Pathology of acute and chronic coronary stenting in humans

Citation
A. Farb et al., Pathology of acute and chronic coronary stenting in humans, CIRCULATION, 99(1), 1999, pp. 44-52
Citations number
14
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
99
Issue
1
Year of publication
1999
Pages
44 - 52
Database
ISI
SICI code
0009-7322(19990112)99:1<44:POAACC>2.0.ZU;2-W
Abstract
Background-Despite the increasing use of stents, few reports have described human coronary artery morphology early and late after stenting. Methods and Results-Histology was performed on 55 stents in 35 coronary ves sels (32 native arteries and 3 vein grafts) from 32 patients. The mean dura tion of stent placement was 39+/-82 days. Fibrin, platelets, and neutrophil s were associated with stent struts less than or equal to 11 days after dep loyment. In stents implanted for less than or equal to 3 days, only 3% of s truts in contact with fibrous plaque had >20 associated inflammatory cells compared with 44% of struts embedded in a lipid core and 36% of struts in c ontact with damaged media (P<0.001). Neointimal growth determined late hist ological success, and increased neointimal growth correlated with increased stent size relative to the proximal reference lumen area. Neointimal thick ness was greater for struts associated with medial damage than struts in co ntact with plaque (P<0.0001) or intact media (P<0.0001). When matched for t ime since treatment, neointimal cell density in stented arteries was simila r to that in unstented arteries that had undergone balloon angioplasty and showed similar proteoglycan deposition. Conclusion-Morphology after coronary stenting demonstrates early thrombus f ormation and acute inflammation followed by neointimal growth. Medial injur y and lipid core penetration by struts result in increased inflammation. Ne ointima increases as the ratio of stent area to reference lumen area increa ses. Deployment strategies that reduce medial damage and avoid stent oversi zing may lower the frequency of in-stent restenosis.