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PURPOSE:To improve the patency rate for angioplasty in chronic occlusion of the superficial femoral artery by deploying stents after angioplasty. MATERIALS AND METHODS:Angioplasty and stent placement were performed in 61 arteries in 48 male patients. The mean occlusion length was 13.5 cm and the mean stent length was 30 cm. Patency rates were analyzed at 6 months and at 1, 2, 3, and 4 years. The predictors of restenosis were analyzed by univariate and multiple logistic regression. RESULTS:Patency rates were 87% at 6 months, consisting of 74% primary, 6% primary assisted, and 7% secondary; 79% at 1 year, consisting of 47% primary, 19% primary assisted, and 13% secondary; 72% at 2 years, consisting of 36% primary, 26% primary assisted, and 10% secondary; 70% at 3 years, consisting of 26% primary, 22% primary assisted, and 22% secondary; and 63% at 4 years, consisting of 25% primary, 0% primary assisted, and 38% secondary. There was a 15% morbidity rate and one mortality as a result of retroperitoneal bleeding. Better patency rates were noted at all time intervals in diabetic limbs, 7-mm-diameter versus 10-mm-diameter stents, shorter obstructions and shorter stents, nonsmokers, in limbs in which urokinase was not necessary after stent deployment, and in limbs with an International Society of Cardiovascular Surgery (ISCVS) classification under 3. Patency rates were not affected by age, race, number of trifurcation vessels patent, experience in performing the procedures, and procedures requiring less time. By multivariate logistic analysis, the independent predictors of patency at 6 months were postprocedure ankle/brachial index (ABI) and shorter stent length; at 1 year, preprocedure ABI, shorter stent length, and the presence of diabetes; at 2 years, preprocedure ABI and the presence of diabetes; and at 3 years, the preprocedure ABI. CONCLUSIONS:The techniques used to reestablish antegrade flow in these superficial femoral arteries yielded a high success rate. In addition, the use of angioplasty with stents may improve patency rates over angioplasty without stents.

BackgroundIntravascular ultrasound (IVUS) images vary in intensity because of the angle of the transducer relative to the plaque. The purpose of this study was to determine the angle dependence of ultrasound backscatter when the IVUS transducer is aligned coaxially in atherosclerotic arteries and to examine its feasibility in tissue characterization of human atherosclerotic tissue.Methods and resultsThirty-nine noncalcified regions of interest (ROI, 0.4 to 0. 6 mm in diameter) within cross sections of formalin-fixed human iliac arterial plaque were imaged with a 3.9F, 25-MHz IVUS catheter in saline at room temperature. The catheter was moved coaxially from 8 to 16 positions and spanned 50 to 122 degrees relative to the ROI and the lumen center. Echo intensity for each ROI was defined as the videointensity relative to a standard reflector. The angle dependence of echo intensity was defined as the slope of the regression line between the angle of incidence and echo intensity. Each ROI was histologically classified into 4 groups: fibro-acellular (fibrous cap, n=7), fibro-cellular (n=9), fibro-fatty (n=13), or fatty tissue (n=10). The echo intensity of the majority (72%) of plaque components in IVUS images are significantly affected by the angle of incidence of the transducer. The angle dependence of fibro-acellular samples was significantly greater than that of the other 3 groups (4.69 +/- 3.29 x 10(-3) x echo intensity/degree vs 1.06 +/- 1.10 in fibro-cellular area, 2.09 +/- 1.75 in fibro-fatty area, and 2.16 +/- 1.92 in fatty area, P

OBJECTIVES:Intravascular ultrasound imaging (IVUS) is limited by the size of the imaging catheter. To facilitate imaging before and during interventions, a 30-MHz ultrasonic imaging device was developed that is the same dimension as a 0.018-inch guide wire. The purpose of this study was to evaluate the clinical feasibility of this device. METHODS AND RESULTS:The imaging core was tested in 8 patients with the use of a monorail guiding sheath that was advanced through a 7F catheter. In addition, after coronary interventions, the standard guide wire was removed, the imaging core was placed inside a compatible balloon, and imaging was performed. In 4 patients, imaging was also performed with a standard 3.2F IVUS catheter. The lumen-plaque interface and the media-plaque interface were clearly visualized in all patients. There was no detectable loss in image quality between the new imaging device and the larger IVUS catheter, and measurements of lumen cross-sectional area were not statistically different. CONCLUSIONS:Improvements in manufacturing technology have permitted the development of a mechanically rotating ultrasound imaging core 0.018 inches in diameter. It is compatible with current balloon catheters without degradation of image quality.

To examine the accuracy of intravascular ultrasound (IVUS) in assessing the biophysical properties of atherosclerotic plaque, 33 human iliac arteries were imaged with a 25 MHz IVUS transducer and classified into four groups on the basis of IVUS appearance: minimally diseased arterial wall, bright echogenic plaque with acoustic shadowing, bright echogenic plaque without shadowing, and hypoechogenic plaque (so-called "soft echoes"). The hardness of each plaque was assessed with an ultrasensitive compression ergonometer. The radial static stress-strain relations fit well (r > 0.98) to exponential curves, providing a compression stiffness constant (K) defined as the coefficient of the exponential power. K for bright echogenic plaque with shadowing was significantly greater than that of the other tissues. However, K among minimally diseased entire arterial wall, hypoechogenic plaque, and bright echogenic plaque without shadowing was not significantly different, but these tissues are not physically soft compared with adipose tissue. Therefore, tissue characterization by IVUS distinguishes calcified from noncalcified plaque and accurately predicts its biomechanical hardness. However, soft echoes, although less firm than calcium, do not necessarily correspond to soft tissue.

ObjectivesOne potential complication of stenting is "stent jail" due to placement of a stent across a side branch, which may impede additional interventions. Another form of stent entrapment may occur if the guidewire is accidentally withdrawn and then unknowingly passes through a stent loop during reentry with subsequent high pressure expansion. The purpose of this study was to evaluate this form of stent entrapment in vitro by intravascular ultrasound (IVUS).MethodsA guidewire was passed through the end or middle diamonds of Palmaz-Schatz and Palmaz stents or the middle of Gianturco-Roubin stents. A 3.5 mm balloon was inflated over the guidewire through the various side holes of the stents.ResultsIVUS images presented three distinct patterns depending on the type of stent and position of balloon entry: 1) external compression and loss of wall continuity in the Palmaz-Schatz and Palmaz stents, 2) displacement of the side diamond across the lumen, and 3) external compression of the Gianturco-Roubin stent. The first and second patterns but not the third one were associated with impairment of lumen access.ConclusionsBased upon this in vitro verification, IVUS imaging can be used to identify the presence of stent entrapment in vivo.

