364

Images in CAD

Images in CAD Coronary Artery Disease 2015, 26:364–365

Correspondence to Ashish H. Shah, MD, MRCP (UK), Department of Cardiology, Toronto General Hospital, Toronto, ON, Canada M5G 0B2 Tel: + 1 416 835 2822; fax: + 1 416 340 3000; e-mail: [email protected]

Recurrent stent thrombosis: where is the clue? Ashish H. Shaha, Timothy D. Kinnairdb and Ashesh N. Buchc, aUniversity Health Network, Toronto, Ontario, Canada, bUniversity Hospital of Wales, Cardiff, UK and cEast Carolina University Hospitals, Greenville, North Carolina, USA

Received 23 November 2014 Revised 6 January 2015 Accepted 7 January 2015

Fig. 1

(a)

(b)

(d)

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(e)

(f)





B Length (10.0 mm) 30 40

A Length (27.7 mm) 10 20

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10

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(g)

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30

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∗C Length (10.6 mm)

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D Stented LAD/D1 (a). Residual thrombus noted in 2012 after presentation with stent thrombosis (b), and angiographic appearance predischarge (c). Optical coherence tomography confirms well expanded but malapposed stent struts (d) that appeared well apposed after further postdilatation (e). Final angiographic appearance (f), and stent apposition observed in longitudinal view before and after postdilatation (g, h). Stented segment marked with arrow and malapposed struts with *. D1, diagonal; LAD, left anterior descending. 0954-6928 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

DOI: 10.1097/MCA.0000000000000230

Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.

Recurrent stent thrombosis Shah et al. 365

Stent thrombosis (ST) is a serious, potentially lifethreatening complication of percutaneous coronary intervention (PCI). Most of the factors responsible for ST are stent or procedure related [1]. A 60-year-old man, known to have hypertension, dyslipidemia and be an exsmoker, underwent PCI to the left anterior descending (LAD) and diagonal artery in 2005, using CYPHER (Cordis Corporation, Miami Lakes, Florida, USA) drug-eluting stents. He represented to the hospital in 2006 with anterior ST elevation myocardial infarction 10 days after stopping 12 months of clopidogrel, as advised after initial PCI. The paramedics treated him with thrombolysis in the ambulance. Coronary angiography demonstrated patent stents in LAD/diagonal. ST was the provisional diagnosis, but no further interventions were offered. The patient was discharged on long-term aspirin and clopidogrel. In 2012, he needed to undergo elective knee arthroscopy. After a negative stress test, he was advised to stop clopidogrel 1 week before the procedure. Four hours into recovery, postarthroscopy, the patient experienced chest pain and ECG confirmed anterior ST elevation myocardial infarction. He underwent primary PCI, and angiography confirmed ST (Fig. 1b), which was treated with thrombus aspiration and IIb/IIIa infusion for 16 h. Angiography post IIb/IIIa infusion was satisfactory (Fig. 1c), so the patient was discharged with long-term dual antiplatelet therapy (DAPT). He was brought back electively for intracoronary imaging with optical coherence tomography that confirmed the presence of well expanded but nearly 10 mm segment of malapposed and uncovered stent struts in proximal LAD (Fig. 1d and g), very likely due to positive vessel remodeling. Malapposed segment of the stent was post dilated with noncompliant balloon and a satisfactory result was achieved (Fig. 1f); confirmed by repeat intracoronary imaging (Fig. 1e and h). After 12 months of further DAPT, the patient has stopped

taking clopidogrel, and remains free of any further cardiovascular events. ST is associated with significant morbidity and mortality. Allergic reaction to the polymer of the drug-eluting stent can result in vessel remodeling and uncovered stent struts [2]. Such malapposed and uncovered struts could have resulted in recurrent ST upon stopping DAPT, even 7 years postindex PCI [3]. Although malapposed stent struts are not an uncommon finding, patients with longer lesions and stents, multiple stents per lesion, overlapping stents and larger incomplete stent apposition area are likely to have very late ST in comparison with patients with drug-eluting stent who did not experience ST [4]. While this does not prove the ‘cause and effect’, optical coherence tomography finding and lack of further ST subsequent to intervention would strongly suggest that in this man’s case, malapposition was the significant etiological factor leading to recurrent ST. Coronary angiography has inherent limitations, and patients presenting with ST should be investigated by intracoronary imaging to understand the underlying mechanism and should be treated accordingly.

Acknowledgements Conflicts of interest

There are no conflicts of interest.

References 1 2 3

4

Kirtane AJ, Stone GW. How to minimize stent thrombosis. Circulation 2011; 124:1283–1287. Azarbal B, Currier JW. Allergic reactions after the implantation of drug-eluting stents: is it the pill or the polymer? J Am Coll Cardiol 2006; 47:182–183. Guagliumi G, Sirbu V, Musumeci G, Gerber R, Biondi-Zoccai G, Ikejima H, et al. Examination of the in vivo mechanisms of late drug-eluting stent thrombosis: findings from optical coherence tomography and intravascular ultrasound imaging. JACC Cardiovasc Interv 2012; 5:12–20. Cook S, Wenaweser P, Togni M, Billinger M, Morger C, Seiler C, et al. Incomplete stent apposition and very late stent thrombosis after drug-eluting stent implantation. Circulation 2007; 115:2426–2434.

Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.

Recurrent stent thrombosis: where is the clue?

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