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      Periprocedural Abciximab Administration in ST Elevation Myocardial Infarction Patients

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          Objectives: The impact of periprocedural (before primary percutaneous coronary angioplasty, PCI) abciximab administration on microvascular obstruction in patients with occluded infarct-related artery (IRA) is unknown. Methods: We studied 36 consecutive patients with first ST elevation myocardial infarction (STEMI) and occluded IRA treated with successful primary PCI within 12 h from symptom onset, who received intravenous abciximab immediately before PCI and 49 matched patients who did not receive abciximab as controls. All patients underwent delayed-enhanced magnetic resonance (DE-MR) 6 ± 2 days after PCI. Necrosis was judged as transmural when DE was extended to ≧75% of left ventricular (LV) segment thickness. Severe microvascular obstruction was identified as areas of late hypoenhancement surrounded by DE. Results: Time to treatment was comparable in the two groups (182 ± 60 vs. 188 ± 110 min, respectively). Transmurality and severe microvascular obstruction were present in 3.03 ± 2.8 versus 3.09 ± 2.9 (p = 0.9) and 1.05 ± 1.5 versus 1.06 ± 1.8 (p = 0.6) of LV segments, respectively, in the abciximab group versus controls. At multivariate analysis, severe microvascular obstruction was independently associated only with transmural necrosis (OR 1.5, p < 0.001) and age (OR 1.1, p = 0.02) but not with the use of abciximab. Conclusions: Severe microvascular obstruction after primary PCI of STEMI patients with occluded IRA is related to transmural necrosis but not to the use of abciximab.

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          Most cited references 16

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          Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction.

          When administered in conjunction with primary coronary stenting for the treatment of acute myocardial infarction, a platelet glycoprotein IIb/IIIa inhibitor may provide additional clinical benefit, but data on this combination therapy are limited. We randomly assigned 300 patients with acute myocardial infarction in a double-blind fashion either to abciximab plus stenting (149 patients) or placebo plus stenting (151 patients) before they underwent coronary angiography. Clinical outcomes were evaluated 30 days and 6 months after the procedure. The angiographic patency of the infarct-related vessel and the left ventricular ejection fraction were evaluated at 24 hours and 6 months. At 30 days, the primary end point--a composite of death, reinfarction, or urgent revascularization of the target vessel--had occurred in 6.0 percent of the patients in the abciximab group, as compared with 14.6 percent of those in the placebo group (P=0.01); at 6 months, the corresponding figures were 7.4 percent and 15.9 percent (P=0.02). The better clinical outcomes in the abciximab group were related to the greater frequency of grade 3 coronary flow (according to the classification of the Thrombolysis in Myocardial Infarction trial) in this group than in the placebo group before the procedure (16.8 percent vs. 5.4 percent, P=0.01), immediately afterward (95.1 percent vs. 86.7 percent, P=0.04), and six months afterward (94.3 percent vs. 82.8 percent, P=0.04). One major bleeding event occurred in the abciximab group (0.7 percent); none occurred in the placebo group. As compared with placebo, early administration of abciximab in patients with acute myocardial infarction improves coronary patency before stenting, the success rate of the stenting procedure, the rate of coronary patency at six months, left ventricular function, and clinical outcomes.
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            Abciximab as adjunctive therapy to reperfusion in acute ST-segment elevation myocardial infarction: a meta-analysis of randomized trials.

            The benefits of abciximab in patients with ST-segment elevation myocardial infarction (STEMI) are still a matter of debate. To combine data from all randomized trials conducted with abciximab in STEMI. Formal searches of electronic databases (MEDLINE, PubMed) from from January 1990 to December 2004. We examined all completed, published, randomized trials of abciximab in STEMI. The following key words were used for study selection: randomized trial, myocardial infarction, reperfusion, primary angioplasty, facilitated angioplasty, stenting, fibrinolysis, IIb-IIIa inhibitors, and abciximab. Information on study design, type and dosage of drugs, inclusion and exclusion criteria, number of patients, and clinical outcome was extracted by 2 investigators. Disagreements were resolved by consensus. Eleven trials were analyzed, involving 27115 patients (12,602 [46.5%] in the abciximab group, 14,513 [53.5%] in the control group). When compared with the control group, abciximab was associated with a significant reduction in short-term (30 days) mortality (2.4% vs 3.4%, P = .047) and long-term (6-12 months) mortality (4.4% vs 6.2%, P = .01) in patients undergoing primary angioplasty but not in those treated with fibrinolysis or in all trials combined. Abciximab was associated with a significant reduction in 30-day reinfarction, both in all trials combined (2.1% vs 3.3%, P<.001), in primary angioplasty (1.0% vs 1.9%, P = .03), and in fibrinolysis trials (2.3% vs 3.6%, P<.001). Abciximab did not result in an increased risk of intracranial bleeding (0.61% vs 0.62%, P = .62) but was associated with an increased risk of major bleeding complications when combined with fibrinolysis (5.2% vs 3.1%, P<.001) but not with primary angioplasty (4.7% vs 4.1%, P = .36). This meta-analysis shows that, when compared with the control group, adjunctive abciximab for STEMI is associated with a significant reduction in 30-day and long-term mortality in patients treated with primary angioplasty but not in those receiving fibrinolysis. The 30-day reinfarction rate is significantly reduced in patients treated with either fibrinolysis or primary angioplasty. A higher risk of major bleeding complications is observed with abciximab in association with fibrinolysis.
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              The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema.

              Acute mitral regurgitation may cause pulmonary edema, but the pathogenetic role of chronic ischemic mitral regurgitation, a dynamic condition, has not yet been characterized. We prospectively studied 28 patients (mean [+/-SD] age, 65+/-11 years) with acute pulmonary edema and left ventricular systolic dysfunction and 46 patients without a history of acute pulmonary edema. The two groups were matched for all baseline characteristics. Patients underwent quantitative Doppler echocardiography during exercise. Exercise-induced changes in the left ventricular volume, the ejection fraction, the mitral regurgitant volume, the effective regurgitant orifice area, and the transtricuspid pressure gradient were compared in patients with and without acute pulmonary edema. The two groups had similar clinical and baseline echocardiographic characteristics. They also had similar exercise-induced changes in heart rate, systolic blood pressure, and left ventricular volumes. In the univariate analysis, patients with recent pulmonary edema had a much higher increase than did the patients without pulmonary edema in mitral regurgitant volume (26+/-14 ml vs. 5+/-14 ml, P<0.001), the effective regurgitant orifice area (16+/-10 mm2 vs. 2+/-9 mm2, P<0.001), and the transtricuspid pressure gradient (29+/-10 mm Hg vs. 13+/-11 mm Hg, P<0.001). In the multivariate analysis, exercise-induced changes in the effective regurgitant orifice area (P<0.001), in the transtricuspid pressure gradient (P=0.001), and in the left ventricular ejection fraction (P=0.02) were independently associated with a history of recent pulmonary edema. In patients with left ventricular systolic dysfunction, acute pulmonary edema is associated with the dynamic changes in ischemic mitral regurgitation and the resulting increase in pulmonary vascular pressure. Copyright 2004 Massachusetts Medical Society.

                Author and article information

                S. Karger AG
                April 2008
                31 October 2007
                : 110
                : 2
                : 129-134
                Department of Cardiac, Thoracic and Vascular Sciences and Department of Radiology, University of Padova, Padova, Italy
                110492 Cardiology 2008;110:129–134
                © 2007 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 29, Pages: 6
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