Drug-Eluting Stent Thrombosis More Than Seven Years After Implantation: Pathophysiology of “Very” Very Late Stent Thrombosis Elucidated by Optical Coherence Tomography and Histological Analysis

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Authors

Alec Vishnevsky, MD (@AVishnevsky_MD)¹; Antony Kaliyadan, MD¹; David L. Fischman, MD (@fischman_david)¹; Nicholas J. Reuggiero II, MD (@DrNickTJU)¹; John Farber, MD¹; Michael P. Savage, MD^1
1From the Department of Medicine, Division of Cardiology, Sidney Kimmel Medical College at Thomas Jefferson University, Thomas Jefferson University Hospital, Philadelphia, PA

Case

Stent thrombosis remains a serious complication of percutaneous coronary intervention (PCI) resulting in myocardial infarction (MI) or death in up to 80% of patients.1–3 Thrombosis occurring more than one year after PCI is classified as very late stent thrombosis (VLST). It remains unknown whether the risk of DES thrombosis eventually abates over time or persists indefinitely. Recently a series of patients with “very” very late stent thrombosis occurring more than 5 years after implantation has been reported4. In this imaging case report, we present a case of VLST occurring more than 7 years after stent implantation; optical coherence tomography (OCT) and histopathological analysis was performed to elucidate the pathophysiology of this event. A 58-year-old male presented to our emergency department with five hours of chest pain. The patient had a history of non-ST elevation myocardial infarction with placement of a Sirolimus-eluting stent seven years and two months previously. The patient admitted to self-discontinuation of his medications, including a baby aspirin, and had resumed smoking. ECG revealed acute postero-lateral ST elevation MI. Emergent coronary angiography revealed a 100% thrombotic occlusion in the first obtuse marginal branch at the site of the previous SES (Figure 1). After flow was re-established with aspiration thrombectomy, OCT was performed (Figure 2). Histologic analysis of the aspirated material demonstrated a large thrombus characterized by dense platelet aggregates (Figure 3). Noteable was the absence of neoatherosclerosis. Following additional thrombectomy and balloon angioplasty, there was an excellent angiographic appearance (Figure 4).

Figures

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  Video 1. Injection of SVG to OM graft with retrograde filling of the entire circumflex system which then provides antegrade flow into the LAD. Stenosis seen both in the proximal circumflex and ostial LAD.
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  Video 2. A wire in the ostial circumflex supported by an OTW balloon and a guide extension catheter. Note the kink just proximal to the anatamosis of the SVG to the OM and poor flow in the distal LAD.
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  Video 3. Crossing the left main CTO from the retrograde approach with a Pilot 200 wire supported by a Corsair microcatheter (currently being withdrawn).
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  Figure 1. Injection of SVG to OM graft with retrograde filling of the entire circumflex system which then provides antegrade flow into the LAD. Stenosis seen both in the proximal circumflex and ostial LAD.
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  Figure 2. A wire in the ostial circumflex supported by an OTW balloon and a guide extension catheter. Note the kink just proximal to the anatamosis of the SVG to the OM and poor flow in the distal LAD.
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  Figure 3. Crossing the left main CTO from the retrograde approach with a Pilot 200 wire supported by a Corsair microcatheter (currently being withdrawn).
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  Figure 4. : Inflating a 3.5mm balloon in the left main CTO to create a channel for antegrade access. The guide in the ascending aorta will not engage the left main despite repeated efforts from a radial approach.
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  Figure 5. An 8F JL3 guide has engaged the left main from a femoral approach and a Runthrough wire is now in the posterior lateral branch and a Fielder XT is in the distal LAD. The guide engaging the vein graft and the retrograde Pilot 200 have been removed.
• 
  Figure 6. Final cranial view of LAD. TIMI 3 antegrade flow into the LAD with reduced flow into the circumflex.

Comments

We demonstrate a case of “very” very late stent thrombosis 7 years after initial implantation due to non-compliance with aspirin and smoking cessation. OCT proved critical for elucidating the pathophysiology of this thrombotic event, demonstrating massive white thrombus and focal areas of stent strut malposition.