2017 Volume 81 Issue 7 Pages 1054-1055
A 63-year-old woman was admitted for the treatment of sick sinus syndrome and atrioventricular block. She had received sirolimus-eluting stent (SES; 2.5×18 mm) in the left anterior descending artery (LAD) 10 years previously. Routine coronary angiography had indicated no stent restenosis 1 year after SES implantation. The patient had a history of hyperlipidemia and hypertension, and coronary risk factors were well controlled after the stenting. She continued taking aspirin at 100 mg/day and cilostazol at 200 mg/day for 10 years. As part of thorough examination of atrioventricular block, 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) was performed to rule out cardiac sarcoidosis. There was no myocardial FDG uptake, but there was a significant uptake around the SES in the LAD (Figure 1). Coronary CT angiography showed aneurysmal dilatation (18×28 mm) with a low-density area surrounding the SES (Figure 2A). Coronary angiography showed aneurysm formation at the carina to diagonal branch as well as diffuse severe in-stent stenosis, with a fractional flow reserve of 0.73 (Figure 2B). Angioplasty was therefore carried out using a paclitaxel-coated balloon. Inflammatory markers, including white blood cells, eosinophils, and C-reactive protein, were not elevated.
18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) showing significant localized FDG uptake around the sirolimus-eluting stent in the left anterior descending artery.
(A) Coronary computed tomography angiography showed aneurysmal dilatation (18×28 mm) with a low-density area surrounding the sirolimus-eluting stent and proximal diagonal branch. (B) Coronary angiography showed aneurysm formation at the carina to diagonal branch as well as diffuse severe in-stent stenosis.
Drug-eluting stents (DES) reduce the subsequent need for target lesion revascularization compared with bare metal stents, but very late stent thrombosis in the late phase after DES implantation remains a critical problem. Various pathologic changes including hypersensitivity reaction, delayed endothelialization, incomplete stent apposition, aneurysm formation, and neoatherosclerosis have been reported in coronary lesions following DES implantation.1,2 In particular, hypersensitivity reaction with subsequent aneurysm formation, most frequently observed in SES, is associated with an increased risk of stent thrombosis.1 Histopathology shows an extensive inflammatory infiltrate consisting of lymphocytes and eosinophilis and giant cells in the stent segment in patients with very late stent thrombosis after SES implantation. This hypersensitivity vasculitis might play a key role in the resulting loss of elastic integrity of the vessel wall leading to aneurysm formation.3 Uncovered strut area decreases with continuous neointimal growth in the late phase after SES implantation, whereas aneurysm formation continually expands.4 This suggests that inflammation reaction due to SES also persists in the late phase. Although the patient presented with atrioventricular block, the relationship between the inflammation and the conduction disturbance is not clear. FDG uptake correlates with macrophage accumulation and inflammation. Hence, FDG-PET can provide sensitive detection of active inflammation. The present case shows that inflammatory reaction to SES may persist over the years, and that such a localized disorder may go undetected in routine daily clinical practice. Careful long-term follow-up and judicious use of antiplatelet therapy is warranted in patients with SES.