Abstract
An 81-year-old male patient with a severe de novo coronary artery stenosis in the proximal left anterior descending artery was treated with a BioFreedom stent (3.5 × 11 mm), three months later, the patient was re-admitted with chest pain and slightly increased troponin. The angiogram showed a significant in-stent restenosis in the recently treated lesion. Optical coherence tomography revealed a fully expanded stent without areas of incomplete stent apposition. Severe immature neointimal hyperplasia without formation of thrombosis was visualized, causing a severe in-stent restenosis. An underlying plaque rupture within the mid-proximal part of the in-stent restenosis was evident.
Highlights
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OCT images revealed an expanded stent without areas of incomplete stent apposition.
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Severe immature neointimal hyperplasia caused a severe in-stent restenosis.
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No formation of thrombosis was visualized.
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A plaque rupture within the mid-proximal part of the in-stent restenosis was evident.
1
Introduction
At present, percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation is the standard strategy to treat coronary artery disease in institutions around the world. However, concerns regarding long-term safety of first generation DES have prompted to development of novel DES systems such as the polymer-free Biolimus A9 coated stent (BioFreedom) (Biosensors Inc., Newport Beach, CA). In the current case report we present a patient with an early in-stent restenosis after implantation of a BioFreedom stent, and supplementary intracoronary imaging with optical coherence tomography (OCT) is used to shed light on the underlying mechanism.
2
Case report
An 81-year-old man was admitted to the department of cardiology due to intermittent chest pain. The patient was previously known with ischemic heart disease and earlier coronary artery bypass grafting (CABG) with a left internal mammary artery (LIMA) to the ramus diagonalis and triple saphenous vein grafts to the right coronary artery, to the left circumflex artery and to the ramus intermedius had been performed back in 1993. The patient had a previous history of arterial hypertension, dyslipidemia and was an earlier smoker. He had no history of diabetes mellitus, neither no known family history of ischemic heart disease. Following CABG, the patient was asymptomatic for many years. One week prior to admission to our hospital the patient developed chest pain and the general practitioner referred him for a diagnostic elucidation at our department. The electrocardiogram (ECG) revealed anterior ST-segment depressions and biochemically troponin I was moderately elevated (143 ng/L), why the patient was diagnosed as having a non ST-segment elevation myocardial infarction (NSTEMI). Following a loading dose of 180 mg of ticagrelor and 300 mg of aspirin, dual antiplatelet therapy (DAPT) with ticagrelor 90 mg twice daily and aspirin 75 mg once daily was ordained. The patient was referred for a subacute coronary angiogram, which revealed a 90% single de novo stenosis in the proximal left anterior descending artery (LAD) ( Fig. 1 ). The patient was treated a BioFreedom stent and a 3.5 × 11 mm stent ( Fig. 1 B). The LIMA to the ramus diagonalis and all 3 vein grafts were angiographically well-functioning.
Three months post-PCI of the proximal LAD, the patient started to experience shortness of breath during physical activity, and complaints of chest pain began to evolve. The patient was re-hospitalized. Troponin I was discreetly increased and ECG revealed unchanged anterior ST-segment depressions. There had been no interruption in DAPT. A repeat subacute coronary angiogram showed a significant in-stent restenosis at the newly LAD-stented segment ( Fig. 2 ). A supplementary OCT (C7 Dragonfly, LightLab Imaging Inc., Westford, MA, USA) was performed in order to investigate the underlying mechanism of the early in-stent restenosis ( Fig. 3 a ). OCT images revealed a fully expanded stent without areas of incomplete stent apposition in its entire length. Severe immature neointimal hyperplasia without formation of thrombosis was visualized, causing a severe in-stent restenosis with a minimal lumen area (MLA) of 2.1 cm 2 . An underlying plaque rupture within the mid-proximal part of the in-stent restenosis was evident. Repeat revascularisation with PCI and implantation of a 3.5 × 12 mm Promus Stent (Everolimus-eluting stent, Boston Scientific, Malborough, MA) overlapping the previous BioFreedom stent was performed in order to cover and repeal the early in-stent restenosis. Repeat OCT post-procedure showed optimal stent expansion and apposition without residual protruding material or edge dissections ( Fig. 3 b). Fig. 4 shows supplementary OCT images of clinically asymptomatic left main (LM) stenosis.
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