Abstract
Peri-stent contrast staining and late acquired malapposition represent pathological vessel wall healing patterns following percutaneous coronary intervention with stent implantation. Earlier studies have described these abnormal vessel wall responses commonly present after implantation of first-generation drug-eluting stents. These coronary vascular changes can cause flow disturbance and thereby dispose for later thrombotic events. This case report, based on coronary optical frequency domain imaging, describes peri-stent contrast staining, major evaginations and severe malapposition occurring 18 months after third-generation biolimus-eluting stent implantation.
1
Introduction
Peri-stent contrast staining and late malapposition represent pathological vessel wall healing patterns following percutaneous coronary intervention with stent implantation. These later abnormal coronary vessel wall changes can induce flow disturbance and cause subsequent thrombotic events . Previous studies have described these pathological findings frequent after implantation of sirolimus- and paclitaxel eluting stents, and association to the pharmacokinetic profile and permanent polymer coating of these first-generation drug-eluting stents have been postulated .
This case report, based on coronary optical frequency domain imaging, describes peri-stent contrast staining, major evaginations and severe malapposition occurring 18 months after third-generation biolimus-eluting stent (BES) implantation.
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Case report
A 63-year old male patient with stable angina pectoris was referred for an elective coronary angiogram (CAG). The patient had previously had percutaneous coronary intervention (PCI) with bare-metal stent (BMS) implantation in the left anterior descending (LAD), and a Biomatrix Flex™ (3.5/14 mm, 10 atm.) had been implanted in the proximal segment of the right coronary artery (RCA) 18 months prior due to stable angina pectoris ( Fig. 1 ).

Risk factors included a family history of ischemic heart disease, active smoking, hypertension and hypercholesterolemia. In accordance with current antithrombotic treatment guidelines post PCI with drug-eluting stent (DES) implantation, the patient was treated with dual antiplatelet therapy (aspirin and clopidogrel) for 12 months after the index PCI, and was on a maintenance dose of aspirin when referred due to recurrent angina. The angiogram revealed thin and gracile left sided vessels with a well-functioning BMS at the proximal LAD with slight angiographic signs of non-significant intimal hyperplasia. The right coronary artery had a severe proximal edge in-stent restenosis (ISR) in relation to the previously stented segment, where also peri-stent contrast staining was present (defined as contrast staining outside the stent contour extending to ≥ 20% of the stent diameter) ( Fig. 2 , left). Pre-dilation with a 2.0 balloon was performed, after which an intravascular optical frequency domain imaging (OFDI) (Lunawave™, Terumo) was performed to assess the region of interest. The analysis was interpreted online, and confirmed severe late malapposition and major evaginations (defined as extending ≥ 3 mm along the vessel length, with a depth ≥ 10% of the stent diameter) at the stented segment, and illuminated the proximal edge ISR, where a minimum lumen area (MLA) of 2.7 mm 2 was measured ( Fig. 3 ). No subclinical thrombi at the malapposition-sites were detected by the OFDI. The severe proximal edge in-stent restenosis was treated with a Nobori™ stent (3.5 × 14 mm, 16 atm.). A final coronary angiogram ( Fig. 2 , right) and control OFDI ( Fig. 4 ) revealed unaltered incomplete stent apposition at the previously stented segment. It was not possible to correct (post-dilation) for the late malapposition, since the cause was extreme positive remodeling with an increase in vessel dimensions without an equal amount of peri-stent plaque growth, and the average lumen diameter was up to 7 mm. The patient was discharged in well being the same day as the procedure was performed. Lifelong dual antiplatelet therapy with aspirin and clopidogrel was recommended. At a 6-month clinical control, the patient was event-free.

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