Journal of atherosclerosis and thrombosis (J Atherosclerosis Thromb)

Publisher: Nihon Dōmyaku Kōka Gakkai

Current impact factor: 2.73

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.733
2013 Impact Factor 2.77
2012 Impact Factor 2.933
2011 Impact Factor 2.692
2010 Impact Factor 2.293
2009 Impact Factor 3.048
2008 Impact Factor 2.625
2007 Impact Factor 2.835

Impact factor over time

Impact factor

Additional details

5-year impact 2.76
Cited half-life 4.50
Immediacy index 0.37
Eigenfactor 0.01
Article influence 0.71
Website Journal of Atherosclerosis and Thrombosis website
Other titles Journal of atherosclerosis and thrombosis (Online)
ISSN 1340-3478
OCLC 53835682
Material type Document, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Flow-mediated vasodilation (FMD) of the brachial artery measures the ability of the artery to dilate after a forearm ischemia lasting for 5 min. During ischemia, and therefore in conditions of low flow, constriction of the brachial artery (L-FMC) has sometimes been reported. The meaning of L-FMC is still unclear. The aims of our study were to establish the prevalence of subjects with L-FMC, to determine whether the magnitude of L-FMC correlates with magnitude of FMD, and to determine whether L-FMC can be used to predict FMD timing. Methods: A total of 179 outpatients were studied, and the brachial artery diameter was measured every minute during the 5 min forearm ischemia. Subjects who had at least one measurement showing a constriction of >1% during ischemia were defined as constrictors. FMD was evaluated at 50 s, 2 min, and 3 min after cuff release. On the basis of time, the subjects in whom maximal dilation had occurred were divided into Early, Late, or No dilators. Results: The brachial artery diameter of 70 subjects (39%) constricted during ischemia. Higher the constriction during ischemia, lower was the dilation after ischemia. Constrictors were more likely to have Late (OR 2.6; ICs 95% 1.19-5.81, p=0.02) or No dilation (OR 4.8; ICs 95% 1.90-12-16, p=0.02) compared with no constrictors. Conclusions: The present study reveals that almost 40% of the subjects had brachial artery L-FMC and a more pronounced constriction during ischemia correlated with a lower dilation after ischemia. Finally, the prevalence of subjects showing L-FMC was significantly higher among subjects with delayed or no vasodilation, suggesting that L-FMC may be a marker of endothelial dysfunction.
    Journal of atherosclerosis and thrombosis 11/2015; DOI:10.5551/jat.32060
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Current Japanese guidelines state the target level of low-density lipoprotein cholesterol (LDL-C) of <100mg/dL for secondary prevention of coronary artery disease (CAD). However, this level was set considering the results of trials mainly conducted in Western countries. In addition, the effect of achieving target LDL-C on secondary prevention is unknown. Methods: We examined the effects of achieving target LDL-C on clinical outcomes. Patients who underwent percutaneous coronary intervention at Juntendo University Hospital (Tokyo, Japan) from 2004 to 2010 and received follow-up coronary angiography (CAG) were analyzed. The study population was divided into two groups based on the follow-up LDL-C. The incidence of major adverse cardiovascular events within 3 years after the follow-up CAG was examined. Results: A total of 1321 consecutive patients were enrolled. Sixty-three percent of the patients achieved the target LDL-C. The rate of 3-year events was lower in the group that achieved the target LDL-C (achieved group). The adjusted relative risk reduction in the achieved group was 26% (p=0.02). In the sub-analysis among the four groups stratified by baseline LDL-C of 140 and follow-up LDL-C of 100, the adjusted hazard ratio for 3-year events was 1.84 (95% confidence interval; 1.10-3.24)in Group 3 (baseline <140, follow-up ≥100) and 2.05 (1.18-3.74) Group 4 (baseline ≥140, follow-up ≥100) [Group 2 (baseline ≥140, follow-up <100) as reference]. Conclusions: Our data suggested that follow-up LDL-C <100mg/dL was appropriate for secondary prevention of CAD in Japanese population.
    Journal of atherosclerosis and thrombosis 11/2015; DOI:10.5551/jat.32284
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: To investigate the relationship between the clustering of metabolic syndrome (MetS) components and non-high-density lipoprotein cholesterol (non-HDL-C) levels in Japanese obese boys. Methods: Subjects were 58 obese boys aged 12.0±2.6 years, which were categorized into three subgroups: abdominal obesity, pre-MetS (abdominal obesity+1 component), and MetS (abdominal obesity+2 or more components). Results: Sixteen (27.6%) and 32 (55.2%) of the obese boys were diagnosed as pre-MetS and MetS, respectively. The mean non-HDL-C level in total subjects was 139.0±36.4 mg/dl and that in boys with abdominal obesity, pre-MetS, and MetS were 112.9±34.4, 135.4±37.9, and 149.0±32.6 mg/dl, respectively (p=0.0183, ANOVA). Conclusions: Japanese obese boys with MetS exhibited elevated non-HDL-C levels, suggesting that they may have a higher risk for the development of atherosclerotic diseases.
