Alveolar hemorrhage: an underdiagnosed complication of treatment with glycoprotein IIb/IIIa inhibitors.
OBJECTIVE
Alveolar hemorrhage (AH) is a rare complication of treatment with GP IIb/IIIa inhibitors. Hemoptysis, a constant sign, lacks in specificity, and may occur in confounding syndromes such as pulmonary edema, pulmonary infarction, and pneumonia. Nonspecific symptoms and signs often delay the diagnosis, thereby allowing serious or even fatal disease progression. Here, we performed a large-scale retrospective analysis to define the incidence and risk factors of AH in the setting of GP IIb/IIIa inhibitors therapy.


BACKGROUND
Randomized controlled trials demonstrate that treatment with glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors may improve the outcome of acute myocardial infarction (AMI) and angioplastic procedures. However, this treatment may rarely lead to severe hemorrhagic complications, in particular AH. Unfortunately, the incidence and risk factors of AH remain poorly defined.


METHODS
We reviewed for the period extending from August 1998 to January 2005 consecutive histories of AMI patients receiving coronary arteriography and treatment with either eptifibatide or abciximab. Concomitantly admitted AMI patients not treated with GP IIb/IIIa inhibitors were reviewed and served as a control group. The diagnosis of AH required the demonstration of typical symptoms and signs including dyspnea, hemoptysis, arterial hypoxemia, pulmonary radiographic changes, and, when available, bronchoscopic signs for AH. Potential covariates including pulmonary disease, pulmonary hypertension, smoking, and use of other anticoagulant or antiplatelet agents were evaluated.


RESULTS
Six of 1,810 patients (0.33%) receiving eptifibatide and five of 3,648 patients (0.14%) receiving abciximab exhibited typical symptoms and signs of AH. Contrarily, only one of 4,136 patients (0.025%) receiving no GP IIb/IIIa inhibitors presented with similar symptoms and signs. There was no fatal outcome, though two patients required blood transfusions. Statistically significant differences were found between control patients and patients receiving eptifibatide alone (P = 0.004). There was also a significant difference between untreated patients and those receiving eptifibatide and abciximab (P = 0.017). No differences were found between eptifibatide and abciximab-treated patients (P = 0.19) or between abciximab and untreated control patients (P = 0.105).


CONCLUSIONS
AH is a rare complication of treatment with GP IIb/IIIa inhibitors. Its incidence ranged from 0.14% in patients treated with abciximab to 0.33% in those receiving eptifibatide. Compared to a control group, patients treated with GP IIb/IIIa inhibitors had a statistically increased risk for AH.
Iskandar
Said B
SB
Division of Cardiology, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee 37604, USA. drsiskandar@hotmail.com
Kasasbeh
Ehab S
ES
Mechleb
Bassam K
BK
Garcia
Israel
I
Jackson
Ann
A
Fahrig
Stephen
S
Albalbissi
Kaiss
K
Henry
Phillip D
PD
D000077284:Abciximab; D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D000077542:Eptifibatide; D005260:Female; D006469:Hemoptysis / Q000139:chemically induced* / Q000453:epidemiology; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy; D010455:Peptides / Q000009:adverse effects; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011650:Pulmonary Alveoli / Q000187:drug effects* / Q000503:physiopathology; D012189:Retrospective Studies; D012307:Risk Factors; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077542:Eptifibatide; D000077284:Abciximab