Detection of Atherosclerotic Progression with Rupture of Degenerated In-Stent Intima (Full title below)

Detection of Atherosclerotic Progression with Rupture of Degenerated In-Stent Intima Five Years after Bare-Metal Stent Implantation Using Optical Coherence Tomography ABSTRACT: In-stent intimal hyperplasia peaks in the early phase (6–12 months) after bare-metal stent (BMS) implantation. However, late luminal re-narrowing due to atherosclerotic progression of in-stent intima is reported beyond 4 years. We report the optical coherence tomographic findings of a case of late restenosis of BMS 5 years after implantation. Remarkable in-stent intimal growth was observed, demonstrating a heterogeneous appearance including low-intensity areas and accompanied by intimal rupture. These findings were similar to the morphology of ruptured fibroatheroma in the native coronary artery, and suggested that atherosclerotic change in the in-stent intima occurred over the 5 years following BMS implantation. J INVASIVE CARDIOL 2009;21:552–553 Case Presentation A 58-year-old male with a history of diabetes mellitus and hypertension underwent percutaneous coronary intervention (PCI) due to stable angina pectoris. A lesion with a chronic total occlusion in the proximal right coronary artery was treated with 2 slotted bare-metal stents (BMS). Follow-up coronary angiography (CAG) 6 months after the index PCI showed mild in-stent luminal narrowing. Myocardial stress scintigraphy performed at 2 and 4 years after the index procedure showed no evidence of ischemia, although the patient’s glycemic and blood pressure control were poor. After being free of pain for 5 years, he experienced a recurrent angina attack on exercise and visited our hospital 1 month after the onset of this recurrent angina episode due to accelerated angina (Braunwald Classification IB). Since his exercise stress test showed a positive result, CAG was performed. This angiogram showed severe in-stent restenosis (Figure 1A). The optical coherence tomographic (OCT) image, acquired prior to the repeat PCI, showed remarkable intimal growth inside the stents, which demonstrated a heterogeneous appearance including low-intensity areas (Figures 1C, D and E). Furthermore, rupture of the in-stent intima, accompanied by an intimal flap and a cavity, was observed (Figures 1B and C). These findings are similar to the morphology observed with ruptured fibroatheroma in the native coronary artery.1 Using a distal embolic protection device, the lesion was successfully treated with a sirolimus-eluting stent without complications such as distal embolization, slow-flow or a major cardiac enzyme rise. Discussion In-stent intimal hyperplasia peaks in the early phase (6–12 months) after stent implantation. In general, the stented lesion stabilizes after the early restenosis phase. However, Kimura et al demonstrated that late luminal re-narrowing was common beyond 4 years following BMS implantation.2 Hasegawa et al also reported that atherosclerotic progression occurred in the in-stent intima of BMS more than 5 years after stent implantation based on pathological analysis.3 OCT, a high-resolution intravascular imaging modality, visualizes microscopic structures of the coronary artery. Usually, in-stent intima of BMS is observed as a homogeneous structure;4 however, in the present case, the observed intima demonstrated a heterogeneous pattern comparable to a fibroatheroma in the native coronary artery. These findings suggest that atherosclerotic progression occurred in the in-stent intima over the 5 years following BMS implantation, which is consistent with previous reports.3 Very late stent thrombosis is a major clinical concern after drug-eluting stent implantation,5 however, it has also been reported in BMS. Although some authors have suggested some mechanisms for this finding, it is not yet clearly known.6,7 OCT is reported to be superior to intravascular ultrasound or coronary angioscopy in the detection of the cause of acute coronary syndromes such as plaque rupture and erosion.1 This case may very well represent one of the poorly understood mechanisms of late stent thrombosis in BMS. From the Division of Cardiovascular Medicine, Toyohashi Heart Center, Toyohashi, Japan. The authors report no conflicts of interest regarding the content herein. Manuscript submitted June 2, 2009, provisional acceptance given June 8, 2009, final version accepted July 7, 2009. Address for correspondence: Mitsuyasu Terashima, MD, Division of Cardiovascular Medicine, Toyohashi Heart Center, 21-1 Gobudori, Oyama-cho, Toyohashi, 441-8530, Japan. E-mail: mterashima-circ@umin.ac.jp

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