The purpose of the study was to compare four intravascular ultrasound (IVUS) machines in vitro for their image representation of coronary arterial walls. There has been considerable variability among reported studies on the accuracy of morphometric measurements of coronary arteries by IVUS. This variability may be caused in part by the difference in the IVUS system used. A total of 24 formalin-fixed coronary arteries were imaged in saline at 37 degrees with four different IVUS systems. The images were interpreted independently and compared with histology. Each system had benefits and limitations: System 1 overestimated the lumen area and had difficulty in identifying the media; System 2 underestimated the media area, but had a lower positive bias for lumen area; System 3 overestimated the lumen area but more clearly identified tissue characteristics such as internal elastic membrane and the echolucent media zone which improved the likelihood of observing a three-layer appearance; and System 4 showed less distinct separation of the arterial components and had poor correlations with histology for media measurements. The ability to make accurate morphometric measurements from IVUS images depends on the clarity of the separation of plaque and media. Among the four systems studied, there is significant variability in the appearance of the ultrasound images and the accuracy of morphometric measurements. These system differences should be considered when comparing IVUS studies performed by different groups.

Different intravascular ultrasound (IVUS) systems vary in their image presentation. The purpose of this study was to compare four IVUS systems in vitro to determine the accuracy of tissue characterization of atherosclerotic plaque compared with histology. Ninety-eight plaque segments from 23 formalin-fixed human iliac arteries were imaged in saline at room temperature with four different IVUS systems. To assess the accuracy of IVUS in describing plaque, three types of analysis were performed: (1) the ability to identify the presence and extent of lumen or plaque boundary; (2) sensitivity, specificity, and interobserver variability of IVUS in qualitatively identifying plaque components compared with histology; and (3) quantification of calcification. The synthetic aperture device had a lower sensitivity in identifying lumen and plaque boundaries (87%, 38% respectively) compared with other machines (96%-100%, 95%-100%). All three mechanically rotating systems had fair to good sensitivities for identifying calcification (57%-73%) or lipid filled areas (50%-83%). The sensitivity of discriminating fibrous tissue from fatty areas was low (39%-52%). The synthetic aperture system had a significantly lower sensitivity for identifying all three tissue types (4%-21%). There was significant interobserver variability (kappa value = 0.47-0.68) as well as machine to machine variability (kappa value = 0.52) for tissue characterization. Calcified areas were underestimated by System 1 (p < .05) and System 4 (p < .01) because of weaker echo reflections or poor image quality. There are significant differences in image representation among these four IVUS systems in the diagnosis of tissue components of complex atherosclerotic plaque. These variabilities should be considered when interpreting studies performed with different machines.

The purpose of this investigation was to compare the accuracy of intravascular ultrasound (IVUS) and electron-beam computed tomography (EBCT) in quantitating human atherosclerotic plaque and calcium. In experiment 1, 12 human atherosclerotic arterial segments were obtained at autopsy and imaged by using IVUS and EBCT. The plaque from each arterial segment was dissected and a volume measurement of the dissected plaque was obtained by water displacement. The plaque from each arterial segment was ashed at 700 degrees F, and the weight of the remaining ashes was used as an estimate of the calcium mass. In experiment II, 11 calcified arterial segments were obtained at autopsy and imaged by using IVUS at one site along the artery. A corresponding histologic cross section stained with Masson's trichrome was prepared. In experiment I, the mean plaque volume measured by water displacement was 165.3 +/- 118.4 microliters. The mean plaque volume calculated by IVUS was 166.1 +/- 114.4 microliters and correlated closely with that by water displacement (r = 0.98, p < 0.0001). The mean calcium mass measured by ashing was 19.4 +/- 15.8 mg. The mean calculated calcium mass by EBCT was 19.9 mg and correlated closely with that by ashing (r=0.98, p

Intravascular ultrasound imaging was performed in vitro on six histologically normal and 104 minimally diseased arteries in patients aged 13 to 83 years. This study tested the hypothesis that normal coronary arteries produce a three-layer image that corresponds to the histologic layers of intima, media, and adventitia. The results showed a very good correlation between area of the echolucent ultrasound layer with the media and the inner echogenic layer with intimal area. In addition, a three-layer appearance was consistently seen when the internal elastic membrane was present with or without intimal hyperplasia. If the internal elastic membrane was absent, a three-layer appearance was still seen if the collagen content of the media was low. However, a two-layer appearance was observed when there was absence of the internal elastic membrane as well as a high collagen content of the media.

The purpose of this retrospective study was to examine 732 consecutive patients who underwent dobutamine stress echocardiography (DSE) in order to compare the safety and result profiles of this test between women versus men and in patients > or = 75 and < 75 years of age. Our study included 416 women (57%) and 316 men (43%; mean age 62 +/- 12 years [range 16 to 93]). Patients were divided into 3 age groups: (1) group I (n = 179): < 55 years (mean 47 +/- 6), (2) group II (n = 447): 55 to 74 years (mean 64 +/- 5), and (3) group III (n = 106): > or = 75 years (mean 80 +/- 4). DSE was more likely to have negative results in women than in men (prevalence of positivity = 20% vs 31%, p = 0.001), but DSE had a similar safety profile in both genders. Women required lower doses of dobutamine and atropine to reach an end point. There was a similar incidence of test positivity in older and younger patients (23% in group I, 24% in group II, and 30% in group III, p = NS). DSE was generally a safe test in patients > or = 75 years, but there was a different safety profile in the elderly group compared with younger patients--specifically, more frequent asymptomatic hypotension (7% in group I, 13% in group II, and 25% in group III, p = 0.0002) and ventricular arrhythmias (26% in group I, 30% in group II, and 41% in group III, p = 0.04), but less frequent chest pain (32% in group I, 23% in group II, and 17% in group III, p = 0.009). Multivariate analysis suggested that the baseline usage of beta blockers was also a major determinant of the safety and ischemia profile during DSE. In conclusion, there were significant gender- and/or age-specific differences in the safety and test result profile of DSE. These differences should be considered when performing or interpreting DSE, particularly in women and in patients aged > or = 75 years. [ABSTRACT FROM AUTHOR]

