Abciximab (ReoPro) or IIb/IIIa Class Drugs - Pulmonary Hemorrhage

2/03/2003 

Question: How common are pulmonary bleeding complications in patients receiving abciximab therapy?

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Unique Identifier:12479522

Authors: Choi RK. Lee NH. Lim DS. Hong S. Hwang HK.

Institution: Yoorimbin@hanmail.net

Title: Pulmonary hemorrhage after percutaneous coronary intervention with abciximab therapy.

Source: Mayo Clinic Proceedings. 77(12):1340-3, 2002 Dec.

Abstract: Abciximab has a key role in the treatment of patients with acute coronary syndromes undergoing percutaneous coronary intervention; however, an increased risk of bleeding complications is well recognized. We report a case of serious pulmonary hemorrhage after use of abciximab therapy. A definitive indication and treatment guideline should be available to minimize serious bleeding complications. Additionally, respiratory symptoms should be monitored closely for early detection of serious pulmonary hemorrhage in patients receiving abciximab therapy during percutaneous coronary intervention. CAS Registry/EC Number 0 (Antibodies, Monoclonal). 0 (Immunoglobulins, Fab). 0 (Platelet Glycoprotein GPIIb-IIIa Complex). 143653-53-6 (abciximab).

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Unique Identifier:11451827

Authors: Kalra S. Bell MR. Rihal CS.

Institution: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA. kalra.sanjay@mayo.edu

Title: Alveolar hemorrhage as a complication of treatment with abciximab.

Source: Chest. 120(1):126-31, 2001 Jul.

Abstract: STUDY OBJECTIVE: The use of abciximab, a chimeric monoclonal antibody Fab fragment specific for platelet glycoprotein IIb/IIIa receptors, is associated with improved outcome after angioplasty and stent placement. Major complications include bleeding, but pulmonary hemorrhage has been reported rarely. This study was done to identify patients with pulmonary hemorrhage following abciximab infusion and to define, if possible, any specific risk factors. DESIGN: Retrospective review of institutional coronary angiography and bronchoscopy databases to identify patients who received abciximab and developed pulmonary hemorrhage. SETTING: Tertiary-care teaching hospital. PATIENTS: All patients who underwent coronary angiography and received abciximab between June 1995 and March 2000. INTERVENTION: None. Measurements and results: Seven of 2,553 patients (0.27%) had documented severe pulmonary hemorrhage associated with chest radiographic abnormalities, impaired oxygenation, and the need for blood product transfusions. The initial symptom was hemoptysis in four of the seven patients. There were two early deaths and one late death. No cases of pulmonary hemorrhage were identified in 5,412 patients who underwent coronary procedures without abciximab infusion. No other risk factors predicting hemorrhage were identified. CONCLUSIONS: Severe pulmonary hemorrhage is a complication of abciximab use. Although hemoptysis is an important alerting symptom, it may not be present initially and the diagnosis may be missed or considered late, with the potential for inappropriate treatment until the diagnosis is established. Lesser degrees of bleeding are potentially easily missed, and this report should alert physicians to this complication so that it can be considered early in the evaluation of patients presenting with pulmonary events after abciximab use. CAS Registry/EC Number 0 (Antibodies, Monoclonal). 0 (Immunoglobulins, Fab). 0 (Platelet Aggregation Inhibitors). 0 (Platelet Glycoprotein GPIIb-IIIa Complex). 143653-53-6 (abciximab).

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Unique Identifier:9867573

Authors: Khanlou H. Eiger G. Yazdanfar S.

Title: Abciximab and alveolar hemorrhage.[comment].

Source: New England Journal of Medicine. 339(25):1861-3, 1998 Dec 17.

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Unique Identifier:9676804

Authors: Khanlou H. Tsiodras S. Eiger G. Abousy K. Goldberg S. Nakhjavan F. Yazdanfar S.

