Neoatherosclerosis 16 years following bare-metal stent implantation: Different tissue components in different underlying lesions observed with optical coherence tomography

Abstract

A 61 years old male with a history of multiple treatments ofpercutaneous coronary intervention (PCI) with bare-metal stents (BMS)was admitted for the treatment of acute coronary syndrome (ACS).Sixteen years prior to this admission when he was 45 years old, heexperienced inferior ST-elevation myocardial infarction. He receivedone Palmaz-Schatz Stent (PS) for the treatment of lesion in distal rightcoronary artery (RCA). During the hospitalization, he received one PSfor the treatment of stable lesion in proximal left anterior descendingartery (LAD) (Fig. 1). Routine 3-year follow up angiography revealed norestenosis. The controls of other coronary risk factors were good exceptforobesity(BMI=36).SixteenyearsafterPSimplantation,hefeltsuddenchest pain suggestive of ACS, although there was no signi ficant ST-Tchange in electrocardiography at rest. The angiography revealed focalsevere stenoses in both the PS at the RCA and LAD. Optical coherencetomography(OCT)wasperformedtodecidewhichlesionwastheculprit.OCT findings within both lesion demonstrated intimal hyperplasia overthe BMSs. OCT in the RCA demonstrated diffusely thickened neointimathat exhibited low signal intensity with attenuation, partially coveredwith layered tissue pattern. Disrupted thin fibrous cap with intraluminalthrombus was observed at the culprit lesion ( Fig. 2,PanelA1,A2),whichpresumably caused plaque rupture responsible for ACS. In contrast, OCTin the LAD showed neointima accompanied with homogeneousconcentric high backscatte r structure with calcification in all of thestent area. Within the stable neointima, microvessels with tubularstructures differentiated from any side branches were observed ( Fig. 2,Panel B1, B2). In this LAD lesion, thin cap fibroatheroma was notobserved, which is compatible with a stable plaque. PCI was performedfor in-stent neoatherosclerotic lesions in both distal RCA and proximalLAD with zotarolimus-eluting stents.Inthepresentcase,OCTrevealedtypicalunstableplaquemorphologyin the RCA in-stent lesion, which was the culprit of acute myocardialinfarction treated 16 years prior to the event. Also, OCT found stableplaque morphology in the LAD in-stent segment whose underlyingsegment was the stable lesion. Theref ore, the types of neoatherosclerosiswere different according to the unde rlying plaque, although the BMSimplantation was performed 16years ago.PCI with stenting is the most widely performed procedure for thetreatmentofischemicheartdisease,andthisdeviceimprovedtheclinicalperformance as well [1]. In addition to in-stent restenosis (ISR) and latestent thrombosis, neoatherosclerosis within the stent has been recentlybrought into focus [2,3]. Traditionally, intimal hyperplasia after BMSimplantation has been considered stable, with an early peak between6 months and 1 year at late quiescent period thereafter [4].However,Kimura et al. demonstrated that lat e luminal re-narrowing was commonbeyond 4years following BMS implantation [5]. Hasegawa et al. reportedthat atherosclerotic progression occurred in the in-stent intima of BMSmore than 5years after stent deployment based on pathological analysis[6]. OCT has demonstrated its potential capacity to accurately char-acterize or evaluate the responses after stent deployment. Habara et al.reported that the qualitative OCT findings of BMS restenosis tissuebetween very-late-ISR and early-ISR are signi ficantly different [6].Basedon their OCT analysis, the restenosis lesions N5years after BMSimplantation were found with a high incidence (90.7%) accompaniedwith heterogeneous OCT appearance with low-density area, whereaslesions b1 year after BMS implantation showed extremely lowerincidence (17.9%) of neoatherosclerosis [7]. Nakazawa et al. reportedthat an underlying unstable lesion, which included ruptured plaque andthin-cap fibroatheroma, is an independent risk factor for neo-atheroscrelosis [3]. It has been reported that the quality of underlyingplaque has influenced the incidence of neatherosclerosis after stenting[3], however, it is not known whether the quality of the underlyingplaque affects neoatherosclerotic process. In the present case, based onOCT analysis, the observed neointima demonstrated very similar