Objectives: The objective of this study was to evaluate whether the regressive effects of aggressive lipid-lowering therapy with atorvastatin on coronary plaque volume (PV) in patients with acute coronary syndrome (ACS) are generalized for other statins in multicenter setting. Background: A previous single-center study reported beneficial regressive effects of atorvastatin in patients with ACS on PV of the nonculprit site by intravascular ultrasound (IVUS) evaluation. The effect of statins other than atorvastatin on PV has not been evaluated in the setting of ACS. Methods: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) study was a prospective, randomized, open-label, parallel group study with blind end point evaluation conducted at 33 centers in Japan. A total of 307 patients with ACS undergoing IVUS-guided percutaneous coronary intervention were randomized, and 252 patients had evaluable IVUS examinations at baseline and 8 to 12 months' follow-up. Patients were randomly assigned to receive either 4 mg/day of pitavastatin or 20 mg/day of atorvastatin. The primary end point was the percentage change in nonculprit coronary PV. Results: The mean percentage change in PV was -16.9 +/- 13.9% and -18.1 +/- 14.2% (p = 0.5) in the pitavastatin and atorvastatin groups, respectively, which was associated with negative vessel remodeling. The upper limit of 95% confidence interval of the mean difference in percentage change in PV between the 2 groups (1.11%, 95% confidence interval: -2.27 to 4.48) did not exceed the pre-defined noninferiority margin of 5%. Conclusions: The administration of pitavastatin or atorvastatin in patients with ACS equivalently resulted in significant regression of coronary PV (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome; NCT00242944). [ABSTRACT FROM AUTHOR]

The main cause of acute coronary syndrome (ACS) is plaque rupture and thrombus formation. However, it has not been fairly successful to identify vulnerable plaque to rupture using conventional parameters of intravascular imaging modalities. Fractal analysis is one of the mathematical models to examine geometrical features of picture image using a specific parameter called as fractal dimension (FD) which suggests geometric complexity of the image. This study examined FD of the optical coherence tomography (OCT)-derived images of the culprit plaque in patients with ACS vs stable angina pectoris (SAP) to evaluate the feasibility of FD for identifying vulnerable coronary plaques prone to provoke ACS distinguished from stable plaques only provoking SAP. We examined 65 cases (34 ACS patients, 31 SAP patients) in which the culprit lesion was imaged by OCT before percutaneous coronary intervention in patients with ACS and SAP. The culprit plaque lesion in the ACS group had a significantly larger mean lipid arc (203.8 ± 39.4° vs 152.3 ± 34.5°, p < 0.001) and a larger lipid plaque length (12.6 ± 5.1 mm vs 7.7 ± 2.7 mm, p < 0.001) and a thinner fibrous cap thickness (75.3 ± 22.3 μm vs 134.8 ± 53.2 μm, p < 0.001) than those in the SAP group. The prevalence of OCT-derived macrophage infiltration (Mph) in the entire culprit coronary vessel as well as that of the OCT-derived thin-cap fibroatheroma (TCFA) at the culprit lesion were significantly greater in the ACS group than those in the SAP group, respectively (Mph: 61.8% vs 35.5%, p = 0.048; TCFA: 44.1% vs 6.4%, p < 0.001). The FD of culprit plaque in the ACS group was significantly greater than in the SAP group (2.401 ± 0.073 vs 2.341 ± 0.051, p < 0.001). In multivariate regression analysis, the presence of Mph was a significant determinant of FD (regression coefficient estimate 0.049, CI 0.018-0.079, p = 0.002). The FD of OCT-derived image of culprit coronary plaque in the ACS group was significantly greater than that in the SAP group, indicating that the culprit plaque in ACS were structurally more complex. Therefore, fractal analysis of coronary OCT images might be clinically useful for identifying coronary plaques prone to provoke ACS., (© 2024. Springer Nature Japan KK, part of Springer Nature.)

