title: Use of platelet glycoprotein IIb/IIIa inhibitors and spontaneous pulmonary hemorrhage.
abstract: BACKGROUND
  The use of platelet glycoprotein (GP) IIb/IIIa inhibitors in patients undergoing percutaneous coronary intervention has resulted in an impressive reduction in adverse events. Pulmonary hemorrhage is a rare but potentially lethal complication of antithrombotic and antiplatelet therapy. We analyzed the incidence of spontaneous pulmonary hemorrhage following the use of platelet GP IIb/IIIa inhibitors.
  
  
  METHODS
  The medical records of 1,020 consecutive patients who received GP IIb/IIIa inhibitors and underwent PCI at our institution between August 1997 and December 1999 were reviewed.
  
  
  RESULTS
  Diffuse pulmonary hemorrhage developed in 7 patients (0.68%), two of whom died. Five of 7 patients with pulmonary hemorrhage had activated clotting times > 250 seconds during the procedure. Activated partial thromboplastin time measured at the time of pulmonary hemorrhage was elevated in all patients (mean, 85 seconds; range, 69 95 seconds). All patients had history of congestive heart failure and had elevated pulmonary capillary wedge pressure and/or left ventricular end-diastolic pressure at the time of the index procedure. Six patients also had evidence of baseline radiographic abnormalities.
  
  
  CONCLUSIONS
  Diffuse pulmonary hemorrhage is a potentially disastrous complication of GP Ilb/Illa antagonists. No specific predictors can be identified, but evidence of pulmonary congestion, baseline pulmonary abnormalities and use of higher heparin dosages may predispose patients to this serious complication.
authors.affiliation: Division of ardiology, St Johns Hospital & Medical Center, Detroit, MI, USA. arshadali@aol.com
authors.forename: Arshad
authors.initials: A
authors.lastname: Ali
authors.forename: Mustafa
authors.initials: M
authors.lastname: Hashem
authors.forename: Howard S
authors.initials: HS
authors.lastname: Rosman
authors.forename: Ghassan
authors.initials: G
authors.lastname: Kazmouz
authors.forename: Julius M
authors.initials: JM
authors.lastname: Gardin
authors.forename: Theodore L
authors.initials: TL
authors.lastname: Schrieber
mesh_terms: D000077284:Abciximab; D000368:Aged; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D000077542:Eptifibatide; D005260:Female; D006470:Hemorrhage / Q000139:chemically induced* / Q000453:epidemiology; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000009:adverse effects; D015994:Incidence; D008171:Lung Diseases / Q000139:chemically induced* / Q000453:epidemiology; D008297:Male; D008824:Michigan / Q000453:epidemiology; D008875:Middle Aged; D010455:Peptides / Q000009:adverse effects / Q000037:antagonists & inhibitors; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000009:adverse effects* / Q000037:antagonists & inhibitors*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D000077466:Tirofiban; D017211:Treatment Failure; D014443:Tyrosine / Q000009:adverse effects / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077466:Tirofiban; D000077542:Eptifibatide; D000077284:Abciximab