Late stent thrombosis six months after ultrathin-strut covered stent implantation in lesion with calcified nodule

Abstract

A 72-year-old woman undergoing hemodialysis presented with effort angina pectoris due to severe stenosis with calcified nodules in the right coronary artery. Percutaneous coronary intervention was performed using an excimer laser coronary angioplasty and an ultrathin-strut covered stent (CS) was implanted due to coronary perforation. An additional durable-polymer everolimus-eluting stent (DP-EES) was implanted because of protrusions in the proximal edge of the CS. However, late stent thrombosis occurred six months after ultrathin-strut covered stent implantation for a calcified nodule. After thrombus aspiration, intravascular imaging analyses revealed that the struts within the CS were fully covered with thick neointimal hyperplasia. In contrast, half of the struts in the DP-EES were uncovered and some struts were malapposed. In this case, we speculated that the cause of the current late stent thrombosis was dispersion of the thrombi formed at the uncovered with malapposed sites in the DP-EES into a severe stenosis caused by neointimal hyperplasia in the CS. Neointimal hyperplasia occurs at the edge of the CS, a CS should be implanted locating its edge on the site with less plaque.

Learning objectives

• •To evaluate the mechanism of late stent thrombosis after ultrathin strut-covered stent implantation for lesions with calcified nodules.
• •To discuss the optimal covered stent placement locating its edge on the site with less plaque.
• •To recognize that introduction of an ultrathin-strut covered stent for lesions with calcified nodules requires careful consideration.

Introduction

PK papyrus® ultrathin-strut covered stents (CS) (Asahi Intecc, Aichi, Japan) have shown favorable rates of successful device delivery and perforation sealing [1]. One of the speculated mechanisms of restenosis after percutaneous coronary intervention (PCI) for calcified nodules (CNs) is progression of the underlying CNs [2]. Based on the mechanism of restenosis, CS has been hypothesized to be effective for lesions with CNs, due to the lack of progression of the underlying CNs beyond the CS. However, the outcomes of ultrathin-strut CS implantation for lesions with CNs have not been elucidated. We encountered a case of late stent thrombosis six months after ultrathin-strut CS implantation for CNs.

Case report

A 72-year-old woman was admitted to our hospital due to shortness of breath on exertion. Since an electrocardiogram showed a new negative T wave in II/III/aVF leads, we suspected the presence of chronic coronary syndrome. Coronary angiography demonstrated the severe stenosis with CNs in the right coronary artery (Fig. 1a, b). She had coronary risk factors, such as hypertension, diabetes mellitus, hyperuricemia, and dyslipidemia. She had undergone hemodialysis for 7 years due to diabetic nephropathy. PCI was performed using a 0.9 mm excimer laser coronary atherectomy (ELCA) (Philips, Eindhoven, the Netherlands). After ELCA, an ultrathin-strut CS (PK papyrus® 2.5 mm × 20 mm) was implanted due to coronary perforation (Fig. 1c). An additional durable-polymer everolimus-eluting stent (DP-EES) (Xience Skypoint™ 3.0 mm × 8 mm, Abbott Vascular, Santa Clara, CA, USA) was implanted because of protrusions in the proximal edge of the CS, which resulted in sufficient angiographic results (Fig. 1d). Intravascular ultrasound showed adequate stent expansion. Dual-antiplatelet therapy with aspirin and prasugrel was initiated before the PCI and continued thereafter. However, six months after the PCI, the patient was admitted to our hospital with sudden onset of chest pain at rest. Electrocardiography revealed ST-segment elevation in leads II, III, and VF. Transthoracic echocardiography revealed a reduced ejection fraction and hypokinesis of the posterior-inferior left ventricular wall. Emergency coronary angiography revealed a total occlusion of the CS segment (Fig. 2a). We diagnosed this event as late stent thrombosis (ST). A 0.014-inch guidewire (Amati®, Japan Lifeline, Tokyo, Japan) easily crossed the lesion. After thrombus aspiration and pre-dilatation with a 2.0 mm balloon, intravascular imaging analyses with optical coherence tomography (OCT) (Dragonfly Opstar™, Abbott Vascular) and coronary angioscopy (CAS) (Forwardlooking™, Taisho Biomed Instruments, Osaka, Japan) were performed. OCT revealed that the struts within the CS were fully covered with neointima and organized thrombus, with some exhibiting thick neointimal hyperplasia. In contrast, half of the struts in the DP-EES were uncovered and some struts were malapposed (covered: 57.9 %, uncovered with apposed: 37.0 %, uncovered with malapposed: 5.2 %; Fig. 2b, Video 1). CAS showed that the CS was completely covered by white neointima and red thrombi as well as uncovered struts were detected at the DP-EES implantation site (Fig. 2c, Video 2). We performed pre-dilation with a 3.0 mm scoring balloon (Aperta NSE®, Nipro, Osaka, Japan), followed by 3.0-mm drug-coated balloon inflation (Sequent® Please Neo, Nipro). The final angiography revealed adequate expansion and coronary flow (Fig. 2d). Chest pain improved after PCI. Three months after discharge, the patient had experienced no further episodes of chest pain.