Background and Aims: Previous studies have not found a consistent association between circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) levels and the risk of cardiovascular events partly due to measurement methods that cannot distinguish between uncleaved and furin-cleaved forms of PCSK9., Methods: This is a prespecified sub-study of the REAL-CAD study which is a prospective, multicenter, randomized trial to compare high- versus low-dose statin in patients with stable coronary artery disease (CAD). The primary endpoint was major adverse cerebrovascular and cardiovascular events (MACCE) defined as a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal ischemic stroke, or unstable angina requiring emergency hospitalization. In this case-cohort study, serum mature (uncleaved) and furin-cleaved PCSK9 levels obtained at 6 months after randomization were measured among 426 participants who developed MACCE (cases) and 1,478 randomly selected participants (sub-cohort)., Results: From 1,478 patients in sub-cohort, the Cox proportional hazards models with a pseudolikelihood method for case-cohort design revealed that the risk of the primary endpoint in patients with the highest quartile of mature PCSK9 levels was similar to that in the lowest quartile (hazard ration [HR] 0.809; 95% confidence intervals [CI], 0.541-1.209). Similarly, the HR for the highest to lowest quartiles of furin-cleaved PCSK9 was 0.948 [95% CI, 0.645-1.392] (P = 0.784). Compared to the lowest quartile, neither serum mature nor furin-cleaved PCSK9 levels predicted MACCE., Conclusions: In a large-scale secondary prevention cohort, serum mature and furin-cleaved PCSK9 levels did not provide useful information for predicting future cardiovascular events in statin-treated patients with stable CAD., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Kiyoshi Hibi reports financial support was provided by the Public Health Research Foundation. Kiyoshi Hibi reports financial support was provided by Kowa. Kiyoshi Hibi reports a relationship with Abbott Medical that includes: speaking and lecture fees. Kiyoshi Hibi reports a relationship with Daiichi Sankyo that includes: speaking and lecture fees. Kiyoshi Hibi reports a relationship with Medtronic that includes: speaking and lecture fees. Kiyoshi Hibi reports a relationship with the Research Institute for Production Development that includes: funding grants. Kiyoshi Hibi reports a relationship with Japan Medical Device Corporation that includes: funding grants. Kiyoshi Hibi reports a relationship with Abbott Medical that includes: funding grants. Kiyoshi Hibi reports a relationship with NIPRO that includes: funding grants. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Background: The prognostic implications of persistent low-grade inflammation in patients with chronic coronary syndrome (CCS) are underexplored. The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy with Pitavastatin in Coronary Artery Disease) study demonstrated the benefit of higher intensity pitavastatin in Japanese patients with CCS., Objectives: This prespecified subanalysis of the REAL-CAD study aimed to assess the prognostic effect of the persistent low-grade inflammation represented by high-sensitivity C-reactive protein (hs-CRP) in CCS patients., Methods: The present analysis involved patients without events until 6 months after randomization and whose hs-CRP levels were available at baseline and 6 months (n = 10,460). The primary endpoint was the composite of cardiovascular mortality, myocardial infarction, stroke, and unstable angina hospitalization. Landmark analyses evaluated the prognostic impact of continuous inflammation in 4 groups based on the median levels of hs-CRP (0.5 mg/L for both) at baseline and 6 months. The 4 groups included patient with persistently low, elevated (increased), reduced, and persistently high hs-CRP., Results: Adjusted Cox proportional hazard analyses demonstrated an increased risk of the primary endpoint in the group with persistently high hs-CRP when compared to the group with persistently low hs-CRP as a reference (adjusted HR: 1.48, 95% CI: 1.18-1.89; P  = 0.001), but with a similar risk in the group with elevated (HR: 1.07, 95% CI: 0.77-1.49, P  = 0.68) and reduced (HR: 0.92; 95% CI: 0.66-1.27; P  = 0.60) hs-CRP., Conclusions: The study shows that persistent low-grade inflammation is associated with poor outcomes and underscores the need to address residual inflammatory risk in CCS patients. (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease [REAL-CAD]; NCT01042730)., Competing Interests: The Comprehensive Support Project for Clinical Research of Lifestyle-Related Disease of the Public Health Research Foundation funded this study. The company manufacturing the study drug (Kowa Co Ltd) was one of the entities providing financial support for Public Health Research Foundation projects but was not involved in design, analysis, data interpretation, or manuscript preparation. Dr Iwata has received payment or honoraria for lectures, presentations, Speakers Bureaus from Bayer Yakuhin, Ltd, MSD KK, Kowa Co Ltd, Mitsubishi Tanabe Pharma Corp, Sumitomo Pharma, and Mochida Pharmaceutical Co, Ltd. Dr Miyauchi has received payment or honoraria for lectures, presentations, Speakers Bureaus, manuscript writing, or educational events from AstraZeneca KK, Bayer Yakuhin, Ltd, Bristol-Myers Squibb, Daiichi-Sankyo Co Ltd, Kowa Co Ltd. Dr Iimuro has received all support for the present manuscript (data management fee) from Public Health Research Foundation (REAL-CAD office) to Innovation and Research Support Center, International University of Health and Welfare. Dr Sakuma has received grants or contracts from any entity from Public Health Research Foundation from National Cerebral and Cardiovascular Center, Medical Informatics Study Group, GlaxoSmithKline KK, AstraZeneca KK, Takeda Pharmaceutical Co Ltd, and Boehringer lngelheim Japan Inc. Dr Nakagawa has received payment or honoraria for lectures, presentations, Speakers Bureaus, manuscript writing, or educational events from Kowa Co Ltd and Daiichi Sankyo Co, Ltd. Dr Fukumoto has received royalties or licenses from Daiichi Sankyo Co, Ltd, Otsuka Pharmaceutical Co, Ltd, Teijin Pharma Ltd, Bayer Yakuhin, Ltd, Mochida Pharmaceutical Co, Ltd, Astellas Pharma Inc, Sanwa Kagaku Kenkyusho Co, Ltd, Mitsubishi Tanabe Pharma Corp, Takeda Pharmaceutical Co Ltd, Pfizer Japan Inc, Ono Pharmaceutical Co Ltd, and AstraZeneca KK; and payment or honoraria for lectures, presentations, Speakers Bureaus, manuscript writing, or educational events from AstraZeneca KK, Eisai Co, Ltd, MSD KK, Otsuka Pharmaceutical Co, Ltd, Daiichi Sankyo Co, Ltd, Sumitomo Dainippon Pharma Co, Ltd, Teijin Pharma Ltd, Astellas Pharma Inc, Sanwa Kagaku Kenkyusho Co, Ltd, Mitsubishi Tanabe Pharma Corp, Takeda Pharmaceutical Co Ltd, Pfizer Japan Inc, Ono Pharmaceutical Co Ltd, and AstraZeneca KK. Dr Ogawa has received payment or honoraria for lectures, presentations, Speakers Bureaus, manuscript writing, or educational events from Bayer Yakuhin. Dr Daida has received payment or honoraria for lectures, presentations, Speakers Bureaus, manuscript writing, or educational events from Novartis Pharma K.K., Bayer Yakuhin, Ltd, Sanofi KK, Kowa Co Ltd, Taisho Pharmaceutical Co, Ltd, Abbott Medical Japan LLC, Otsuka Pharmaceutical Co, Ltd, Amgen KK, MSD KK, Daiichi Sankyo Co Ltd, Pfizer Japan Inc, Fukuda Denshi Co Ltd, Tsumura & Co, TOA EIYO LTD; and grants or contracts from any entity (trust research/joint research funds/scholarship fund) from Philips Japan, Ltd, FUJIFILM Holdings Co, Asahi Kasei Co, Inter Reha Co, Ltd, TOHO HOLDINGS Co Ltd, GLORY LTD, BMS KK Abbott Japan LLC, Boehringer Ingelheim Japan, Inc, Eisai Co Ltd, Bayer Yakuhin Ltd, and Daiichi Sankyo Co, Ltd. Dr Nagai has received payment or honoraria for lectures, presentations, Speakers Bureaus, manuscript writing, or educational events from Kowa Co Ltd and Shionogi & Co Ltd. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)

