Diffuse alveolar hemorrhage following administration of tirofiban in a patient with acute coronary syndrome: a fatal complication

It is now established that glycoprotein (GP) IIb/IIIa 62-year-old female patient was admitted to a local receptor blockers are indicated in patients with definite acute coronary syndrome where there is continuing ischemia or with high risk features or with planned percutaneous coronary intervention (PCI) [1]. The GP IIb/IIIa receptor is abundant on the platelet surface. When platelets are activated, this receptor undergoes a change in configuration conformation that increases its affinity for binding to fibrinogen and other ligands. The binding of molecules of fibrinogen to receptors on different platelets results in platelet aggregation. This mechanism is independent of the stimulus for platelet aggregation and represents the final and obligatory pathway for platelet aggregation [2]. The platelet GP IIb/IIIa receptor antagonists act by occupying the receptors, preventing fibrinogen binding, and thereby preventing platelet aggregation. Tirofiban is a nonpeptide, competitive antagonist of GP IIb/IIIa receptors [3]. It has a half-life of 2–3 h and is highly specific for the GP IIb/IIIa receptor, with no effect on the vitronectin receptor (a-h3 integrin). Platelet aggregation returns to normal in 4–8 h after discontinuation of the drug, a finding that is consistent with the relatively short half-life of the drug [4]. The efficacy of GP IIb/IIIa antagonists in prevention of the complications associated with PCI has been shown in trials, many of which composed totally or largely of patients with acute coronary syndrome [4]. The use of GP IIb/IIIa antagonists is associated with a slight increase in bleeding complications [5]. We report a patient who succumbed to pulmonary hemorrhage following administration of tirofiban, which was administered following PCI.