SummaryA 58-year-old male with a history of prior myocardial infarction, hypertension, and dyslipidemia was admitted due to deteriorating exertional angina. A bare metal stent (Multilink plus TM , GUIDANT Corporation, Santa Clara, CA, USA) had been implanted into the proximal left anterior descending artery because of ST-elevation myocardial infarction 7 years earlier. Optical coherence tomography (OCT) showed a disruption of the atherosclerotic neointima overlying the stent. Intravascular imaging studies and pathological studies have shown that neointima within a bare-metal stent often transform into atherosclerotic tissue during an extended period of time. In the current report, OCT demonstrated that a disruption of the atherosclerotic neointima has the potential to cause the development of unstable clinical features. OCT examinations therefore help to understand the pathogenesis of acute coronary syndrome after stent implantation. ( imaging technology that provides cross-sectional tomographic imaging, which yields detailed structural information superior to any other currently available modality. The image is formed with a 15-20 μm axial resolution, which is about 10 times that of intravascular ultrasound (IVUS). Moreover, atherosclerotic lesions can be identified by their distinctive borderlines and the intensity, uniformity, and attenuation of the associated signal. Lipid plaques are diffusely bordered, and exhibit lower signal intensity with high attenuation. OCT examinations help to clarify the course of vascular healing and the cause of stent failure after stent implantation. This report presents a case of deteriorating exertional angina in which OCT showed a rupture of the atherosclerotic neointima 7 years after bare-metal stent (BMS) implantation.
Case ReportA 58-year-old male with a history of prior myocardial infarction, hypertension, and dyslipidemia was admitted for deteriorating exertional angina. A bare metal stent (Multilink plus TM , 3.5/15 mm; GUIDANT Corporation, Santa Clara, CA, USA) had been implanted into the proximal left anterior descending artery (LAD) 7 years earlier because of ST-elevation myocardial infarction. Aspirin, statin, and ACE inhibitory therapy were continued after stent deployment and he had an uneventful course for 7 years. Since he developed worsening exer-