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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angioplasty in acute coronary syndromes without ST elevation (angina + non Q wave infarction) is traditionally associated with an increased risk of major cardiac complications compared with angioplasty in stable angina. The recent development of instrumental techniques, in particular the introduction of stenting and pharmacological support for angioplasty have transformed the immediate prognosis in unstable angina. Consequently, angioplasty has become better tolerated and more easily recommended. Angioplasty cannot be considered without active medical therapy, including aspirin, betablockers, and non-fractionated or low molecular weight heparin, the use of the only inhibitor of GP IIb/IIIa receptors available in France, abciximab, remaining limited to the pharmacological environment of angioplasty in the absence of governmental authorization for its use in other indications. In high risk clinical situations, refractory angina, angina complicated by ventricular arrhythmias, left ventricular failure, mitral regurgitation, patients with a history of infarction or coronary bypass surgery, the indications of angioplasty and revascularization should be liberal as the prognosis of this patient group is improved. In situations of intermediate or low risk, there is no consensus about the best strategy, systematic or elective invasive procedures, that is to say guided by residual or recurrent myocardial ischaemia after initial stabilisation. However, the most recent trials, in particular FRISC II, seem to prove that systematic invasive procedures after stabilization by medical treatment, have a favourable influence on the prognosis compared with a conservative strategy. Other on-going trials may provide a definitive answer to this very controversial question.
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PMID:[Angioplasty in unstable chest angina. Angioplasty in unstable angina]. 1059 43

During the past 15 years, we have learned an enormous amount about the pathogenesis and treatment of unstable angina. In most cases of unstable rest angina, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. However, any process that acutely changes the supply-demand ratio (decreased supply or increased demand in the presence of a decrease in supply) can precipitate the clinical presentation of unstable angina. Standard acute antithrombotic drug therapy is effective in decreasing progression to infarction. Newer agents (low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibitors) are more effective, and their use is evolving. Percutaneous intervention and bypass surgery can reduce symptoms and multiple hospitalizations, in most cases without a decrease in the long-term mortality rate. Because the cost of hospitalization is extremely high and the clinical presentation and outcome are heterogeneous, better triage methods are required.
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PMID:Unstable angina: current concepts of pathogenesis and treatment. 1063 2

1999 has been a good year in the field of innovation in thrombosis. In coronary syndrome without ST elevation: low molecular weight heparin has been confirmed to be more effective than non-fractionated heparin (enoxaparin) and to improve the prognosis of non-revascularised patients (dalteparin) after the hospital phase; hirudin has been shown to be more effective in terms of incidence of myocardial infarction and recurrence of angina than non-fractionated heparin without a higher incidence of bleeding complications; the anti-GP IIb-IIIa (abciximab) has confirmed all its advantages at 6 months and 1 year after a coronary event. The association of heparin and aspirin, which has been the mainstay of antithrombotic treatment of acute coronary syndromes without ST elevation, will soon be improved upon at the beginning of the third millennium. In myocardial infarction, medical thrombolysis has probably reached a turning point in its history. The association of half doses of rt-Pa and anti-GP IIb-IIIa has been shown to be more effective in obtaining good reflow than the thrombolytic agent alone at conventional doses. These results were obtained without any increase in bleeding complication. The same anti-GP IIb-IIIa also improve mechanical revascularisation by optimising reperfusion after the 24th hour. This benefit is rapidly transformed into reduced left ventricular dysfunction. Pulmonary embolism remains a critical illness as the ICOPER registry reports a 3 year mortality of nearly 16%. This emphasises the importance of early diagnosis which is usually possible without resorting to invasive procedures and by modulating all the results of paraclinical investigations with respect to the pretest clinical probability.
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PMID:[The best of thrombosis and thromboembolic disease in 1999]. 1072 51

