Showing papers by "Elliott M. Antman published in 1999"
TL;DR: Enoxaparin is superior to UFH for reducing a composite of death and serious cardiac ischemic events during the acute management of UA/NQMI patients without causing a significant increase in the rate of major hemorrhage.
Abstract: Background—Low-molecular-weight heparins are attractive alternatives to unfractionated heparin (UFH) for management of unstable angina/non–Q-wave myocardial infarction (UA/NQMI). Methods and Results—Patients (n=3910) with UA/NQMI were randomized to intravenous UFH for ≥3 days followed by subcutaneous placebo injections or uninterrupted antithrombin therapy with enoxaparin during both the acute phase (initial 30 mg intravenous bolus followed by injections of 1.0 mg/kg every 12 hours) and outpatient phase (injections every 12 hours of 40 mg for patients weighing <65 kg and 60 mg for those weighing ≥65 kg). The primary end point (death, myocardial infarction, or urgent revascularization) occurred by 8 days in 14.5% of patients in the UFH group and 12.4% of patients in the enoxaparin group (OR 0.83; 95% CI 0.69 to 1.00; P=0.048) and by 43 days in 19.7% of the UFH group and 17.3% of the enoxaparin group (OR 0.85; 95% CI 0.72 to 1.00; P=0.048). During the first 72 hours and also throughout the entire initial ho...
1,057 citations
TL;DR: The guidelines have been updated to include the most significant advances that have occurred in the management of patients with acute myocardial infarction (AMI) during that time frame and were developed to keep the guidelines current without republishing the entire document.
Abstract: The American College of Cardiology/American Heart Association (ACC/AHA) Guidelines for the Management of Patients With Acute Myocardial Infarction have been reviewed over the past 2.5 years since their initial publication in the Journal of the American College of Cardiology (1996;28:1328–1428) to ensure their continued relevancy. The guidelines have been updated to include the most significant advances that have occurred in the management of patients with acute myocardial infarction (AMI) during that time frame. This update was developed to keep the guidelines current without republishing the entire document. This effort represents a new procedure of the ACC/AHA Task Force on Practice Guidelines. These guidelines will be reviewed and updated as necessary until it is deemed appropriate to revise and republish the entire document.
The guidelines, incorporating the update, are available on the Web sites of both the American College of Cardiology (www.acc.org) and the American Heart Association (www.americanheart.org). In the Web site version, deleted text is indicated by strikeout, and new/revised text is presented as double-underlined type. Reprints of the original document with the revised sections appended are available from both organizations (see information below).
The following is a listing of the recommendations made by the ACC/AHA Task Force on Practice Guidelines in the ACC/AHA Task Force Report “ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction.” More detailed information regarding the evidence and the rationale for these recommendations can be found in the full text of the guidelines themselves, which appears in the November 1996 and September 1999 (update) issues of the Journal of the American College of Cardiology.
As in previous guidelines, the American College of Cardiology and the American Heart Association have used the following classification system in which indications for a diagnostic procedure, a particular therapy, or intervention are designated as:
Class I: Conditions for …
749 citations
TL;DR: Abciximab facilitates the rate and extent of thrombolysis, producing early, marked increases in TIMI 3 flow when combined with half the usual dose of alteplase, and substantial reductions in heparin dosing may reduce the risk of bleeding even further.
Abstract: Background—The TIMI 14 trial tested the hypothesis that abciximab, the Fab fragment of a monoclonal antibody directed to the platelet glycoprotein (GP) IIb/IIIa receptor, is a potent and safe addition to reduced-dose thrombolytic regimens for ST-segment elevation MI. Methods and Results—Patients (n=888) with ST-elevation MI presenting <12 hours from onset of symptoms were treated with aspirin and randomized initially to either 100 mg of accelerated-dose alteplase (control) or abciximab (bolus 0.25 mg/kg and 12-hour infusion of 0.125 μg · kg−1 · min−1) alone or in combination with reduced doses of alteplase (20 to 65 mg) or streptokinase (500 000 U to 1.5 MU). Control patients received standard weight-adjusted heparin (70-U/kg bolus; infusion of 15 U · kg−1 · h−1), whereas those treated with a regimen including abciximab received low-dose heparin (60-U/kg bolus; infusion of 7 U · kg−1 · h−1). The rate of TIMI 3 flow at 90 minutes for patients treated with accelerated alteplase alone was 57% compared with 3...
694 citations
TL;DR: Accumulated evidence indicates that enoxaparin should be considered as a replacement for unfractionated heparin as the antithrombin for the acute phase of management of patients with high-risk unstable angina/non-Q-wave myocardial infarction.