Background: This study aimed to examine whether high-sensitivity cardiac troponin-I (hsTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) could predict future major adverse cardiovascular events (MACE) in stable coronary artery disease (CAD) patients with high- or low-dose of pitavastatin., Methods: This was a case-cohort analysis of the REAL-CAD study, a randomized trial of high- or low-dose (4 or 1 mg/day) pitavastatin therapy in patients with stable CAD. We examined the MACE risk according to the quartile of hsTnI and NT-proBNP at baseline., Results: A total of 1336 and 1396 patients including 582 MACE cases were randomly examined into the hsTnI and NT-proBNP cohort, respectively. Both higher levels of hsTnI and NT-proBNP at baseline were significantly associated with increased risk of MACE (p < 0.001, respectively). When separately analyzed in statin dose, the higher marker levels were significantly associated with higher MACE risk in all cohorts (p < 0.001 in all cohorts). After multivariable adjustment, hsTnI levels were significantly associated with MACE risk in low-dose statin group (HR 2.54, p = 0.0001); however, in high-dose pitavastatin therapy, a significant association was diminished in MACE risk among the quartiles of baseline hsTnI levels (p = 0.154). Conversely in the NT-proBNP cohort, the association between NT-proBNP levels and MACE risk was constantly observed regardless of pitavastatin dose even after multivariable adjustment (both p < 0.0001)., Conclusions: Patients with high hsTnI levels had high risk of MACE in low-dose statin group, but not in high-dose, suggesting that high-dose statin treatment might decrease MACE risk in stable CAD patients with high hsTnI levels., Competing Interests: Declaration of Competing Interest Dr. J. Ishii received a research grant from Sysmex Corp. and honoraria from Daiichi Sankyo Co. Ltd., Kowa Pharmaceutical Co. Ltd., Siemens Healthineers Japan, and LSI Medience Corp. Dr. Fukumoto received research grant from Sanofi KK, Shionogi & Co, Ltd., honoraria from Public Health Research Foundation, AstraZeneca KK, Eisai Co, Ltd., Kowa Pharmaceutical Co Ltd., research grant and honoraria from MSD KK, Otsuka Pharmaceutical Co, Ltd., Daiichi Sankyo Co, Ltd., Sumitomo Dainippon Pharma Co, Ltd., Teijin Pharma Ltd., Bayer Yakuhin, Ltd., Mochida Pharmaceutical Co, Ltd., Astellas Pharma Inc., Sanwa Kagaku Kenkyusho Co, Ltd., Takeda Pharmaceutical Co Ltd., Mitsubishi Tanabe Pharma Corp, Pfizer Japan Inc., Ono Pharmaceutical Co Ltd., AstraZeneca KK. Dr. Ozaki received research grant and honoraria from Mochida Pharmaceutical Co., Ltd., Pfizer Japan Inc., Takeda Pharmaceutical Company Limited, Sanofi K.K., Shionogi & Co., Ltd., MSD K.K., Mitsubishi Tanabe Pharma Corporation, Otsuka Pharmaceutical Co., Ltd., Bayer Yakuhin, Ltd., Daiichi Sankyo Company, Limited, Sumitomo Dainippon Pharma Co., Ltd., research grant, other reserch support and honoraria from Public Health Research Foundation. Dr. Iimuro received research grant from Amgen Astellas BioPharma K.K., research grant and honoraria from Public Health Research Foundation. Dr. Iwata received other research support from Public Health Research Foundation, honoraria from Bayer Yakuhin, Ltd., Daiichi Sankyo Company, Limited, Takeda Pharmaceutical Company Limited, MSD K.K., Kowa Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Corporation. Dr. Sakuma received honoraria from GlaxoSmithKline, AstraZeneca, Takeda, Bayer, Pfizer, Bristol-Myers Squibb, Boehringer lngelheim, MSD, Kyowa Hakko Kirin, Daiichi Sankyo, Novartis, Sanofi, Kowa, Shionogi, Kissei, Astellas, Amgen, Ono, Otsuka, Novonordisk, Mochida, Teijin, Sysmex, Nipro, Kyorin, Fuji and Sumitomo Dainippon, research grants from Public Health Research Foundation, Kowa, National Cerebral and Cardiovascular Center and Medical Informatics Study Group. Dr. Nakagawa received honoraria from Kowa Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Bayer Yakuhin, Ltd., Sanofi K.K., Daiichi Sankyo Company, Limited, Shionogi & Co., Ltd., Astellas Pharma Inc., MSD K.K., Mitsubishi Tanabe Pharma Corporation, Sumitomo Dainippon Pharma Co., Ltd., AstraZeneca K.K., Amgen Astellas BioPharma K.K., Eisai Co., Ltd., Otsuka Pharmaceutical Co., Ltd., Pfizer Japan Inc., research grant, other research support and honoraria from Public Health Research Foundation. Dr. Hibi received research grants from Public Health Research Foundation, Abott Vascular Japan Co. Ltd., and Sanofi KK. Dr. Hiro received research grants from Otsuka Pharmaceutical Co. Ltd., Shionogi & Co. Ltd., and Takeda Pharmaceutical Co. Ltd., honoraria from Amgen Astellas BioPharma KK, Kowa Pharmaceutical Co. Ltd., Kissei Pharmaceutical Co. Ltd., and Chugai Pharmaceutical Co. Ltd., research grants and honoraria from Astellas Pharma Inc., Eisai Co. Ltd., MSD KK, Sanofi KK, Daiichi Sankyo Co. Ltd., Sumitomo Dainippon Pharma Co. Ltd., Mitsubishi Tanabe Pharma Corp., Bayer Yakuhin, Ltd., Pfizer Japan Inc., and AstraZeneca KK, and research grant, other research support, and honoraria from Public Health Research Foundation. Dr. Hokimoto received honoraria from Daiichi Sankyo Co. Ltd. and AstraZeneca KK. Dr. Miyauchi received honoraria from Sanofi KK, Daiichi Sankyo Co. Ltd., AstraZeneca KK, Amgen Astellas BioPharma KK, Takeda Pharmaceutical Co. Ltd., Bayer Yakuhin, Ltd., and MSD KK. Dr. Daida received honoraria from Amgen Astellas BioPharma KK, Daiichi Sankyo Co., Ltd., Kowa Pharmaceutical Co., Ltd., MSD KK, and research grant from Canon, and scholarship grant from Otsuka Pharmaceutical Co., Ltd., Sanofi KK, MSD KK, Pfizer Japan Inc., Mitsubishi Tanabe Pharma Corp., Astellas Pharma Inc., Takeda Pharmaceutical Co., Ltd., Teijin Pharma Ltd., Shionogi & Co., Ltd., Actelion Pharmaceuticals Japan, Ltd. Bayer Yakuhin, Ltd., Boehringer Ingelheim Japan Co., Ltd., and courses endowed by Phillips, Resmed, Fukuda Denshi, Asahikasei, Inter-Reha. Dr. Shimokawa received research grant from Shionogi & Co, Ltd., Teijin Pharma Ltd., Astellas Pharma Inc., Otsuka Pharmaceutical Co, Ltd., honoraria from Kowa Pharmaceutical Co Ltd., Sanofi KK, AstraZeneca KK, Bayer Yakuhin, Ltd., research grant and honoraria from MSD KK, Mitsubishi Tanabe Pharma Corp, Daiichi Sankyo Co, Ltd., research grant, other research support, and honoraria from Public Health Research Foundation. Dr. Saito received honoraria from Otsuka Pharmaceutical Co. Ltd., Mitsubishi Tanabe Pharma Corp., Mochida Pharmaceutical Co. Ltd., and Kowa Pharmaceutical Co. Ltd. and other research support and honoraria from Public Health Research Foundation. Dr. Kimura received research grant from Sumitomo Dainippon Pharma Co, Ltd., Astellas Pharma Inc., Otsuka Pharmaceutical Co, Ltd., Mitsubishi Tanabe Pharma Corp, Takeda Pharmaceutical Co Ltd., other research support and honoraria from Kowa Pharmaceutical Co Ltd., Bayer Yakuhin, Ltd., research grant, other research support, and honoraria from MSD KK, Sanofi KK, Mochida Pharmaceutical Co, Ltd., Daiichi Sankyo Co, Ltd., Public Health Research Foundation, Amgen Astellas BioPharma KK. Dr. Matsuzaki received honoraria from Mochida Pharmaceutical Co. Ltd. Dr. Nagai received honoraria from Kowa Pharmaceutical Co Ltd., Takeda Pharmaceutical Co Ltd., Bayer Yakuhin, Ltd., Daiichi Sankyo Co, Ltd., Shionogi & Co, Ltd., MSD KK, Mitsubishi Tanabe Pharma Corp, Amgen Astellas BioPharma KK, Eisai Co, Ltd., Astellas Pharma Inc., Sumitomo Dainippon Pharma Co, Ltd., Mochida Pharmaceutical Co, Ltd., honoraria and expert witness from Public Health Research Foundation. Other coauthors report no conflicts., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: The ability to predict secondary cardiovascular events could improve health of patients undergoing statin treatment. Circulating ANGPTL8 (angiopoietin-like protein 8) levels, which positively correlate with proatherosclerotic lipid profiles, activate the pivotal proatherosclerotic factor ANGPTL3. Here, we assessed potential association between circulating ANGPTL8 levels and risk of secondary cardiovascular events in statin-treated patients., Methods: We conducted a biomarker study with a case-cohort design, using samples from a 2018 randomized control trial known as randomized evaluation of high-dose (4 mg/day) or low-dose (1 mg/day) lipid-lowering therapy with pitavastatin in coronary artery disease (REAL-CAD [Randomized Evaluation of Aggressive or Moderate Lipid-Lowering Therapy With Pitavastatin in Coronary Artery Disease])." From that study's full analysis set (n=12 413), we selected 2250 patients with stable coronary artery disease (582 with the primary outcome, 1745 randomly chosen, and 77 overlapping subjects). A composite end point including cardiovascular-related death, nonfatal myocardial infarction, nonfatal ischemic stroke, or unstable angina requiring emergent admission was set as a primary end point. Circulating ANGPTL8 levels were measured at baseline and 6 months after randomization., Results: Over a 6-month period, ANGPTL8 level changes significantly decreased in the high-dose pitavastatin group, which showed 19% risk reduction of secondary cardiovascular events compared with the low-dose group in the REAL-CAD [Randomized Evaluation of Aggressive or Moderate Lipid-Lowering Therapy With Pitavastatin in Coronary Artery Disease] study. In the highest quartiles, relative increases in ANGPTL8 levels were significantly associated with increased risk for secondary cardiovascular events, after adjustment for several cardiovascular disease risk factors and pitavastatin treatment (hazard ratio in Q4, 1.67 [95% CI, 1.17-2.39). Subgroup analyses showed relatively strong relationships between relative ANGPTL8 increases and secondary cardiovascular events in the high-dose pitavastatin group (hazard ratio in Q4, 2.07 [95% CI, 1.21-3.55]) and in the low ANGPTL8 group at baseline (166

