Akiko Fujino

TCT-387 Morphological Correlates of Symptomatic Progression After Coronary Computed Tomography Angiography-derived High Risk Lesions Are Assessed by Optical Coherence Tomography

Low attenuation plaque (LAP) by coronary computed tomography angiography (CTA) is known to predict coronary ischemic events. We hypothesized that in stable pts in whom CTA showed LAP and who were subsequently treated by PCI after worsening ischemia, OCT may reveal evidence of recent plaque rupture

TCT-836 Unique Calcification Patterns in the Left Main Bifurcation in Patients After Coronary Artery Bypass Grafting

Coronary artery bypass grafting (CABG) accelerates calcium (Ca) proximal to the anastomosis of a patent graft. Optical coherence tomography (OCT) is uniquely able to assess coronary Ca. OCT imaging of the LM bifurcation from either the LAD or LCX was performed in 76 pts with at least one patent

PREDICTORS OF LEFT MAIN CORONARY ARTERY STENT DIMENSIONS: AN EXCEL TRIAL INTRAVASCULAR ULTRASOUND SUBSTUDY

A small minimum stent area (MSA) after left main (LM) PCI has been associated with poor clinical outcomes. The predictors of (LM) stent MSA have not been described. EXCEL was a multicenter, randomized trial comparing PCI with everolimus-eluting stents (n=948) to CABG (n=957) in pts with LM disease

Predictors of Calcium Fracture Derived From Balloon Angioplasty and its Effect on Stent Expansion Assessed by Optical Coherence Tomography

Calcium fracture during percutaneous coronary intervention (PCI) is associated with better stent expansion [(1,2)][1]. Optical coherence tomography (OCT) can penetrate calcium, evaluate calcium thickness, and identify the severity and pattern of calcium requiring additional lesion modification.

Neoatherosclerosis after paclitaxel-eluting stent implantation: Ex vivo intravascular image and histopathology: Pathology of neoatherosclerosis

To the Editor: In-stent neoatherosclerosis is a new problem for the late drug-eluting stent (DES) failure. Although a previous paper described that neoatherosclerosis accounts for approximately one third of late and very late stent thrombosis after first-generation DES implantation, we harbor doubts for the high prevalence of the neoatherosclerosis by our expert experiences as pathologist. We need to clarify the clinical prevalence of neoatherosclerosis after DES implantation in the real world, particularly vulnerable neoathorosclerosis which initiate the prospective clinical events. In addition, the etiology of the neoatherosclerosis remains unclear and accumulation of cases with pathological examination is of importance. Recent clinical observation demonstrated that secondgeneration DES is not more protective against neoatherosclerosis compared with the first-generation DES. Although a few histological studies of neoatherosclerosis had been described using the specimens of cadavers, the comparison between intravascular imaging and histopathology of neoatherosclerosis at the consistent section has not been sufficiently demonstrated. We could speculate that the number of patients with long-term DES implantation in their coronary artery tree will increase annually. In this viewpoint, it is of great importance to understand the intravascular image of neoatherosclerosis with histological validation. We examined postmortem ex vivo optical frequency domain imaging (OFDI) for vulnerable neoatherosclerosis after DES implantation, which may contribute to the future clinical event. Comparison between intravascular imaging and corresponding histology of neoatherosclerosis was clearly documented and illustrated in this report. A seventy-year-old female was admitted to our hospital due to cardiogenic shock and died of heart failure one day after administration. She suffered diabetic nephropathy and had hemodialysis for 12 years. Paclitaxel-eluting stent (PES; TAXUS, 3.0 32, Boston Scientific, Natick, MA) was implanted in the proximal portion of right coronary artery 5 years before. An autopsy revealed no evidence of acute myocardial necrosis and acute coronary thrombosis including stent implanted segment. Epicardial coronary arteries were removed from the heart and side branches were tied off to preserve the perfusion pressure of 80mm Hg during the following procedures. Ex vivo OFDI (Terumo Corporation, Tokyo, Japan) was examined before fixation by 20% buffered formalin. After recording the ex vivo imaging, the whole stent implanted segment was fixed and embedded in plastic in order to prepare the histological tissue section with stent struts. Five micrometer thick plastic sections with stent struts were cut by a sharp tungsten knife and stained with hematoxylin-eosin. The ex vivo OFDI clearly demonstrated low intensity signal with high-backscattering in the neointima at the mid portion of stent implanted segment (Fig. 1a). In lowintensity-signal lesions, stent struts cannot be clearly visualized by OFDI because of the high-backscattering. Histology of corresponding lesion demonstrated by OFDI showed that the PES was implanted over the eccentric fibrocalcific plaque and the lumen was narrowed down by intimal hyperplasia (Fig. 1b). Cholesterin crystals and cluster of foam cells (Fig. 1c) within the neointima were clearly identified and these histological features were consistent with neoatherosclerosis. Massive inflammation remained in the media close to the stent struts. Inflammatory cells were composed by lymphocytes and plasma cells, predominantly (Fig. 1d). Necrotic core in the neointima was covered with a thin fibrous cap. These histological features indicated vulnerable neointima formation over fibrocalcific plaque 5 years after PES implantation. On OFDI, it is widely accepted that lipid-rich necrotic core of native coronary plaque appears as low signal intensity mass. In contrast, it had been described that a high intensity signal with high backscattering reflects the presence of foamy macrophages in the intima. However, by our comparison study between ex vivo intravascular image and histopathology, lesion of dense macrophage infiltration in the intima demonstrated a low intensity signal with high backscattering by OFDI. Dense macrophage infiltration in the neointima as shown in the current case, which is more alarming lesion than scattering macrophage infiltration, presented as a low intensity signal with high backscattering. In this manner, it is reasonable that the stent struts underneath the neoatherosclerosis cannot be visualized by high-backscattering on OFDI. Stent struts behind organized fibrin thrombus can be visible because OFDI signals are not attenuated by these materials. Therefore, it is crucial to detect the neoatherosclerosis whether stent struts behind the low signal intensity area are visible or invisible by OFDI. The question arises whether the “neoatherosclerosis” is derived from penetrated native plaque or newly developed

