In Myocardial Infarction (TIMI) III B trial found similar clinical outcomes for the 2 strategies, but the Veterans Administration Non-Q-Wave Infarction Strategies in-Hospital trial found a higher mortality with the invasive strategy. Both these trials were conducted before platelet glycoprotein IIb/IIIa inhibition and coronary stenting, both of which improve clinical outcome. Thus, there is a need to reexamine the question of which management strategy is optimal in the current era of platelet glycoprotein IIb/IIIa inhibition and new coronary interventions. The Treat Angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy (TACTICS-TIMI 18) trial is an international, multicenter, randomized trial that is evaluating the clinical efficacy of early invasive and early conservative treatment strategies in patients with unstable angina or non-Q-wave AMI treated with tirofiban, heparin, and aspirin. Patients are randomized to an invasive strategy, involving cardiac catheterization within 4 to 48 hours and revascularization with angioplasty or bypass surgery if feasible, versus a conservative strategy, where patients are referred for catheterization only for recurrent pain at rest or provokable ischemia. The primary end point is death, MI, or rehospitalization for acute coronary syndromes through a 6-month follow-up. The trial is also testing the "troponin hypothesis," that baseline troponins T and I will be useful in selecting an optimal management strategy.
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PMID:Invasive versus conservative strategies in unstable angina and non-Q-wave myocardial infarction following treatment with tirofiban: rationale and study design of the international TACTICS-TIMI 18 Trial. Treat Angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy. Thrombolysis In Myocardial Infarction. 976 Oct 82

A review of the most important findings published during 1997 in cardiovascular papers is presented: Chlamydia pneumoniae was recognised as a potential risk factor for coronary artery disease (CAD) and possible pathogenic agent for valvular aortic stenosis. Valvular changes similar to the valvular disease reported after ergotamine and methylsergide were also detected in obese women treated with a combination of phentermine and fenfluramine. In CAD, several new laboratory methods were introduced for early diagnosis, such as serum troponin levels, and arbutamine and adenosine stress echocardiography. Laser transmyocardial revascularisation can be performed in patients unsuitable for PTCA and CABG. In patients with end-stage heart failure, implantable ventricular-assist devices can be used, and dynamic cardiomyoplasty or partial ventriculectomy may be useful temporary measures until a suitable heart donor is available. In pharmacotherapy, fluvastatin was registered as an antiatherosclerotic agent, and mibefradil and moxonidin in hypertension and angina. Digoxin was shown to reduce the number of hospitalisations in patients with CHF but still in sinus rhythm. In the future, several improvements in anti-thrombotic therapy are expected: antithrombins, platelet glycoprotein IIb/IIIa receptor blockers and tissue factor inhibitors are all potentially more potent than presently available drugs. Also, efforts are under way to introduce genes directly into the cells of the vascular wall to prevent atherosclerosis and restenosis, as well as to transform cardiac mesenchymal cells into the cardiac myocytes of hearts that have suffered large infarctions.
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PMID:[Cardiology in 1997]. 981 70

Antithrombotic therapy is a basic part in the treatment of acute as well as chronic coronary syndromes. The rationale is an enhanced platelet activity with predomination of procoagulatory mechanisms in coronary artery disease. The current status of antiplatelet drugs, anticoagulation, and chronic thrombolysis used in the treatment of chronic coronary syndromes is discussed. It is concluded that low-dose aspirin is the current drug of choice for long term oral treatment in patients with stable chronic coronary artery disease. In contrast, oral anticoagulation with coumadin should be considered in patients with higher risk for atrial or ventricular thrombosis. The impact of long-term intermittent urokinase therapy in patients with end-stage coronary artery disease and refractory angina pectoris leads to a marked improvement of clinical symptoms. Oral blockade of platelet membrane glycoprotein IIb/IIIa receptor and clinical trials regarding antiischemic effects of low-molecular weight heparins in chronic coronary syndromes are expected for the future.
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PMID:[Antithrombotic therapy in chronic coronary syndromes--value of thrombocyte aggregation inhibition, anticoagulation and chronic thrombolysis]. 982 73

