Polymorphonuclear blood leukocytes and restenosis after intracoronary implantation of drug-eluting stentsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

Abstract

Peripheral blood contents of osteonectin-positive progenitor cells and polymorphonuclear granulocytes were examined by flow cytometry in 38 patients after myocardial revascularisation with drug-eluting stents. Repeat coronary angiography performed 6-12 months after stent implantation revealed in-stent restenosis in 15 patients and its absence in 23 patients. The plasma levels of osteonectin-positive progenitor cells, neutrophils, and basophils did not differ in patients with and without restenosis. Eosinophil blood levels in patients with and without restenosis were 262+/-68 and 124+/-67 cells/microL (mean+/-SD, p<0.001), respectively. Only one of 19 patients (5%) with eosinophil content lower than the distribution median for the entire group developed restenosis, whereas in the group with eosinophil contents higher than the median (n=19) restenosis occurred in 14 patients (74%, p<0.001). Our findings suggest that the frequency of restenoses after stenting is related to high peripheral blood eosinophil content.

Coronary stent implantation links to the occurrence of eosinophilia and interstitial pneumonia: a case report and systematic review

“…Studies have demonstrated that eosinophils accumulate in tissues near metal components of coronary artery stents, particularly polymer scaffolds [ 9 ]. Additionally, a previous study indicated that peripheral blood eosinophil count increases during restenosis [ 29 ]. Hajizadeh R et al further established the predictive value of peripheral eosinophils for in-stent restenosis following coronary artery stent therapy for stable angina [ 30 ].…”

“…A smattering of indistinct granulomas in the bronchiolar region featuring multinucleated giant cells. High-dose steroids (2 weeks, dose unknown); Cefoxitin; roxithromycin Improved Jun Liu [ 29 ] 2018 54 F Sirolimus 4 days Fever, chest stuffiness No increase Thickened interstitial texture of outer lower lobe of both lungs, increased flake density, and uneven density NA Methylprednisolone (started at 80 mg/ day, gradually transitioned to 4 mg/ day); Imipenem; Oseltamivir Improved Kobayashi H [ 30 ] 2022 68 F Everolimus 9 months Dyspnea NA Mechanical pneumonia, including diffuse patchy air space consolidation, ground-glass shadows, and small nodular shadows NA No treatment Improved F, female; NA, not available Onset time: The interval between the insertion of drug-eluting stents and the manifestation of interstitial pneumonia …”

In-Stent Restenosis Exacerbated by Drug-Induced Severe Eosinophilia after Second-Generation Drug-Eluting Stent Implantation

“…Of interest, eosinophils infiltrating surrounding stent struts have been described after bare metal stent implantation, and eosinophils appear to be even more involved in DES than in BMS restenosis [13]. On the other hand, Gabbasov et al demonstrated the frequency of restenoses after stenting is related to high peripheral blood eosinophil content, suggesting the increase in eosinophil count itself may be a risk factor for the progression of ISR after stent deposition [14]. Indeed, bronchial asthma, the pathologic process to which eosinophils are closely related, was exacerbated by the increase of eosinophil contribution [15].…”

Hypersensitivity and in-stent restenosis in coronary stent materials

“…Similarly, some case reports have revealed histopathological findings of lymphocytic and eosinophilic infiltration following Cipher stent implantation. Eosinophils may accumulate late and secrete inflammatory factors, initiate inflammatory and hypersensitivity reactions, and exacerbate tissue damage, thereby promoting smooth muscle cell migration and proliferation, leading to lumen narrowing and the occurrence and development of ISR ( Gabbasov et al, 2009 ). Notably, eosinophils are equally important in the promotion of thrombosis ( Sakai et al, 2009 ).…”