Mechanisms of Very Late Stent Thrombosis After Drug ... · After Drug-Eluting Stent Implantation...

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IMAGING VIGNETTE Mechanisms of Very Late Stent Thrombosis After Drug-Eluting Stent Implantation Findings From Coronary Angioscopy and Optical Coherence Tomography Hiroki Ikenaga, MD, Masaharu Ishihara, MD, PHD, Kazuoki Dai, MD, Yasuharu Nakama, MD, Takayuki Ohtani, MD DRUG-ELUTING STENTS (DES) ARE NOW WIDELY USED FOR PATIENTS WITH CORONARY ARTERY DISEASE UNDERGOING PERCUTANEOUS COR- ONARY INTERVENTIONS . A current major concern of using DES is very late stent thrombosis (VLST) that may occur beyond 1 year after DES implantation (1). VLST is an infrequent, albeit catastrophic complication, which can lead to myocardial infarction or sudden cardiac death (2). However, the underlying mechanisms of VLST remain unclear. In the current report, we show 3 cases of VLST after sirolimus-eluting stent (SES) implantation. Findings from coronary angioscopy (CAS) and optical coherence tomography (OCT) suggested 3 differential mechanisms of VLST in each case. In the first case (Fig. 1), CAS and OCT showed uncovered and malapposed stent struts at the culprit lesion. Late stent malapposition is caused by stent underexpansion and thrombus resolution or by positive vessel remodeling. The later mechanism is characteristic of DES (3). In this case, CAS findings revealed yellow plaque, which might reflect inflammatory reaction. Delayed neointimal coverage over stent struts and late stent malapposition are ordinarily thought to be associated with VLST in patients treated with DES. In the second case (Fig. 2), coronary rupture was observed in the yellow plaque which completely covered stent struts. Rupture of thin-cap fibroatheroma is a common cause of acute coronary syndrome. It has been reported that neointimal atherosclerotic change (neoatherosclerosis) occurred with DES earlier than with a bare-metal stent; and unstable features of neoatherosclerosis were identified after shorter implantation duration then with DES (4). Enhanced inflammation after DES implantation may promote atherosclerosis and exaggerate vulnerability of the plaque. In the third case (Fig. 3), ruptured plaque was observed under the stent struts. The rupture continued to a large cavity behind the completely covered stent struts. To our knowledge, this is the first report of such a case. This is likely associated with delayed arterial healing following DES implantation in a patient with acute myocardial infarction (AMI). The underlying plaque in this patient might have been lipid-rich necrotic plaque, which was not covered by thick neointima following stent implantation because of the drug effect. This may have created another thin-cap fibroatheroma, which finally ruptured. From the Department of Cardiology, Hiroshima City Hospital, Hiroshima, Japan. All authors have reported that they have no relationships relevant to the contents of this paper to disclose. JACC: CARDIOVASCULAR IMAGING VOL. 4, NO. 11, 2011 © 2011 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 1936-878X/$36.00 PUBLISHED BY ELSEVIER INC. DOI:10.1016/j.jcmg.2011.05.008

Transcript of Mechanisms of Very Late Stent Thrombosis After Drug ... · After Drug-Eluting Stent Implantation...

Page 1: Mechanisms of Very Late Stent Thrombosis After Drug ... · After Drug-Eluting Stent Implantation Findings From Coronary Angioscopy and Optical Coherence Tomography Hiroki Ikenaga,

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I M A G I N G V I G N E T T E

Mechanisms of Very Late Stent ThrombosisAfter Drug-Eluting Stent ImplantationFindings From Coronary Angioscopy and Optical Coherence Tomography

Hiroki Ikenaga, MD, Masaharu Ishihara, MD, PHD, Kazuoki Dai, MD,Yasuharu Nakama, MD, Takayuki Ohtani, MD

D R U G - E L U T I N G S T E N T S ( D E S ) A R E N O W W I D E L Y U S E D F O R P A T I E N T S

W I T H C O R O N A R Y A R T E R Y D I S E A S E U N D E R G O I N G P E R C U T A N E O U S C O R -

O N A R Y I N T E R V E N T I O N S . A current major concern of using DES is very late stent thrombosis

(VLST) that may occur beyond 1 year after DES implantation (1). VLST is an infrequent, albeit

catastrophic complication, which can lead to myocardial infarction or sudden cardiac death (2).

However, the underlying mechanisms of VLST remain unclear. In the current report, we show 3 cases

of VLST after sirolimus-eluting stent (SES) implantation. Findings from coronary angioscopy (CAS) and

optical coherence tomography (OCT) suggested 3 differential mechanisms of VLST in each case.

In the first case (Fig. 1), CAS and OCT showed uncovered and malapposed stent struts at the culprit

lesion. Late stent malapposition is caused by stent underexpansion and thrombus resolution or by

positive vessel remodeling. The later mechanism is characteristic of DES (3). In this case, CAS findings

revealed yellow plaque, which might reflect inflammatory reaction. Delayed neointimal coverage over

stent struts and late stent malapposition are ordinarily thought to be associated with VLST in patients

treated with DES.

In the second case (Fig. 2), coronary rupture was observed in the yellow plaque which completely

covered stent struts. Rupture of thin-cap fibroatheroma is a common cause of acute coronary syndrome.

