interventionaL CARDIOLOGY


Cardiology Journal

2022, Vol. 29, No. 4, 718–719

DOI: 10.5603/CJ.2022.0063

Copyright © 2022 Via Medica

ISSN 1897–5593

eISSN 1898018X

Neoatherosclerosis with silent plaque rupture in a saphenous vein graft causing no re-flow phenomenon assessed by optical coherence tomography and histopathology

Takao Konishi1Yuki Takahashi1Sho Kazui1Yutaro Yasui1Kohei Saiin1Seiichiro Naito1Sakae Takenaka1Yoshifumi Mizuguchi1Atsushi Tada1Yuta Kobayashi1Kazunori Omote1Takuma Sato1Kiwamu Kamiya1Toshiyuki Nagai1Shinya Tanaka23Toshihisa Anzai1
1Department of Cardiovascular Medicine, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan
2Department of Cancer Pathology, Faculty of Medicine, Hokkaido University, Sapporo, Japan
3Institute for Chemical Reaction Design and Discovery (WPI-ICReDD), Hokkaido University, Sapporo, Japan

Address for correspondence: Takao Konishi, MD, PhD, Department of Cardiovascular Medicine, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, West 7, North 15, Kita-ku, Sapporo, 060-8638, Japan, tel: +81-11-706-6973, fax: +81-11-706-7874, e-mail:

Received: 7.04.2021 Accepted: 23.05.2022

This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.

A 79-year-old man with a history of coronary artery bypass grafting 22 years earlier was hospitalized due to stable angina. A bare metal stent was implanted in his saphenous vein graft (SVG) 15 years ago and then, a drug-eluting stent was implanted for the in-stent restenosis 8 years ago. Coronary angiography revealed a severe in-stent restenosis in the SVG anastomosed to the right coronary artery (Fig. 1A). Optical coherence tomography (OCT) showed plaque fissure, cholesterol crystals, and low-intensity area without attenuation adjacent to the lipid-rich plaque (LRP), which suggested the intraplaque hemorrhage (IPH) (Fig. 1B, a, b). OCT also revealed the disrupted intimal flap within the stent (Fig. 1B, c) and mild to moderate stenosis with LRP outside the stent. Following balloon dilatation for the target lesion, no-reflow phenomenon occurred. The coronary flow resumed by aspiration thrombectomy and nitroprusside administration. Histopathological examination of the aspirated specimens showed that they were composed of atherosclerotic plaques with fibrin, cholesterol clefts and inflammatory cells including foam cells (Fig. 1C, 1D). Previous reports have shown that IPH is one of the factors contributing to coronary plaque destabilization and plaque progression, which might cause effort angina. This case showed for the first time an in-stent neoatherosclerosis with silent plaque rupture in SVG that caused no-reflow phenomenon detected with OCT and confirmed by histopathology. Observations suggested that the use of a distal protection device and the administration of vasodilators should be strongly considered when OCT identifies the characteristics of vulnerable plaque during percutaneous coronary intervention.

Figure 1. A. The initial coronary angiogram showing the in-stent restenosis in saphenous vein graft (white arrow). B. Optical coherence tomography images showing (a) plaque fissure (thick yellow arrow), lipid-rich plaque (LRP), (b) cholesterol crystals (thin yellow arrow), intraplaque hemorrhage (light blue area), and (c) disruption of the intimal flap (yellow arrowhead). C, D. Histopathology of aspirated specimens showing fibrin thrombi with cholesterol clefts and inflammatory cells including foam cells (red arrows).
Conflict of interest: None declared


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