Acute coronary syndromes not associated with ST-segment elevation, i.e. unstable angina and non-Q wave myocardial infarction, represent a heterogeneous group of clinical disorders sharing similar pathogenic mechanisms, clinical presentation and medical management. Current guidelines recommended an early anti-thrombotic and anti-ischemic treatment in these patients, as well as their prompt risk evaluation based on easily available clinical and instrumental data, to identify those subjects at greater risk in whom a more aggressive management is warranted. Despite the association of aspirin, heparin and anti-ischemic drugs, the 30-day rate of death or myocardial infarction remains high (9-15%) in patients with markers of greater risk (i.e. Braunwald class III, ST-segment depression, abnormal creatine kinase or troponin values). Moreover, in patients with acute coronary syndromes undergoing percutaneous coronary interventions (PCI), complex coronary lesions increase the peri-procedural risk of thrombotic complications. Regardless of the agonist responsible for platelet activation and aggregation, platelet glycoprotein (GP) IIb/IIIa receptor activation is the key factor in thrombosis formation. Several clinical trials in the past few years have documented the beneficial value of GP IIb/IIIa inhibitors in patients treated with aspirin and heparin, with a significant reduction in the cumulative end-point of death and/or myocardial infarction at 48-96 hours (odds ratio--OR 0.81, 95% confidence interval--CI 0.71-0.92, p < 0.01). Such therapeutical benefit is still present at 30 days (OR 0.88, 95% CI 0.81-0.97, p < 0.001) and 6 months (OR 0.88, 95% CI 0.79-0.97, p < 0.001). In patients treated with abciximab, eptifibatide or tirofiban, undergoing early PCI, a remarkable relative reduction in the risk of death and non-fatal acute myocardial infarction was shown before PCI (-34%, p < 0.001). The pre-PCI administration of GP IIb/IIIa inhibitors is associated with a significant reduction in peri-procedural complications (-41% relative reduction of death or acute myocardial infarction in the 48 hours after PCI, p < 0.001). In this subset of patients the benefit correlates with abnormal pre-PCI values of troponin, a reliable surrogate marker of active thrombosis. The greatest clinical benefit from GP IIb/IIIa inhibitors is expected in patients presenting high-risk features (early post-infarction angina; older age with a history of left ventricular dysfunction or diabetes; heart failure symptoms, ST-segment depression, abnormal troponin, creatine kinase, and C-reactive protein values at admission) as well as in patients with recurrent ischemic attacks and those undergoing early PCI. Although the combination of GP IIb/IIIa inhibition and standard doses of unfractionated heparin is associated with an increased risk of major bleeding, such risk can be remarkably reduced adopting simple technical suggestions.
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PMID:[The clinical use of the GPIIb/IIIa inhibitors eptifibatide and tirofiban in the treatment of acute coronary syndromes of the "non-ST elevation" type]. 1093 49

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

The recent availability of novel antiplatelet and antithrombin agents has revolutionized the therapeutic options for intermediate- and high-risk unstable angina (UA). Current guidelines recommend aspirin, unfractionated heparin (UFH), and antianginal therapy. Low-molecular-weight heparin (LMWH) and direct thrombin inhibitors have significant theoretical advantages and apparent clinical benefits compared with UFH and are good alternatives in selected patients. Glycoprotein (GP) IIb/IIIa receptor inhibition reduces the future risk of myocardial infarction (MI) and may reduce the incidence of death in patients with unstable angina. In particular, these drugs should be considered for use in combination with aspirin and UFH in patients undergoing an "early invasive" approach. Coronary revascularization plays an important role in high-risk patients and in those with refractory angina, but its routine application continues to be controversial. Issues regarding the use of LMWH in combination with GP IIb/IIIa inhibitors and during percutaneous transluminal coronary angioplasty (PTCA) are being addressed in clinical trials. Ideally, the incidence of serious cardiac events in patients with UA will continue to decrease with the ongoing search for potent drug combinations that achieve early control of intracoronary thrombosis.
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PMID:Unstable Angina. 1109 9