Institution: Department of Pulmonary and Critical Care Medicine, Albert Einstein Medical Center, Philadelphia, PA 19141, USA.

Title: Fatal alveolar hemorrhage and Abciximab (ReoPro) therapy for acute myocardial infarction.

Source: Catheterization & Cardiovascular Diagnosis. 44(3):313-6, 1998 Jul.

Abstract: We describe two cases of diffuse alveolar hemorrhage and development of ARDS in patients who underwent percutaneous transluminal coronary angioplasty (PTCA) with stenting in whom Abciximab (ReoPro) was used in combination with other agents interfering with the hemostatic mechanism. The development of pulmonary infiltrates, associated with a fall in hemoglobin after the administration of Abciximab, should strongly suggest the possibility of diffuse alveolar hemorrhage. Physicians should be aware of the possible association between the use of Abciximab and the development of alveolar hemorrhage. CAS Registry/EC Number 0 (Antibodies, Monoclonal). 0 (Immunoglobulins, Fab). 143653-53-6 (abciximab).

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Unique Identifier:9476687

Authors: Sitges M. Villa FP.

Institution: Institut Clinic de Malalties Cardiovasculars, Barcelona, Spain.

Title: Massive pulmonary hemorrhage in a patient treated with a platelet glycoprotein IIb/IIIa inhibitor.

Source: International Journal of Cardiology. 62(3):269-71, 1997 Dec 19.

Abstract: Novel platelet glycoprotein IIb/IIIa receptor inhibitors have appeared as promising antithrombotic agents. However, their increased risk of bleeding complications, although known, is not well established. We report the case of a serious bleeding complication, a massive pulmonary hemorrhage, in a patient who was treated with one of these agents. Further studies defining guidelines and indications of treatment with platelet glycoprotein IIb/IIIa inhibitors are needed before their routine application to daily practice. CAS Registry/EC Number 0 (Antibodies, Monoclonal). 0 (Immunoglobulins, Fab). 0 (Platelet Aggregation Inhibitors). 0 (Platelet Glycoprotein GPIIb-IIIa Complex). 143653-53-6 (abciximab).

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Unique Identifier:9054741

Authors: Ohman EM. Kleiman NS. Gacioch G. Worley SJ. Navetta FI. Talley JD. Anderson HV. Ellis SG. Cohen MD. Spriggs D. Miller M. Kereiakes D. Yakubov S. Kitt MM. Sigmon KN. Califf RM. Krucoff MW. Topol EJ.

Institution: Duke University Medical Center, Durham, NC 27710, USA.

Title: Combined accelerated tissue-plasminogen activator and platelet glycoprotein IIb/IIIa integrin receptor blockade with Integrilin in acute myocardial infarction. Results of a randomized, placebo-controlled, dose-ranging trial. IMPACT-AMI Investigators.[comment].

Source: Circulation. 95(4):846-54, 1997 Feb 18.

Abstract: BACKGROUND: Platelet activation and aggregation may be key components of thrombolytic failure to restore and maintain perfusion in acute myocardial infarction. We performed a placebo-controlled, dose-ranging trial of Integrilin, a potent inhibitor of platelet aggregation, with heparin, aspirin, and accelerated alteplase. METHODS AND RESULTS: We assigned 132 patients in a 2:1 ratio to receive a bolus and continuous infusion of one of six Integrilin doses or placebo. Another 48 patients were randomized in a 3:1, double-blind fashion to receive the highest Integrilin dose from the first phase or placebo. All patients received accelerated alteplase, aspirin, and intravenous heparin infusion; all but two groups also received an intravenous heparin bolus. The highest Integrilin dose group from the nonrandomized phase and the randomized patients were pooled for analysis and compared with placebo-treated patients. The primary end point was Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow at 90-minute angiography. Secondary end points were time to ST-segment recovery, an in-hospital composite (death, reinfarction, stroke, revascularization procedures, new heart failure, or pulmonary edema), and bleeding variables. The highest Integrilin dose groups had more complete reperfusion (TIMI grade 3 flow, 66% versus 39% for placebo-treated patients; P = .006) and a shorter median time to ST-segment recovery (65 versus 116 minutes for placebo; P = .05). The groups had similar rates of the composite end point (43% versus 42% for placebo-treated patients) and severe bleeding (4% versus 5%, respectively). CONCLUSIONS: The incidence and speed of reperfusion can be enhanced when a potent inhibitor of the glycoprotein IIb/IIIa integrin receptor, such as Integrilin, is combined with accelerated alteplase, aspirin, and intravenous heparin. CAS Registry/EC Number 0 (Fibrinolytic Agents). 0 (Peptides). 0 (Placebos). 0 (Platelet Aggregation Inhibitors). 0 (Platelet Glycoprotein GPIIb-IIIa Complex). 0 (eptifibatide). 9005-49-6 (Heparin). EC 3-4-21-68 (Tissue Plasminogen Activator).