Abstract: Background—Two phase III trials of enoxaparin for unstable angina/non–Q-wave myocardial infarction have shown it to be superior to unfractionated heparin for preventing a composite of death and cardiac ischemic events. A prospectively planned meta-analysis was performed to provide a more precise estimate of the effects of enoxaparin on multiple end points. Methods and Results—Event rates for death, the composite end points of death/nonfatal myocardial infarction and death/nonfatal myocardial infarction/urgent revascularization, and major hemorrhage were extracted from the TIMI 11B and ESSENCE databases. Treatment effects at days 2, 8, 14, and 43 were expressed as the OR (and 95% CI) for enoxaparin versus unfractionated heparin. All heterogeneity tests for efficacy end points were negative, which suggests comparability of the findings in TIMI 11B and ESSENCE. Enoxaparin was associated with a 20% reduction in death and serious cardiac ischemic events that appeared within the first few days of treatment, and...
473 citations
TL;DR: Acute MI slows flow globally, and slower global flow is associated with adverse outcomes, especially in patients who died and patients who survived.
150 citations
TL;DR: There is no evidence that the intensity of anticoagulation associated with heparin or hirudin administration influences the occurrence of rupture, and cardiac rupture following thrombolytic therapy tends to occur in older patients and may explain the disproportionately high mortality rate among women in prior dinical trials.
140 citations
TL;DR: Lumen geometry is not the sole determinant of coronary blood flow at 90 min following thrombolytic administration, and other variables such as the location of the culprit artery, the duration of patency, a pulsatile flow pattern and thrombus are also related to slower flow.
73 citations
TL;DR: Serum marker determinations at baseline and 60-min after thrombolysis may permit rapid triage of patients receiving thromBOlytic therapy by ruling out IRA occlusion and early invasive interventions to establish IRA patency may not be necessary in this group.
73 citations
TL;DR: Physicians who design and/or implement RCTs translate the results of the medical literature more promptly and to a greater extent than physicians in routine clinical practice.
54 citations
TL;DR: A 3 cardiac cycle definition of TIMI grade 3 flow results in rates of normal perfusion that are approximately 10% higher than if the original definition of timIgrade 3 flow is applied.
36 citations
TL;DR: Understanding current concepts in the pathogenesis and pathology of atherosclerosis is fundamental for physicians concerned with coronary care.
Abstract: Unstable angina and acute myocardial infarction account for over 90% of admissions to coronary care units. During the past decade, the expanded use of aspirin, heparin, beta-blockade, thrombolysis, electrical and hemodynamic monitoring, and a variety of interventional techniques has dramatically reduced inhospital mortality for these acute ischemic syndromes. For the great majority of patients, however, the underlying pathophysiologic process leading to admission relates directly to complications of atherosclerotic coronary heart disease. Current research indicates that complex interactions between the in_ammatory response to vascular injury, oxidation of lipids, local endothelial dysfunction, and alterations in hemostasis and thrombosis all interact in the initiation, progression, and acute rupture of the atherosclerotic plaque [1,2] Thus, understanding current concepts in the pathogenesis and pathology of atherosclerosis is fundamental for physicians concerned with coronary care.
TL;DR: It is demonstrated that direct antithrombins reduce rates of death and myocardial infarction early in patients without ST elevation, but the treatment effect diminishes over time, and treatment with enoxaparin shows superiority versus unfractionated heparin, and thetreatment effect is durable over time.
TL;DR: Clinical studies evaluating the combination of thrombolytic therapy and glycoprotein IIb/IIIa inhibitors appear most promising, with evidence of improved angiographic outcomes, and reduced-dose reteplase with abciximab and eptifibatide with reduced- dose alteplasing will be investigated.
Abstract: Limitations in the standard treatment of acute myocardial infarction have focused attention on inhibition of platelet activity by its final common pathway of activation, the glycoprotein IIb/IIIa receptor. Animal studies have suggested that a glycoprotein IIb/IIIa inhibitor could accelerate thrombolysis and prevent reocclusion after successful thrombolysis. Studies evaluating the use of a glycoprotein IIb/IIIa inhibitor alone without thrombolysis or percutaneous transluminal coronary revascularization do not suggest that isolated use of glycoprotein IIb/IIIa inhibitors restores TIMI 3 flow in a sufficient proportion of patients. Clinical studies evaluating the combination of thrombolytic therapy and glycoprotein IIb/IIIa inhibitors appear most promising, with evidence of improved angiographic outcomes. Reducing the dose of thrombolytic agents may result in reduction in bleeding risk. Current and future trials will investigate reduced-dose reteplase with abciximab and eptifibatide with reduced-dose alteplase. Available evidence suggests that glycoprotein IIb/IIIa inhibition may facilitate thrombolysis, thus adding a new element to future reperfusion regimens.
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