It has been reported that neointimal atherosclerotic change (neoatherosclerosis) occurred with DES

earlier than with a bare-metal stent; and unstable features of neoatherosclerosis were identified after

shorter implantation duration then with DES (4). Enhanced inflammation after DES implantation may

promote atherosclerosis and exaggerate vulnerability of the plaque.

In the third case (Fig. 3), ruptured plaque was observed under the stent struts. The rupture continued

to a large cavity behind the completely covered stent struts. To our knowledge, this is the first report

of such a case. This is likely associated with delayed arterial healing following DES implantation in a

patient with acute myocardial infarction (AMI). The underlying plaque in this patient might have been

lipid-rich necrotic plaque, which was not covered by thick neointima following stent implantation

because of the drug effect. This may have created another thin-cap fibroatheroma, which finally

ruptured.

From the Department of Cardiology, Hiroshima City Hospital, Hiroshima, Japan. All authors have reported that they have no

relationships relevant to the contents of this paper to disclose.
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J A C C : C A R D I O V A S C U L A R I M A G I N G , V O L . 4 , N O . 1 1 , 2 0 1 1

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Ikenaga et al.

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Figure 1. Uncovered and Malapposed Stent Struts

A 70-year-old man underwent a 2.5 mm � 28 mm sirolimus-eluting stent (SES) implantation in the mid-left anterior descending artery (LAD) for acute myocar-dial infarction (AMI). Aspirin (100 mg/day) with clopidogrel (75 mg/day) was prescribed, but clopidogrel was stopped because of drug-induced liver injury 1month after SES implantation. Thirty-four months after SES implantation, the patient suddenly suffered from recurrence of angina and was admitted to our hos-pital. Emergent coronary angiography (CAG) showed thrombus-like shadow in SES (A). After aspiration thrombectomy (B), optical coherence tomography (OCT)and coronary angioscopy (CAS) were performed. OCT and CAS revealed no coverage of neointima over stent struts in the distal and proximal portion of stent(a). At thrombus sites, OCT revealed malapposition and red and white thrombus on the stent struts which were not covered by neointima (b, c and d). CAS

revealed malapposition and yellow plaque under stent struts (b, c and d, yellow arrow).

Figure 2. In-Stent Restenosis With Neoatherosclerosis

A 68-year-old man underwent 2 SES implantations in the mid-LAD for AMI (2.5 mm � 18 mm and 2.5 mm � 18 mm). Aspirin (100 mg/day) with ticlopidine (200mg/day) was prescribed. Aspirin and ticlopidine were stopped 1 year after SES implantation by a self-judgment. Fifty-four months after SES implantation, thepatient suddenly suffered from recurrence of angina on exertion and was admitted to our hospital. Emergent CAG revealed total occlusion at proximal SES inthe mid LAD (A). After balloon angioplasty (B), OCT and CAS were performed. OCT and CAS revealed neointimal coverage over stent in the distal and proximalportion of stent (a). OCT revealed cavity formation (white arrow) over stent struts (b, c). CAS revealed yellow plaque rupture (C, yellow arrow) and cavity forma-

tion (b, c, red arrow) over stent struts. Abbreviations as in Figure 1.
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Address for correspondence: Masaharu Ishihara, MD, PHD, Department of Cardiology, Hiroshima City Hospital, 7-33, Moto-machi,Naka-ku, Hiroshima, 730-8518 Japan. E-mail: [email protected].

Figure 3. Rupture Continued to Lipid Core Behind Covered Stent Struts

A 70-year-old man underwent a 2.5 mm � 28 mm SES implantation in the mid-LAD for AMI. Aspirin (100 mg/day) and ticlopidine (200 mg/day) was prescribedthereafter. Ticlopidine was stopped 6 months after SES implantation. Fifty-nine months after SES implantation, the patient suddenly suffered from recurrence ofangina and was admitted to our hospital. Emergent CAG showed total occlusion at the site of SES (A). After aspiration thrombectomy (B), OCT and CAS was per-formed. In the distal and proximal portion of stent, OCT and CAS revealed neointimal coverage over stent struts and no stent underexpansion (a). OCT revealedmixed thrombus, plaque rupture (b), and cavity formation behind neointima-covered stent (c, d, white arrow). CAS revealed ruptured yellow plaque under stentstruts (b, c, yellow arrow). The stent struts were floating over the ruptured plaque (b, red arrow). Abbreviations as in Figure 1.

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R E F E R E N C E S

1. Kastrati A, Mehilli J, Pache J, et al.Analysis of 14 trials comparingsirolimus-eluting stents with bare-

metal stent. N Engl J Med 2007;356:1030 –9.

. Cutlip DE, Baim DS, Ho KK, et al.Stent thrombosis in the modern era: apooled analysis of multicenter coronarystent trial. Circulation 2001;103:1967–71.

. Kang SJ, Mintz GS, Park DW, et al.

Late and very late drug-eluting stentmalapposition: serial 2-year quantita-

tive IVUS analysis. Circ CardiovascInterv 2010;3:335–40.

4. Nakazawa G, Otsuka F, Nakano M, etal. The pathology of neoatherosclerosisin human coronary implants. Bare-

metal and drug-eluting stents. J AmColl Cardiol 2011;57:1314–22.