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Unique Identifier:7796496

Authors: Aguirre FV. Topol EJ. Ferguson JJ. Anderson K. Blankenship JC. Heuser RR. Sigmon K. Taylor M. Gottlieb R. Hanovich G. et al.

Institution: Division of Cardiology, St. Louis University Health Sciences Center, MO 63110, USA.

Title: Bleeding complications with the chimeric antibody to platelet glycoprotein IIb/IIIa integrin in patients undergoing percutaneous coronary intervention. EPIC Investigators.

Source: Circulation. 91(12):2882-90, 1995 Jun 15.

Abstract: BACKGROUND: The potential for novel antiplatelet and antithrombin agents to contribute to periprocedural bleeding complications of percutaneous coronary revascularization is poorly defined. In the Evaluation of c7E3 Fab in Preventing Ischemic Complications of High-Risk Angioplasty (EPIC) trial, the periprocedural use of aspirin, heparin, and a chimeric antibody to the platelet glycoprotein IIb/IIIa integrin c7E3 Fab in 2099 patients significantly reduced postprocedural ischemic complications and 6-month clinical restenosis but was associated with increased procedural bleeding complications. We review these complications and describe clinical and procedural variables associated with increased bleeding complications in the EPIC trial. METHODS AND RESULTS: Patients with high-risk clinical or lesion morphological characteristics were randomized to receive placebo bolus plus placebo infusion, c7E3 Fab bolus plus placebo infusion, or c7E3 Fab bolus plus c7E3 Fab infusion. Patients received periprocedural aspirin and intravenous heparin continued for a minimum of 12 hours after the procedure. Outcomes reflecting bleeding complications were measured: transfusions, decreased hemoglobin, and an index including both parameters. Major bleeding complications unrelated to bypass surgery occurred in 3.3%, 8.6%, and 10.6%, and blood product transfusions were used in 7.5%, 14.0%, and 16.8% of patients treated with placebo, bolus c7E3 Fab, and bolus plus infusion c7E3 Fab, respectively (both P < .001). Most major bleeding complications occurred at the femoral access site, regardless of treatment. Intracranial hemorrhage (0.3%) and death (0.09%) attributable to major bleeding complications were rare. Multivariable regression analyses identified several variables significantly and independently related to major bleeding complications or greater blood loss, including greater age, female sex, lower weight, c7E3 Fab therapy, and duration and complexity of the index procedure. Major bleeding complications and blood loss in patients receiving bolus plus infusion were not significantly greater than in those receiving bolus alone (P = .38 and P = .14, respectively). CONCLUSIONS: Bleeding complications unrelated to bypass surgery were two to three times more frequent in patients receiving c7E3 Fab than in those receiving placebo, but most were transient and well tolerated. Risk-factor analysis and modification of concomitant antithrombotic and antiplatelet treatment strategies may aid in reducing bleeding complications and enhancing clinical benefit in patients receiving c7E3 Fab during percutaneous coronary revascularization. CAS