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Wall shear stress (WSS) has been considered a major determinant of aortic atherosclerosis. Recently, nonobstructive general angioscopy (NOGA) was developed to visualize various atherosclerotic pathologies, including in vivo ruptured plaque (RP) in the aorta. However, the relationship between aortic RP and WSS distribution within the aortic wall is unclear. This study aimed to investigate the relationship between aortic NOGA-derived RP and the stereographic distribution of WSS by computational fluid dynamics (CFD) modeling using threedimensional computed tomography (3D-CT) angiography. Methods:We investigated 45 consecutive patients who underwent 3D-CT before coronary angiography and NOGA during coronary angiography. WSS in the aortic arch was measured by CFD analysis based on the finite element method using uniform inlet and outlet flow conditions. Aortic RP was detected by NOGA.Results: Patients with a distinct RP showed a significantly higher maximum WSS value in the aortic arch than those without aortic RP (56.2 30.6 Pa vs 36.2 19.8 Pa, p 0.017), no significant difference was noted in the mean WSS between those with and without aortic RP. In a multivariate logistic regression analysis, the presence of a maximum WSS value more than a specific value was a significant predictor of aortic RP (odds ratio 7.21, 95% confidence interval 1.78-37.1, p 0.005).Conclusions: Aortic RP detected by NOGA was strongly associated with a higher maximum WSS in the aortic arch derived by CFD using 3D-CT. The maximum WSS value may have an important role in the underlying mechanism of not only aortic atherosclerosis, but also aortic RP. vessel wall. Since WSS is involved in the endothelial function, WSS significantly influences site-specific susceptibility and progression of atherosclerosis 2) . Regarding the coronary artery, previous studies have suggested that WSS affects local plaque morphology or vulnerability 3,4) and its progression 5

Smaller low-density lipoprotein (LDL) particle size has been suggested to result in the development of endothelial dysfunction, atherosclerosis, and in-stent restenosis (ISR); however, little is known regarding the impact of the LDL particle size on the neointima formation leading to ISR after everolimus-eluting stent (EES) implantation.Methods: In this study, we have included 100 patients to examine the relationship between an LDL-C/ apolipoprotein B (Apo B) ≤ 1.2, reportedly representing the LDL particle size, and the neointimal characteristics using optical coherence tomography (OCT) and coronary angioscopy (CAS) during the follow-up coronary angiography (CAG) period (8.8 2.5 months) after EES implantation. We divided them into two groups: LDL-C/Apo B ≤ 1.2 group (low LDL-C/Apo B group, n 53) and LDL-C/Apo B 1.2 group (high LDL-C/Apo B group, n 47). Results:The low LDL-C/Apo B group had a significantly larger neointimal volume (12.8 5.3 vs. 10.3 4.9 mm 3 , p 0.021) and lower incidence of a neointimal homogeneous pattern (71 vs. 89 %), higher incidence of a neointimal heterogeneous pattern (25 vs. 9 %) (p 0.006) and higher prevalence of macrophage accumulation (9 vs. 2 %) (p 0.030) as assessed via OCT, and, as per the CAS findings, a higher prevalence of yellow grade ≥ 2 (grade 2; adjusted residual: 2.94, grade 3; adjusted residual: 2.00, p 0.017) than the high LDL-C/Apo B group. Conclusions:A low LDL-C/Apo B ratio was found to be strongly associated with neointimal proliferation and neointimal instability evidenced chronically by OCT and CAS. An LDL-C/Apo B ≤ 1.2 will be of aid in terms of identifying high-risk patients after EES implantation.(sd-LDL-C). The sd-LDL-C has been often associated with atherosclerosis lipoproteins because of its low affinity for the LDL receptors, easy penetrance into the vessel walls, long blood half-life, and high oxidizability 1) . Numerous reports have suggested a relationship between sd-LDL-C and the onset of cardiovascular diseases (CVDs) 2-4) , but a direct measurement of sd-LDL-C has not been widely used Copyright©2021 Japan Atherosclerosis Society This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.

ObjectiveThe aim of this study was to compare how prasugrel and clopidogrel affect platelet aggregation reactivity, cardiac enzyme release, cardiac remodeling, and the formation of in‐stent thrombi after primary percutaneous coronary intervention (PCI).BackgroundThe advantages of using prasugrel over clopidogrel in cardiac injury following acute coronary syndrome (ACS) remain unclear.MethodsA total of 78 ACS patients were randomly allocated into clopidogrel (300 mg loading/75 mg maintenance) or prasugrel (20 mg loading/3.75 mg maintenance) treatment groups, followed by undergoing primary PCI. Platelet reactivity and cardiac enzymes were measured before and after primary PCI. Moreover, cardiac function was measured by ultrasound echocardiography and coronary angioscopic observation was after primary PCI up to 8 months later.ResultsAntiplatelet reactivity in the prasugrel treatment group reached optimal levels (P2Y12 reaction units [PRU] less than 262) immediately after the administration and was maintained even at 8 months, independently of the CYP2C19 genotype. Prasugrel treatment significantly suppressed creatine kinase elevation compared to clopidogrel treatment (median value 404 IU/L to 726 IU/L vs. 189 IU/L to 1,736 IU/L, p = 0.018 for maximum values) and reduced left ventricular mass (217.2–168.8 g in prasugrel, p = 0.045; 196.9–176.4 g in clopidogrel, p = 0.061). There were no significant differences in the incidence of in‐stent attached thrombi between the two groups.ConclusionsCompared to clopidogrel, prasugrel produced a stable platelet aggregation inhibitory effect in patients with ACS regardless of CYP2C19 genotype, reduced cardiac enzyme release, and prevented cardiac remodeling after ACS.