Inflammatory Reaction After Sirolimus-Eluting Stent Implant

Comparison of the Systemic Levels of Inflammatory Markers after Percutaneous Coronary Intervention with Bare Metal versus Sirolimus‐Eluting Stents

“…Recent data also show that sirolimus exposure induces an early inflammatory reaction in the vessel wall characterized by upregulation of superoxide release leading to significant increase in transmural reactive oxygen species 16 . Histologic findings in coronary artery segments treated with SES have shown them to harbor intense mural inflammatory reactions in the months following PCI 17 . Clinical studies have shown that impairment of coronary endothelial function by SES is persistent for several months following PCI as well 18 …”

“…16 Histologic findings in coronary artery segments treated with SES have shown them to harbor intense mural inflammatory reactions in the months following PCI. 17 Clinical studies have shown that impairment of coronary endothelial function by SES is persistent for several months following PCI as well. 18 The polymeric coating of SES is another potential trigger of inflammation.…”

Angioplasty for the late stent thrombosis, the new technical challenge: A single centre experience

“…We feel that these difficulties could be secondary to a greater element of fibrosis in these thrombotic lesions which possibly have developed more gradually over time than the true acute thrombi producing acute total occlusions of AMI in native vessels or the early subacute stent thrombosis producing early stent occlusions. W. J. Gomes and others in pathological studies have commented on a greater level of fibrosis in thrombotic occlusions secondary to drug-eluting stents [7].…”

Does the use of paclitaxel or rapamycin-eluting stent decrease further need for coronary-artery bypass grafting when compared with bare-metal stent?

“…25 Endothelial function becomes altered, thereby generating cytokine hypersecretion that preserves the infl ammatory process and leads to changes in the quantities of endothelial mediators released, which may decrease the nitric oxide levels (vasodilatation) or increase the endothelin-1 levels (vasoconstriction). 26,27 Studies have shown that drug-eluting stents may exacerbate the inflammatory process, such that they may accentuate the restenosis process at the stent extremities 28 and boost the strength of some platelet agonists, thus promoting thrombus formation. 29 Moreover, it has been demonstrated that sirolimus (rapamycin) reduces the production of nitric oxide.…”