PROCEDURAL CALCIUM FRACTURE AND ITS EFFECT ON STENT EXPANSION ASSESSED BY OPTICAL COHERENCE TOMOGRAPHY

Background: Severe coronary calcium (Ca) may limit stent expansion. We hypothesized that Ca fracture during stent implantation may mitigate its impact. Methods: Pre-intervention and final optical coherence tomography (OCT) were performed in 196 pts. Maximum superficial Ca angle and minimum Ca

A multidirectional approach to risk assessment in patients with three-vessel coronary artery disease undergoing percutaneous intervention

BACKGROUND The SYNTAX score (SS) and Clinical SYNTAX score (CSS) have demonstrated utility as risk-stratifying tools following percutaneous coronary intervention (PCI). However, useful determinants for predicting hard clinical events (HCE: death, nonfatal myocardial infarction, and stroke) in the setting of routinely-performed-angiographic follow-up have yet to be elucidated. METHODS AND RESULTS We retrospectively examined the clinical outcomes of 252 three-vessel disease (TVD) patients following PCI. The incidence of HCE at 3 years significantly differed according to CSS (High, 20.2%; Intermediate, 1.2%; and Low, 6.0%; log-rank p<0.001), but not according to SS (High, 14.0%; Intermediate, 5.8%; and Low, 7.3%; log-rank p=0.13). The incidence of repetitive revascularization at 3 years did not differ significantly both among SS (High, 45.2%; Intermediate, 36.5%; and Low, 38.2%; log-rank p=0.22) and CSS (High, 36.9%; Intermediate, 41.7%; and Low, 41.7%; log-rank p=0.88,). CONCLUSION Prediction of HCE in patients with TVD following PCI was more accurate with CSS than with SS.

Serial 3-Vessel Optical Coherence Tomography and Intravascular Ultrasound Analysis of Changing Morphologies Associated With Lesion Progression in Patients With Stable Angina PectorisCLINICAL PERSPECTIVE

Background— Optical coherence tomographic (OCT) morphologies associated with lesion progression are not well studied. The aim of this study was to determine the morphological change for untreated lesion progression using both OCT and intravascular ultrasound (IVUS). Methods and Results— We used baseline and 8-month follow-up 3-vessel OCT and IVUS to assess 127 nonculprit lesions (IVUS plaque burden ≥40%) in 45 patients with stable angina after target lesion treatment. Lesion progression was defined as an IVUS lumen area decrease >0.5 mm2. A layered pattern was identified as a superficial layer that had a different optical intensity and a clear demarcation from underlying plaque. Lesion progression was observed in 19% (24/127) lesions, and its pattern was characterized into 3 types: type I, new superficial layered pattern at follow-up that was not present at baseline (n=9); type II, a layered pattern at baseline whose layer thickness increased at follow-up (n=7); or type III, no layered pattern at baseline or follow-up (n=8). The increase of IVUS plaque+media area was largest in type I and least in type III (1.9 mm2 [1.6–2.1], 1.1 mm2 [0.9–1.4], and 0.3 mm2 [−0.2 to 0.8], respectively; P=0.002). Type III, but not types I or II, showed negative remodeling during follow-up (IVUS vessel area; from 14.3 mm2 [11.4–17.2] to 13.5 mm2 [10.4–16.7]; P=0.02). OCT lipidic plaque was associated with lesion progression (odds ratio, 13.6; 95% confidence interval, 3.7–50.6; P<0.001). Conclusions— Lesion progression was categorized to distinct OCT morphologies that were related to changes in plaque mass or vessel remodeling.