Introduction: Data are lacking on the extent to which patients with non-valvular atrial fibrillation (AF) who are aged ≥80 years benefit from ablation treatment. The question pertains especially to patients' postablation quality of life (QoL) and long-term clinical outcomes., Methods and Analysis: We are initiating a prospective, registry-based, multicentre observational study that will include patients aged ≥80 years with non-valvular AF who choose to undergo treatment by catheter ablation and, for comparison, such patients who do not choose to undergo ablation (either according to their physician's advice or their own preference). Study subjects are to be enrolled from 52 participant hospitals and three clinics located throughout Japan from 1 June 2022 to 31 December 2023, and each will be followed up for 1 year. The planned sample size is 660, comprising 220 ablation group patients and 440 non-ablation group patients. The primary endpoint will be the composite incidence of stroke/transient ischaemic attack (TIA) or systemic embolism (SE), another cardiovascular event, major bleeding and/or death from any cause. Other clinical events such as postablation AF recurrence, a fall or bone fracture will be recorded. We will collect standard clinical background information plus each patient's Clinical Frailty Scale score, AF-related symptoms, QoL (Five-Level Version of EQ-5D) scores, Mini-Mental State Examination (optional) score and laboratory test results, including measures of nutritional status, on entry into the study and 1 year later, and serial changes in symptoms and QoL will also be secondary endpoints. Propensity score matching will be performed to account for covariates that could affect study results., Ethics and Dissemination: The study conforms to the Declaration of Helsinki and the Ethical Guidelines for Clinical Studies issued by the Ministry of Health, Labour and Welfare, Japan. Results of the study will be published in one or more peer-reviewed journals., Trial Registration Number: UMIN000047023., Competing Interests: Competing interests: The following authors have potential conflicts of interest: YO received research funding from Bayer Healthcare, Daiichi-Sankyo, Bristol-Meyers Squibb, Nippon Boehringer Ingelheim, Pfizer and Boston Scientific Japan, and accepted remuneration from Bayer Healthcare, Daiichi-Sankyo and Bristol-Meyers Squibb. KNas accepted remuneration from Johnson & Johnson K.K. TK received lecture fees from Daiichi-Sankyo, Bristol-Myers Squibb, Bayer Healthcare, Boston Scientific and Medtronic Japan. HF accepted remuneration from Daiichi-Sankyo, Bayer Yakuhin, Nippon Boehringer Ingelheim, Johnson & Johnson K.K., Abbott Medical Japan, Medtronic Japan and Japan Lifeline. SN received speaker honoraria from Bayer Healthcare, Daiichi-Sankyo, Bristol-Meyers Squibb and Medtronic Japan. WS received grants from Daiichi Sankyo Co., Ltd, and Nippon Boehringer Ingelheim; and remuneration for lectures, presentations, speakers bureaus, manuscript writing or educational events from Daiichi Sankyo, Nippon Boehringer Ingelheim, Bristol-Meyers Squibb, K.K., Bayer Yakuhin, Pfizer, Ono Pharmaceutical and Medtronic Japan. YM received lecture fees from Bayer Healthcare, Daiichi-Sankyo, Bristol-Meyers Squibb, Nippon Boehringer Ingelheim, Johnson & Johnson K.K., Japan Lifeline K.K, Medtronic Japan, Pfizer and Boston Scientific Japan. SSu received research funding from Daiichi Sankyo and remuneration from Bristol-Myers Squibb and Daiichi Sankyo. MHar received research funding from BIOTRONIK Japan, Medtronic Japan, Abbott Japan, Japan Lifeline, Nihon Kohden and Boston Scientific Japan, and accepted remuneration from Nippon Boehringer Ingelheim, Daiichi-Sankyo, Bristol-Meyers Squibb, Medtronic Japan, Japan Life Line and Abbott Japan. TY received speaker honoraria from Medtronic Japan and Abbott Medical Japan. MTo received research funding from Japan Lifeline and consulting fee from Medtronic Japan. MTa belongs to the Section of Arrhythmia, Division of Cardiovascular Medicine, Department of Internal Medicine. This section supported by an endowment from Abbott Japan, Medtronic Japan and Boston Scientific Japan. MS is affiliated with an endowed division supported by BIOTRONIK Japan, Boston Scientific Japan K.K., Medtronic Japan and Abbott Medical Japan. AO taught courses endowed by BIOTRONIK, Abbott, Medtronic, Boston Scientific Japan and Japan Lifeline. KSa accepted remuneration from Abbott Japan, Medtronic Japan and Japan Lifeline. HKi accepted remuneration from Otsuka Pharmaceutical., AstraZeneca, Bristol-Meyers Squibb, Ono Pharmaceutical, Pfizer and Novo Nordisk. KMu received honoraria for Chugai Pharmaceutical, AstraZeneca, Taiho Pharmaceutical, MSD, Kyowa Kirin, Yakult Pharmaceutical and Boehringer Ingelheim. KKus received speaker honoraria from Daiichi-Sankyo, Nippon Boehringer Ingelheim, Bayer Yakuhin, Pfizer and Medtronic Japan, and research grants from Medtronic Japan and JSR. KoM received speaker honoraria from Medtronic Japan and Abbott Japan, and research funding from Bristol-Meyers Squibb, Pfizer, Medtronic Japan, Japan Lifeline and Boston Scientific Japan., (© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Aim: We investigated the relationship between small dense low-density cholesterol (sdLDL-C) and risk of major adverse cardiovascular events (MACE) in patients treated with high- or low-dose statin therapy., Methods: This was a prospective case-cohort study within the Randomized Evaluation of Aggressive or Moderate Lipid-Lowering Therapy with Pitavastatin in Coronary Artery Disease (REAL-CAD) study, a randomized trial of high- or low-dose (4 or 1 mg/d pitavastatin, respectively) statin therapy, in patients with stable coronary artery disease (CAD). Serum sdLDL-C was determined using an automated homogenous assay at baseline (randomization after a rule-in period, ＞1 month with 1 mg/d pitavastatin) and 6 months after randomization, in 497 MACE cases, and 1543 participants randomly selected from the REAL-CAD study population., Results: High-dose pitavastatin reduced sdLDL-C by 20% than low-dose pitavastatin (p for interaction ＜0.001). Among patients receiving low-dose pitavastatin, baseline sdLDL-C demonstrated higher MACE risk independent of LDL-C (hazard ratio [95% confidence interval], 4th versus 1st quartile, 1.67 [1.04-2.68]; p for trend=0.034). High-dose (versus low-dose) pitavastatin reduced MACE risk by 46% in patients in the highest baseline sdLDL-C quartile (＞34.3 mg/dL; 0.54 [0.36-0.81]; p=0.003), but increased relative risk by 40% in patients with 1st quartile (≤ 19.5 mg/dL; 1.40 [0.94-2.09]; p=0.099) and did not alter risk in those in 2nd and 3rd quartiles (p for interaction=0.002)., Conclusions: These findings associate sdLDL-C and cardiovascular risk, independent of LDL-C, in statin-treated CAD patients. Notably, high-dose statin therapy reduces this risk in those with the highest baseline sdLDL-C.

