Document Detail


Directional atherectomy for treatment of restenosis within coronary stents: clinical, angiographic and histologic results.
MedLine Citation:
PMID:  1360479     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The safety and long-term results of directional coronary atherectomy in stented coronary arteries were determined. In addition, tissue studies were performed to characterize the development of restenosis. METHODS: Directional coronary atherectomy was performed in restenosed stents in nine patients (10 procedures) 82 to 1,179 days after stenting. The tissue was assessed for histologic features of restenosis, smooth muscle cell phenotype, markers of cell proliferation and cell density. A control (no stenting) group consisted of 13 patients treated with directional coronary atherectomy for restenosis 14 to 597 days after coronary angioplasty, directional coronary atherectomy or laser intervention. RESULTS: Directional coronary atherectomy procedures within the stent were technically successful with results similar to those of the initial stenting procedure (2.31 +/- 0.38 vs. 2.44 +/- 0.35 mm). Of five patients with angiographic follow-up, three had restenosis requiring reintervention (surgery in two and repeat atherectomy followed by laser angioplasty in one). Intimal hyperplasia was identified in 80% of specimens after stenting and in 77% after coronary angioplasty or atherectomy. In three patients with stenting, 70% to 76% of the intimal cells showed morphologic features of a contractile phenotype by electron microscopy 47 to 185 days after coronary intervention. Evidence of ongoing proliferation (proliferating cell nuclear antigen antibody studies) was absent in all specimens studied. Although wide individual variability was present in the maximal cell density of the intimal hyperplasia, there was a trend toward a reduction in cell density over time. CONCLUSIONS: Although atherectomy is feasible for the treatment of restenosis in stented coronary arteries and initial results are excellent, recurrence of restenosis is common. Intimal hyperplasia is a nonspecific response to injury regardless of the device used and accounts for about 80% of cases of restenosis. Smooth muscle cell proliferation and phenotypic modulation toward a contractile phenotype are early events and largely completed by the time of clinical presentation of restenosis. Restenotic lesions may be predominantly cellular, matrix or a combination at a particular time after a coronary procedure.
Authors:
B H Strauss; V A Umans; R J van Suylen; P J de Feyter; J Marco; G C Robertson; J Renkin; G Heyndrickx; V D Vuzevski; F T Bosman
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Publication Detail:
Type:  Clinical Trial; Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  20     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  1992 Dec 
Date Detail:
Created Date:  1992-12-31     Completed Date:  1992-12-31     Revised Date:  2010-03-24    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1465-73     Citation Subset:  AIM; IM    
Affiliation:
Catheterization Laboratory, Erasmus University, Rotterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Actins / chemistry
Adult
Aged
Angioplasty, Transluminal, Percutaneous Coronary*
Atherectomy, Coronary / methods,  standards*
Belgium
Biopsy
Cell Count
Cell Division
Coronary Angiography
Coronary Disease / diagnosis,  epidemiology,  surgery*
Diagnosis, Computer-Assisted
Equipment Design / standards
Feasibility Studies
Female
France
Humans
Hyperplasia
Immunohistochemistry
Male
Middle Aged
Muscle, Smooth, Vascular / chemistry,  pathology,  ultrastructure
Netherlands
Nuclear Proteins / chemistry
Phenotype
Proliferating Cell Nuclear Antigen
Recurrence
Reoperation / methods,  standards*
Stents*
Time Factors
Treatment Outcome
United States
Chemical
Reg. No./Substance:
0/Actins; 0/Nuclear Proteins; 0/Proliferating Cell Nuclear Antigen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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