Late coronary thrombosis secondary to a sirolimus-eluting stent.

Sirolimus-Eluting Stent A report by Virmani et al1 described a localized hypersensitivity and late coronary thrombosis secondary to a sirolimuseluting stent in a 58-year-old man who died 18 months after stent implantation. The authors discussed a localized hypersensitivity vasculitis in response to the Cypher stents, resulting in an acute myocardial infarction, secondary to late in-stent thrombosis at 18 months. The hypersensitivity reaction was thought to be either due to the metallic stent, the polymer, or the sirolimus coating. The exact mechanism, however, remained unclear, and it was postulated that polymers, like those used for coating of the metallic stent, may have been responsible for the hypersensitivity vasculitis. In October 2003, the US Food and Drug administration notified physicians of a possible generalized hypersensitivity reaction in 50 patients from 290 reports of subacute stent thrombosis. Sixty patients of those 290 reports died as a result of subacute stent thrombosis.2 Although the authors postulate a hypersensitivity reaction to the polymer, we have previously observed in a rat model enhanced thrombus formation in synthetic vascular grafts treated by systemic or local administration of rapamycin.3 Thrombus formation was largest in animals that received high-dose oral rapamycin (3.0 mg/kg), or the same dose of rapamycin intraperitoneally, when compared with the control group, or animals treated with mycophenolate mofetil (Cell Cept). Thus, our data suggest that rapamycin is effective for prevention of intimal proliferation but enhances thrombus formation. This observation would support the hypothesis of Virmani et al1 that rapamycin, rather than the polymer coating, induces the hypersensitivity reaction.