Ulcerated plaque of coronary artery: Insights from ex vivo images of optical frequency domain imaging and histopathology

To the Editor: It is known that episodes of plaque rupture are frequent and occasionally result in acute coronary syndrome (ACS). In vivo imaging studies in patients with ACS demonstrated evidence of multiple plaque ruptures other than the culprit lesion. Furthermore, recent intravascular ultrasound study demonstrated that the natural evolution and long-term impact of plaque ruptures in untreated segments were not accompanied by clinical events. However the ulcerated coronary artery plaque is still a thorny lesion in the clinical practice. A 78-year-old male died of sepsis and an autopsy was performed. The ex vivo optical frequency domain imaging (OFDI; TerumoCorporation, Tokyo, Japan) revealed a large ulceration, which was directly connected to the true lumen at the proximal portion of right coronary artery (Fig. 1a). The false lumen, which was separated by tissue showing a homogeneous, high intensity signal from the true vessel lumen, was clearly illustrated at the distal segment of ulceration by OFDI (Fig. 1b). Pathological examination revealed the ulcer formation without a necrotic core in the intima. Large disruption of fibrous cap and connection between true and false lumen were apparent (Fig. 1c). The adjacent distal section demonstrated the true and false lumen separated by fibrous septum (Fig. 1d). Fresh mural thrombus was not identified in the false lumen, and the false cavity was completely covered with endothelial cells, which were confirmed byCD31 immunohistochemistry (Fig. 1d, inset). The remodeling index of the ulcerated plaque was 1.05. Approximately 5 mm proximal section from the ulcerated plaque showed atherosclerotic plaque with necrotic core formation. The segment demonstrated a remodeling index of 1.45. The patient’s coronary artery demonstrated severe stenosis with atherosclerotic plaque formation in the left anterior descending artery and circumflex artery. We believe that the pathogenesis of coronary ulcerated lesion is a plaque rupture followed by the washing away of the necrotic core content. Although the histological finding of these sections indicated a previous plaque rupture (healed plaque rupture), no scar was observed in the posterior wall of the left ventricle. Plaque rupture is the most common lesion underlying ACS. However, pathological study has suggested evidence of silent

Ex vivo optical frequency domain imaging and histopathology of malapposed drug eluting stent in coronary artery

To the Editor: Drug eluting stents (DESs) significantly reduce the incidence of stent restenosis and target lesion revascularization in the coronary artery tree. However, late and very late stent thrombosis have been raised as the new problem after DES implantation. Stent malapposition is observed frequently by intravascular imaging in patients who underwent DES implantation. Although some previous studies have suggested that stent malapposition is associated with stent thrombosis, others have failed to demonstrate such association. We have identified malapposed DES 65 months after stent deployment in our autopsy case, and compared the ex vivo intracoronary imaging and histopathology of corresponding lesion. A 70-year-old female was admitted to our hospital due to cardiogenic shock and died of heart failure 1 day after administration. A paclitaxel-eluting stent (Taxus, Boston Scientific, Valencia, CA, USA) was implanted to the right coronary artery 65 months previously. Dual-antiplatelet therapy (DAPT) had been continued for five years until her death. An autopsy was performed followed by an ex vivo optical frequency domain imaging (ODFI; Terumo Corporation, Tokyo, Japan) and a pathological examination. Optical frequency domain imaging revealed malapposed struts at the proximal stent edge (Fig. 1a). The serial movie of OFDI revealed that the malapposition site was covered by homogenous membranous tissue without evidence of plaque and/or thrombus prolapse into the lumen. Histopathology of the corresponding site demonstrated that part of the stent struts were not attached to the vessel wall (Fig. 1b). These struts were completely covered by connective tissue with superficial