The interactions between leukocytes and endothelial cells have been studied extensively under conditions of ischemia and reperfusion. In contrast, attraction of leukocytes by platelets at the site of damage is poorly understood. This recruitment facilitates inflammation and atherogenesis. Studies performed ex vivo in coronary artery disease show that neutrophil-platelet adhesion increases in unstable angina, coronary angioplasty and coronary artery bypass surgery, in comparison with stable angina. Experimental works have shown the major role of platelet P-selectin in platelet-leukocyte interactions, and of fibrinogen, which is the ligand of both platelets and leukocytes (B2 integrins). Studied performed in anti-GPIIb/IIIa-treated patients demonstrate a modulation, as inhibition, of platelet-leukocyte interactions. This new drug inhibits platelet function and coagulation, and moreover inflammation.
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PMID:[Platelet-leukocyte interactions in coronary heart disease: pathophysiology, clinical relevance, pharmacological modulation]. 1114 96

Aspirin in a dose of 160 to 325 mg should be administered on day 1 of an acute MI and continued indefinitely on a daily basis. Thrombolytic therapy should be administered within 6 to 12 hours after the onset of an acute MI with ST segment elevation or with left bundle branch block. Primary coronary angioplasty when available should be used rather than thrombolytic therapy in the treatment of older persons with acute MI who are poor candidates for thrombolytic therapy. Intravenous heparin should be given in persons with acute MI undergoing primary coronary angioplasty or surgical coronary revascularization and in persons with acute MI at high risk for systemic embolization. Long-term oral warfarin should be given after MI for the secondary prevention of MI in post-MI persons unable to tolerate daily aspirin, in post-MI persons with persistent atrial fibrillation, and in post-MI persons with left ventricular thrombus. Platelet GP IIb/IIIa inhibitors should be administered along with aspirin and enoxaparin in the acute phase of management of persons with unstable angina pectoris or non-Q wave MI. Aspirin should be administered daily indefinitely to persons after MI, to persons with unstable angina pectoris, to persons with stable angina pectoris, and to persons undergoing coronary revascularization. Aspirin plus ticlopidine or aspirin plus clopidogrel should be used in persons undergoing coronary artery stenting. Platelet GP IIb/IIIa inhibitors should be used at the time of coronary angioplasty, coronary atherectomy, or coronary stenting. Aspirin, 160 to 325 mg daily, is recommended in older men and postmenopausal women who are at high risk for developing coronary events in addition to treating their coronary risk factors.
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PMID:Thrombolysis and antithrombotic therapy for coronary artery disease. 1127 Jan 30

During the last 10 years a new group of drugs was developed--platelet glycoprotein IIb/IIIa blockers that is nowadays largely and efficiently used as for the prevention of percutaneous coronary intervention complications as well as in the treatment of acute coronary syndromes. In the period February-June 2000--19 patients (18 males, 1 female, of average age 53.3 years) were administered Abciximab in the bolus dose of 10 mg immediately before the intervention and afterwards 10 mg by 12-hour infusion. All patients received aspirin and ticlopidine hydrochloride if the stent was introduced and heparin by the standard protocol. Elective intervention was done in 17 patients (non-Q infarction in 3 patients, unstable angina pectoris in 5 patients, postinfarction angina pectoris in 2 patients, acute myocardial infarction at least 1 month before the intervention in 6 patients and 1 patient with myocardiopathy) and in 2 patients the intervention was performed during the myocardial infarction. In 15 patients (79%) intracoronary stent was introduced and in 5 patients (21%) the intervention was performed on 2 arteries. Maximal immediate effect of the dilatation was achieved in 18 patients (94.7%). In the first 60 days of the follow-up 1 patient (5%) died of some other disease, and in no patients symptomatic myocardial ischemia was found. No adverse effects were observed.
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PMID:[Clinical study of administration of abciximab--a monoclonal antibody to platelet glycoprotein IIb/IIIa in percutaneous intracoronary interventions]. 1176 14


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