Platelet membrane glycoproteins play a crucial role in ischemic complications after coronary stenting. Glycoprotein IIb-IIIa blockade reduces adverse clinical events after angioplasty but is associated with rare but profound thrombocytopenia that might increase hemorrhagic complications. Changes in platelet membrane glycoproteins of patients with angina who underwent coronary stenting and were treated with the GPIIb-IIIa antagonist abciximab (n=20) or with heparin (n=23) were studied. GPIb-IIIa receptor blockade and membrane glycoproteins were evaluated with immunological markers in venous blood samples taken before. 10, 24, 48, 72, and 96 h after initial treatment with either abciximab or heparin. Patients receiving abciximab therapy showed a rapid inhibition of binding of fluorochrome-conjugated mAb CD41 and c7E3 concomitant with a reduction in platelet aggregation which was restored in part in the days after termination of abciximab infusion. Induction of ligand-induced binding sites on GPIIb-IIIa was increased in patients receiving abciximab. The expression of ligand-induced binding sites correlated inversely with platelet count. No significant change in platelet membrane markers were found in the heparin group. In vitro studies showed that abciximab induces ligand-induced binding sites on isolated platelets and on nuclear cells bearing recombinant GPIIb-IIIa. Abciximab rapidly achieves GPIIb-IIIa receptor blockade after coronary stent placement that might be beneficial in high-risk settings to bridge the delayed action of ticlopidine. Significant alterations of platelet membrane glycoproteins during GPIIb-IIIa antagonism might contribute to development of acute profound thrombocytopenia.
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PMID:Effect of glycoprotein IIb-IIIa receptor antagonism on platelet membrane glycoproteins after coronary stent placement. 986 73

Fibrinogen is the major ligand of platelet glycoprotein IIb/IIIa platelet receptor. Genes coding for platelet fibrinogen receptor glycoprotein IIb/IIIa are polymorphic. The PLA alloantigen has two antigenic determinants, PLA1 and PLA2, located in a 17-23 kD fragment of glycoprotein IIIa. We analyzed whether PLA genotype has any effect on plasma fibrinogen concentration and investigated if the effect has different magnitude in myocardial infarction patients compared with subjects free of angina or myocardial infarction. One hundred sixteen consecutive patients who suffered a myocardial infarction and 136 subjects recruited by random sampling from the local census were included in the study. PLA genotype distribution and allele frequencies in patients did not significantly differ from those in the control group. Mean fibrinogen concentration tended to be higher in controls with genotype PLA1PLA1 than in those with genotype PLA1PLA2 or PLA2PLA2, and in patients this difference reached statistical significance (p < 0.001). We conclude that the PLA polymorphism may be in linkage disequilibrium with another functional mutation in or near the promoter area of the fibrinogen gene or even in another gene, which controls the production or the clearance of fibrinogen.
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PMID:Platelet glycoprotein IIb/IIIa genetic polymorphism is associated with plasma fibrinogen levels in myocardial infarction patients. The REGICOR Investigators. 987 97

