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      Histopathological Correlates of Early Arterial Recoil following Directional Coronary Atherectomy

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          Abstract

          Elastic recoil has been implicated in the pathophysiology of restenosis after conventional balloon angioplasty alone. Directional atherectomy may attenuate arterial recoil by removing the internal elastic lamina and medial smooth muscle cells and altering the vessel wall architecture. This study sought to evaluate early recoil after directional atherectomy and its relation with excision of deep arterial wall structures. We prospectively evaluated the correlation of the histopathologic evidence of media or adventitia as assessed in the atheroma retrieved during the procedure with the early changes in minimal lumen diameter after directional atherectomy followed by adjunct balloon dilatation in 50 consecutive cases. Recoil was assessed by routinely performed 1- and 15-min postprocedure angiograms, and patients were divided into two groups according to the absence (group I, n = 26) or presence (group II, n = 24) of recoil. The mean changes in minimal luminal diameter between 1 and 15 min was +0.22 mm in group I and –0.14 mm in group II. The absence of recoil was strongly associated with evidence of media tissue in the pathologic analysis as compared with cases with recoil (42 vs. 18%, respectively; p = 0.02). Similarly, retrieval of adventitia was seen exclusively in the group without recoil (15 vs. 0%; p = 0.06). Vessels that underwent recoil had significantly larger reference and immediate postprocedure minimal luminal diameters (3.62 ± 0.57 and 3.02 ± 0.45 mm, respectively) as compared with arteries with no recoil (3.28 ± 0.35 and 2.75 ± 0.43 mm, respectively; p < 0.05 for both). Therefore, early luminal changes, likely related to elastic recoil, correlated with excision of deep wall structures during directional atherectomy. Arteries that showed recoil were larger, possibly due to thicker muscular layer and/or larger plaque burden as compared with arteries that did not recoil. Thus, optimal tissue debulking during directional atherectomy appears to attenuate recoil, providing an additional insight into the mechanism of action of this percutaneous revascularization device.

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          Quantitative assessment with intracoronary ultrasound of the mechanisms of restenosis after percutaneous transluminal coronary angioplasty and directional coronary atherectomy.

          The mechanisms of immediate and late changes after percutaneous transluminal coronary angioplasty (PTCA) and directional coronary atherectomy (DCA) were assessed by serial ultrasound imaging in 18 patients treated with PTCA and 16 treated with DCA before, immediately after, and 6 months after coronary interventions. A reduction in plaque area was the main operative mechanism of DCA, explaining 66% of lumen enlargement. In the PTCA group, the increase in lumen area was the result of a more balanced combination of plaque reduction (52% of lumen increase) and increase in total lumen area (48%); p < 0.05 versus DCA. In the PTCA group, this last mechanism was prevalent (p < 0.05) in the lesions showing wall fracture or dissection after treatment and in the lesions with a mixed or calcific composition. In the PTCA group, concentric lesions showed a greater plaque compression than eccentric lesions (p < 0.02). Plaque increase was responsible for 92% and 32% of the late lumen loss after DCA and after PTCA, respectively (p < 0.05). In PTCA patients, a chronic reduction in total vessel area was the main operative mechanism of lumen reduction (67%) and was prevalent in lesions with a mixed or calcific composition. (p < 0.05).
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            Author and article information

            Journal
            CRD
            Cardiology
            10.1159/issn.0008-6312
            Cardiology
            S. Karger AG
            0008-6312
            1421-9751
            1998
            July 1998
            14 August 1998
            : 90
            : 1
            : 32-36
            Affiliations
            Cardiovascular Institute, Mount Sinai Medical Center, New York, N.Y., USA
            Article
            6813 Cardiology 1998;90:32–36
            10.1159/000006813
            9693168
            © 1998 S. Karger AG, Basel

            Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

            Page count
            Pages: 5
            Categories
            Catheterization and Interventional Cardiology

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