Aim: Coronary plaque rupture is the main cause of acute coronary syndrome (ACS), but the role of blood flow features around plaque rupture for ACS is still unknown. The present study aimed to assess the relationship between the geometric configuration of ruptured plaque and ACS occurrence using computational fluid dynamics (CFD) by moving particle method in patients with coronary artery disease., Methods: In this study, 45 patients with coronary artery disease who underwent three-dimensional intravascular ultrasound (IVUS) and had a coronary ruptured plaque (24 plaques with provoked ACS, 21 without) were included. To compare the difference in blood flow profile around ruptured plaque between the patients with and without ACS, the IVUS images were analyzed via the novel CFD analysis., Results: There were no significant differences in localized flow profile around ruptured plaque between the two groups when the initial particle velocity was 10.0 cm/s corresponded to a higher coronary flow velocity at ventricular diastole. However, when it was 1.0 cm/s corresponded to lower coronary flow velocity at ventricular systole, particles with lower velocity (0 ≤ V ≤ 5 cm/s) were more prevalent around ACS-PR ( p=0.035), whereas particles with higher velocity (10 ≤ V ≤ 20 cm/s) were more often detected in silent plaque ruptures (p=0.018)., Conclusions: Three-dimensional IVUS revealed that coronary plaque rupture was a complex one with a wide variety of its stereoscopic configuration, leading to various patterns of the local coronary flow profile. A novel CFD analysis suggested that the local flow was more stagnant around ACS-provoked ruptures than in silent ones.

