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Right arrow Catheter-based coronary interventions: stents
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(Circulation. 1999;99:44-52.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Pathology of Acute and Chronic Coronary Stenting in Humans

Andrew Farb, MD; Giuseppe Sangiorgi, MD; Andrew J. Carter, DO; Virginia M. Walley, MD; William D. Edwards, MD; Robert S. Schwartz, MD; Renu Virmani, MD

From the Department of Cardiovascular Pathology (A.F., A.J.C., R.V.), Armed Forces Institute of Pathology, Washington, DC; the Mayo Clinic (G.S., W.D.E., R.S.S.), Rochester, Minn; and The University of Ottawa Heart Institute and Ottawa Civic Hospital (V.M.W.), Ottawa, Ontario, Canada.

Correspondence to Renu Virmani, MD, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000.

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 vessels (32 native arteries and 3 vein grafts) from 32 patients. The mean duration of stent placement was 39±82 days. Fibrin, platelets, and neutrophils were associated with stent struts <=11 days after deployment. In stents implanted for <=3 days, only 3% of struts 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 contact with damaged media (P<0.001). Neointimal growth determined late histological success, and increased neointimal growth correlated with increased stent size relative to the proximal reference lumen area. Neointimal thickness was greater for struts associated with medial damage than struts in contact with plaque (P<0.0001) or intact media (P<0.0001). When matched for time since treatment, neointimal cell density in stented arteries was similar to that in unstented arteries that had undergone balloon angioplasty and showed similar proteoglycan deposition.

Conclusions—Morphology after coronary stenting demonstrates early thrombus formation and acute inflammation followed by neointimal growth. Medial injury and lipid core penetration by struts result in increased inflammation. Neointima increases as the ratio of stent area to reference lumen area increases. Deployment strategies that reduce medial damage and avoid stent oversizing may lower the frequency of in-stent restenosis.


Key Words: stents • coronary disease • restenosis • angioplasty • pathology




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