Generalized atherosclerosis and coronary artery disease (CAD) are associated with endothelial dysfunction and during acute myocardial ischemia platelet activation has been reported. Activated platelets exert activated fibrinogen receptors (GP IIb/IIIa) and express CD 62p being regarded as reliable marker for platelet activation. Patients with angiographically proven CAD performed a bicycle exercise test until the onset of angina or ST-segment depression. We studied the ischemia-induced alterations in fibrinogen binding to activated platelet GP IIb/IIIa receptors and CD 62p expression. Therefore, the basal fibrinogen binding to GP IIb/IIIa and CD 62p expression and the thrombin-concentration for half-maximal platelet activation before and after exercise testing were determined. Additionally, inhibition of thrombin-induced platelet activation by increasing concentrations of the prostacyclin-analog iloprost and the NO-donor SIN-1 was examined. In patients with CAD, a significantly reduced basal activation and a highly significant reduction in sensitivity towards thrombin was measured. The thrombin-induced expression of GP IIb/IIIa and CD 62p was significantly diminished in patients with CAD after physical exercise and their platelets were significantly more sensitive towards the inhibitory effects of iloprost and SIN-1. These data demonstrate a significant reduction in platelet activation in response to physical exercise in patients with CAD and advanced atherosclerosis. Despite exercise induced myocardial ischemia as evidenced by angina and ECG-changes, the platelets are not generally activated, as it could be expected. Thus, patients with myocardial ischemia experienced a reduced platelet activity and enhanced sensitivity towards prostacyclin (PGI2) and nitric oxide, probably due to an augmented release of endogenous platelet inhibitory mediators.
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PMID:Increased platelet sensitivity toward platelet inhibitors during physical exercise in patients with coronary artery disease. 995 Feb 58

Transluminal extraction catheter (TEC) is a percutaneous device that performs simultaneous thrombus aspiration and plaque excision. Clinical indications for its application are acute myocardial infarction, unstable angina, and stable angina caused by atherosclerotic, thrombotic lesions located within native coronary arteries and degenerated saphenous vein grafts. The device is useful in management of ischemic patients with contraindications to either pharmacologic thrombolytics or platelet GPIIb/IIIa receptor inhibitors, and can also effectively be used in combination with these agents. A successful TEC procedure requires careful patient selection, strict adherence to recommended indications, optimal equipment selection, familiarity with mechanical components of the device, full understanding of safe and efficacious techniques for deployment and activation, as well as recognition of unique associated angiographic manifestations such as the "empty-pouch phenomenon." As with other debulking devices, the incidence of restenosis post-TEC appears to be directly related to acute luminal gain at the time of procedure and therefore requires the need for adjunct stenting. This communication describes and illustrates various clinical, technical, and angiographic aspects of TEC procedure in patients with acute ischemic-thrombotic coronary syndromes. Cathet. Cardiovasc. Intervent. 48:406-420, 1999.
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PMID:Acute thrombotic-ischemic coronary syndromes: the usefulness of TEC. 1055 25

Coronary artery stenting has definitely been proven to improve results of percutaneous revascularisation in a large number of patients. Stenting reduces restenosis in large vessels above 3 mm diameter. Stenting has not solved the problem of restenosis but in spite of the inevitable in-stent restenosis due to neointimal proliferation seems to yield better long-term results than conventional PTCA. Adjunctive pharmacological treatment with aspirin and clopidogrel in combination with improved stent deployment techniques has reduced the incidence of subacute stent thrombosis. GP IIb/IIIa inhibition is a promising mean for the reduction of procedure related ischaemic events and complications not only with stent implantation but also with conventional PTCA. Other new devices may further influence the treatment choices of stenting versus conventional PTCA in the future. Novel approaches such as brachytherapy and molecular genetic approaches to reduce in-stent restenosis are currently being investigated but to date no conclusions can be drawn as to their future place in clinical practice. From a mechanistic standpoint it seems obvious to give all our efforts to protect patients with coronary atherosclerosis from loss of myocardium either with coronary artery bypass grafting or percutaneous revascularisation. As both approaches are palliative in nature, it may be useful to attempt percutaneous revascularisation in patients amenable to this therapy and thus obviate or delay the need for definitive revascularisation by coronary artery bypass grafting. At the end of this discussion we would like to remind that medical therapy for coronary artery disease is of utmost importance as all revascularisation procedures do not influence the underlying disease. Besides symptomatic relief of angina, treatment of heart failure, and other beneficial strategies to improve endothelial function, medical therapy with lipid lowering compounds together with risk factor control offers the possibility to delay progression of coronary artery disease.
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PMID:To stent or not to stent. 1059 78


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