Fig. 1.

Coronary angiography (CAG) and intravascular ultrasound (IVUS) at the time of initial percutaneous coronary intervention (PCI). (a) CAG showed severe stenosis with eccentric plaques in the middle part of the right coronary artery. (b) IVUS showed severe stenosis with calcified nodules. (c) IVUS showed coronary perforation (white arrows). (d) Sufficient angiographic results were obtained with the implantation of a durable-polymer everolimus-eluting stent (yellow dashed line) and an ultrathin-strut covered stent (yellow solid line) for a severely calcified lesion in the right coronary artery.

Fig. 2.

Coronary angiography (CAG), optical coherence tomography (OCT), and coronary angioscopy (CAS) at the time of the second percutaneous coronary intervention (PCI). (a) CAG showed total occlusion of the covered stent (CS) implantation site (yellow solid line) with patency of the durable-polymer everolimus-eluting stent (DP-EES) site (yellow dashed line). (b) OCT showed that the struts within the CS are fully covered with neointima, with some exhibiting thick neointimal hyperplasia. Half of the struts in the DP-EES were uncovered and some struts were malapposed. (c) CAS showed that the CS was completely covered by white neointima and red thrombi as well as uncovered struts were detected at the DP-EES implantation site. (d) Final angiography showed adequate expansion and coronary flow.

Discussion

Here, we report a case of late ST after ultrathin-strut CS implantation, in which the intravascular status was evaluated using OCT and CAS. This is the first recorded case of late ST of an ultrathin-strut CS in which the mechanism was investigated in detail using intravascular imaging devices.

PK papyrus® ultrathin-strut CS is constructed of an ultrathin (60 μm) strut cobalt chromium design covered on the abluminal side with an electrospun polyurethane matrix. Ultrathin-strut CS have shown favorable rates of successful device delivery and perforation sealing [1]; in addition, ultrathin-strut CS demonstrated target lesion revascularization and ST rates comparable to other polytetrafluoroethylene covered stents [1,2]. Based on the intravascular imaging findings, we speculated that the cause of the current late ST was dispersion of the thrombi formed at the uncovered with malapposed sites in the DP-EES into a severe stenosis caused by neointimal hyperplasia in the CS, resulting in total occlusion of the CS implantation site. Even with the usage of ultrathin-strut, PK papyrus® does not contain an anti-proliferating drug, which would be necessary to prevent the neointimal hyperplasia leading to restenosis. Also, OCT within the covered stent showed possible acute thrombus formation which could have developed over the organized thrombus in the CS. This would be caused by the high thrombogenicity of CS. In addition, because neointimal hyperplasia occurs at the edge of the CS [3], a CS should be implanted locating its edge on the site with less plaque.

The clinical outcomes after PCI for the lesion with CNs have been unsatisfactory even with the current drug-eluting stent (DES), and there is currently no established treatment for CNs [4]. One of the speculated mechanisms of restenosis after PCI for CNs is progression of the underlying CNs [4]. Herein, we have reported a case of early in-stent restenosis caused by this mechanism [5]. Based on the mechanism of restenosis, CS has been hypothesized to be effective for lesions with CNs, due to the lack of progression of the underlying CNs beyond the CS. However, in the current case, the ultrathin-strut CS showed thick intimal hyperplasia and could not prevent in-stent restenosis. This may be because CS does not contain an anti-proliferative drug, and drug technology is necessary to prevent neointimal hyperplasia caused by smooth muscle cell proliferation. Therefore, the use of a CS for lesions with CNs should be carefully considered.

Conclusions

We encountered a case of late ST six months after ultrathin-strut CS implantation in a lesion with CNs. Even if a CS can prevent the protrusion and progression of underlying CNs, introduction of a CS for lesions with CNs should be carefully considered.

Patient permission/consent statement

Written informed consent was obtained from the patient for publication of this case report.

Declaration of competing interest

T. Ishihara received lecture fee from Nipro, and T. Mano received a research grant from Abbott Vascular Japan.