An Infected Drug-Eluting Stented Coronary Aneurysm Forming Intracardiac Fistula

Many cardiologists have usually operated percutaneous coronary intervention (PCI) for coronary artery disease practically. Sometimes, complications following stent implantation rarely include thrombosis, rupture, sepsis and infected coronary aneurysm [Baddour, 2004; Berkalp, 1999]. Particularly, infected coronary aneurysm causes fatal outcome. In addition to contamination at the time of catheterization, there are other mechanisms how stents can become infected, including transient bacteremia from skin flora via access-site hematomas, pseudoaneurysms, delayed bleeding, prolonged arterial sheath insertion, and several procedures performed from the same access site over a short time period [Baddour, 2004]. Previous report demonstrated that 18% of patients who underwent complex PCIs had detectable bacteremia [Ramsdale, 2004]. However, prophylactic antibiotics administarations are not conducted routinely prior to coronary stenting in the current PCI procedures, because the incident rate of stent infections was reported to be less than one in 10,000 cases [Myles, 2000]. The drug-eluting stent (DES) era was ushered in with the first published human study by Sousa et al. in 2001, showing a nearly complete abolition of neointimal hyperplasia by use of sirolimus-eluting stent (SES) [Sousa, 2001]. The role of DES is very questionable, because of long term anticoagulant therapy, but in the patients with comorbidity (diabetes mellitus) DES are recommend. Despite the dramatic capacity of SES to reduce the restenosis rate after PCI, several SES-related problems have been raised [Ong & Serruys, 2005]; 1) the requirement of a prolonged dual anti-platelet regimen to avoid the risk of DES thrombosis [McFadden, 2004], 2) the occurrence of acquired late malapposition 3) the late formation of coronary artery aneurysm (SES having an antiproliferative action may be responsible for the delayed and inappropriate healing, which should lead to weakening of the arterial wall and delayed aneurysm formation) [Abreu, 2005; Degertekin, 2003], 4) a severe localized hypersensitivity consisting predominantly of T lymphocytes and eosinophils, which was caused by the metallic stent, polymer, or sirolimus [Virmani, 2004; Nebeker, 2005; Stabile, 2004].