Aim: The association between high-density lipoprotein cholesterol (HDL-C) level after statin therapy and cardiovascular events in patients with stable coronary artery disease (CAD) remains unclear. Thus, in this study, we sought to determine how HDL-C level after statin therapy is associated with cardiovascular events in stable CAD patients., Methods: From the REAL-CAD study which had shown the favorable prognostic effect of high-dose pitavastatin in stable CAD patients with low-density lipoprotein cholesterol (LDL-C) ＜120 mg/dL, 9,221 patients with HDL-C data at baseline and 6 months, no occurrence of primary outcome at 6 months, and reported non-adherence for pitavastatin, were examined. The primary outcome was a composite of cardiovascular death, non-fatal myocardial infarction, non-fatal ischemic stroke, or unstable angina requiring emergent admission after 6 months of randomization. Absolute difference and ratio of HDL-C levels were defined as (those at 6 months-at baseline) and (absolute difference/baseline)×100, respectively., Results: During a median follow-up period of 4.0 (IQR 3.2-4.7) years, the primary outcome occurred in 417 (4.5%) patients. The adjusted risk of all HDL-C-related variables (baseline value, 6-month value, absolute, and relative changes) for the primary outcome was not significant (hazard ratio [HR] 0.99, 95% confidence interval [CI] 0.91-1.08, HR 1.03, 95% CI 0.94-1.12, HR 1.05, 95% CI 0.98-1.12, and HR 1.08, 95% CI 0.94-1.24, respectively). Furthermore, adjusted HRs of all HDL-C-related variables remained non-significant for the primary outcome regardless of on-treatment LDL-C level at 6 months., Conclusions: After statin therapy with modestly controlled LDL-C, HDL-C level has little prognostic value in patients with stable CAD.

Aim: According to recent clinical trials, a combination of direct oral anticoagulants with antiplatelet drugs is often recommended for atrial fibrillation patients who receive drug-eluting stents (DESs). Although the optimal combination comprises direct factor Xa inhibitors and a P2Y 12 receptor antagonist (or aspirin), their influence on vascular responses to DESs remains unclear., Methods: Pigs were given either aspirin and clopidogrel (dual antiplatelet therapy [DAPT] group), aspirin and rivaroxaban (AR group), or clopidogrel and rivaroxaban (CR group), followed by everolimus-eluting stent (Promus Element) implantation into the coronary artery. Stented coronary arteries were evaluated via intravascular optical coherence tomography (OCT) and histological analysis at 1 and 3 months., Results: OCT revealed lower neointimal thickness in the DAPT group and comparable thickness among all groups at 1 and 3 months, respectively. Histological analyses revealed comparable neointimal area among all groups and the smallest neointimal area in the CR group at 1 and 3 months, respectively. In the DAPT and AR groups, the neointima continued to grow from 1 to 3 months. A shortened time course for neointima growth was observed in the CR group, with rapid growth within a month (maintained for 3 months). A higher incidence of in-stent thrombi was observed in the AR group at 1 month; no thrombi were found in either group at 3 months. More smooth muscle cells with contractile features were found in the CR group at both 1 and 3 months., Conclusions: Our results proved the noninferiority of the combination of rivaroxaban with an antiplatelet drug, particularly the dual therapy using rivaroxaban and clopidogrel, compared to DAPT after DES implantation.

Background: It has not yet been established whether higher-dose statins have beneficial effects on cardiovascular events in patients with stable coronary artery disease (CAD) and renal dysfunction., Methods: The REAL-CAD study is a prospective, multicenter, open-label trial. As a substudy, we categorized patients by an estimated glomerular filtration rate (eGFR) as follows: eGFR ≥60 (n = 7,768); eGFR ≥45 and <60 (n = 3,176); and eGFR <45 mL/Min/1.73 m 2 (n = 1,164), who were randomized to pitavastatin 4mg or 1mg therapy. The primary endpoint was a composite of cardiovascular death, non-fatal myocardial infarction, non-fatal ischemic stroke, or unstable angina, and was assessed by the log-rank test and Cox proportional hazards model., Results: The baseline characteristics and medications were largely well-balanced between two groups. The magnitude of low-density lipoprotein cholesterol (LDL-C) reduction at 6 months in high- and low-dose pitavastatin groups was comparable among all eGFR categories. During a median follow-up of 3.9 years, high- compared with low-dose pitavastatin significantly reduced cardiovascular events in patients with eGFR ≥60 (hazard ratio (HR) 0.73; 95% confidence interval (CI) 0.58-0.91; P = .006), and reduced but not significant for patients with eGFR ≥45 and <60 (HR 0.85; 95% CI, 0.63-1.14; P = .27) or eGFR <45 mL/Min/1.73 m 2 (HR 0.90; 95% CI 0.62-1.33; P = .61). An interaction test of treatment by eGFR category was not significant (P value for interaction = .30)., Conclusion: Higher-dose pitavastatin therapy reduced LDL levels and cardiovascular events in stable CAD patients irrespective of eGFR level, although the effect on events appeared to be numerically lower in patients with lower eGFR., (Copyright © 2021. Published by Elsevier Inc.)

Aims: Wall shear stress (WSS) has been considered a major determinant of aortic atherosclerosis. Recently, non-obstructive 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 three-dimensional 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.

The significance of microvessels within atherosclerotic plaques is not yet fully clarified. Associated with plaque vulnerability. The aim of this study is to examine tissue characteristics of plaque with microvessels detected by optical coherence tomography (OCT) by use of a commercially available color-coded intravascular ultrasound (IVUS) and coronary angioscopy (CAS). The subjects examined comprised of 44 patients with stable angina pectoris who underwent percutaneous coronary intervention. Microvessels were defined as a tiny tubule with a diameter of 50-300 µm detected over three or more frames in OCT. We compared the total volume of microvessels with tissue component such as fibrotic, lipidic, necrotic, and calcified volume and the number of yellow plaque. In IVUS analysis, % necrotic volume and % lipidic volume were significantly correlated and % fibrotic volume was inversely significantly correlated with the total volume of microvessel (r = 0.485, p = 0.0009; r = 0.401, p = 0.007; r = - 0.432, p = 0.003, respectively). The number of plaque with an angioscopic yellow grade of two or more was significantly correlated with the total volume of microvessel (r = 0.461, p = 0.002). The greater the luminal volume of microvessels, the more the percent content of necrotic/lipidic tissue volume within plaque and the more the number of yellow plaques. These data suggested that microvessels within coronary plaque might be related to plaque vulnerability.