Abstract
A 90-year-old man was admitted to our hospital with acute ST-segment elevation myocardial infarction. He had a history of post-infarction angina pectoris 79 months ago and had a bare-metal stent (BMS) implanted in the proximal left anterior descending artery at our hospital. Emergent coronary angiography demonstrated thrombotic occlusion in the previously stented segment. After catheter thrombectomy, antegrade flow was restored, but 90% stenosis with haziness persisted in the proximal and distal portions of the previously stented segment. Intravascular ultrasound imaging showed interstrut cavities or stent malapposition at the proximal and distal sites of stented segment. In close proximity to the sites, residual thrombi were also observed. Optical coherence tomography (OCT) demonstrated neither lipid-laden neointimal tissue nor rupture but clearly demonstrated residual thrombus adjacent to the malapposed region in addition to the stent malapposition. PCI with balloon was successfully performed and stent apposition was confirmed by OCT. Stent malapposition is an unusual mechanism of very late stent thrombosis after BMS implantation. OCT can clearly reveal the etiology of stent thrombosis.
1
Introduction
Stent thrombosis is an acute thrombotic occlusion of a previously stented segment that most often occurs within 30 days after percutaneous coronary intervention with stents. Following the introduction of the drug-eluting stent (DES), very late (> 1 year after implantation) stent thrombosis (VLST) was recognized as a rare, but life-threatening, complication . Several studies have demonstrated that incomplete neointimal coverage, local hypersensitivity reactions and late stent malapposition due to excessive positive remodeling may be possible mechanisms of VLST after DES implantation . A meta-analysis by Hassan et al. suggested that late stent malapposition was more frequent after DES implantation than after bare-metal stent (BMS) implantation and was associated with VLST. In contrast to DES, in-stent neoatherosclerosis could play an important role in VLST occurrence after BMS implantation . To the best of our knowledge, VLST due to stent malapposition after BMS implantation has not been reported. Here we report a case of VLST due to stent malapposition after BMS implantation, evaluated by intravascular ultrasound (IVUS) and optical coherence tomography (OCT).
2
Case report
A 90-year-old male farmer was admitted to our hospital with acute ST-segment elevation myocardial infarction. He had a history of post-infarction angina pectoris 79 months ago and had a bare-metal stent (BMS) (Driver stent 3.00 × 24 mm; Medtronic, Santa Clara, USA) implanted ( Fig. 1 ) in the proximal left anterior descending artery at our hospital. Follow-up coronary angiography (CAG) 6 months after the procedure confirmed in-stent restenosis and he underwent repeat balloon angioplasty ( Fig. 2 ). At 9 months after the first procedure, re-restenosis was not observed by CAG. He was discharged on aspirin (100 mg once daily). His coronary risk factors were hypertension and mild hyperlipidemia.
Emergent CAG demonstrated thrombotic occlusion in the previously stented segment ( Fig. 3 A ). Successful thrombectomy was performed with a thrombus aspiration catheter (Rebirth Pro; Goodman Co Ltd, Nagoya, Japan) and antegrade flow was restored, but 90% stenosis with haziness persisted in the proximal and distal portions of the previously stented segment ( Fig. 3 B). IVUS (Volcano Corporation, Rancho Cordova, CA, USA) imaging showed interstrut cavities or stent malapposition at the proximal and distal sites of stented segment ( Fig. 3 C, E). The presence of cavities or malapposition was unclear from the IVUS. Residual thrombi were also observed at both edges of previously stented segment ( Fig. 3 D, F). Subsequently, frequency-domain OCT was performed to evaluate the lesion using a non-occlusive technique with 18 mm/s pullback (Image catheter; Dragonfly JP TM Imaging Catheter, Image system; ILUMIEN TM OPTIS TM , St Jude Medical LightLab, St Paul, MN, USA). In addition to the stent malapposition, residual thrombus adjacent to malapposed region was also identified by OCT at the distal site of stented segment ( Fig. 4 B–D ). Distal stent struts protruding into the lumen without neointimal coverage were observed ( Fig. 4 D, F). Neither neointimal plaque rupture nor lipid-laden neointimal tissue defined as a region with marked signal attenuation and a diffuse border was observed in the stented segment ( Fig. 4 E). The lesion was treated with plain old balloon angioplasty. OCT after balloon angioplasty revealed that the stent was adequately expanded and well-apposed. Thereafter, the patient was maintained on 100 mg aspirin once daily and 75 mg clopidogrel once daily. The patient remains symptom-free at 6 months.
2
Case report
A 90-year-old male farmer was admitted to our hospital with acute ST-segment elevation myocardial infarction. He had a history of post-infarction angina pectoris 79 months ago and had a bare-metal stent (BMS) (Driver stent 3.00 × 24 mm; Medtronic, Santa Clara, USA) implanted ( Fig. 1 ) in the proximal left anterior descending artery at our hospital. Follow-up coronary angiography (CAG) 6 months after the procedure confirmed in-stent restenosis and he underwent repeat balloon angioplasty ( Fig. 2 ). At 9 months after the first procedure, re-restenosis was not observed by CAG. He was discharged on aspirin (100 mg once daily). His coronary risk factors were hypertension and mild hyperlipidemia.