    Journal of atherosclerosis and thrombosis 09/2015; DOI:10.5551/jat.30692
  • [Show abstract] [Hide abstract]
    ABSTRACT: Microparticles (MPs) are small membrane vesicles that are released from many different cell types by exocytotic budding of the plasma membrane in response to cellular activation or apoptosis. MPs may be involved in both physiological processes and clinical treatments because they express phospholipids, which function as procoagulants. Elevated levels of platelet-derived MPs, endothelial cell-derived MPs, and monocyte-derived MPs are observed in almost all thrombotic diseases occurring in venous and arterial beds. Several studies have shown that the quantity, cellular origin, and composition of circulating MPs depend on the type of disease, the disease state, and medical treatment. Although MPs were initially thought to be small particles with only procoagulant activity, they are now known to have many different functions. An increasing number of studies have identified new implications of elevated MPs in clinical disorders. On the basis of evidence available till date, the present review suggests that MPs may be a useful biomarker in identifying atherothrombosis.
    Journal of atherosclerosis and thrombosis 09/2015; DOI:10.5551/jat.32326
  • [Show abstract] [Hide abstract]
    ABSTRACT: Interleukin-1 receptor-associated kinase 1 (IRAK1) and IRAK4 play essential roles in the induction of inflammatory gene products. We aimed to investigate the effect of the inhibition of IRAK1 and IRAK4 kinase activities on neointimal formation in rats with carotid artery balloon injuries using the IRAK1/4 inhibitor N-(2-Morpholinylethyl)-2-(3-nitrobenzoylamido)-benzimidazole, a cell-permeable benzimidazole compound. Wistar rats and vascular smooth muscle cells (VSMCs) isolated from the thoracic aortas were used. Toll-like receptor 4 (TLR4)-mediated nuclear factor kappa B (NFκB) signaling pathway was revealed by microarrays analysis. In addition, the differential expression of the TLR4 pathway genes, including TLR4, IRAK1, IκBα, and interleukin-1β (IL-1β), was confirmed by quantitative real-time polymerase chain reaction. Immunohistochemical staining, elastic-van Gieson and Masson staining, 5-ethynyl-2´-deoxyuridine staining, enzyme-linked immunosorbent assay, transwell migration assay and western blotting were also contributed for relevant detection. The expression of TLR4 protein gradually increased at days 1, 3, 7, and 21 after balloon injury compared with the uninjured group. The dual inhibition of IRAK1 and IRAK4 attenuated neointimal formation and fibrotic remodeling after injury in vivo and suppressed VSMC proliferation and migration in vitro. The production of mediators such as tumor necrosis factor-α and IL-1β in injured arteries were also reduced by the inhibition of IRAK1 and IRAK4. The expression of NFκB p65- and F4/80-positive cells in inhibitor rats were fewer than those in control rats at day 7, while IRAK1 expression was markedly higher at day 3 in inhibitor rats. Furthermore, western blotting analysis revealed that the IRAK1/4 inhibitor suppressed the IRAK1 and IRAK4 kinase activities and the activation of the TLR4-mediated NFκB pathway in vivo and in vitro. This study suggested that IRAK1/4 could serve as a potential therapeutic target to suppress neointimal formation in carotid arteries after balloon injury through the TLR4/NFκB signaling pathway.
    Journal of atherosclerosis and thrombosis 08/2015; DOI:10.5551/jat.29421
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The optimal fractional flow reserve (FFR) measurement method for superficial femoral artery (SFA) lesions remains to be established. We clarified the optimal measuring procedure for FFR for SFA lesions and investigated the necessary dose of papaverine for inducing maximal hyperemia in SFA lesions. Forty-eight patients with SFA lesions who underwent measurement of peripheral FFR (pFFR: distal mean pressure divided by proximal mean pressure) after endovascular treatment by the contralateral femoral crossover approach were prospectively enrolled. In the pFFR measurement, a guide sheath was placed on top of the common iliac bifurcation and pressure equalization was performed. After advancing the pressure wire distal to the SFA lesion, sequential papaverine administration selectively to the affected common iliac artery was performed. There were no symptoms, electrocardiogram changes, and significant pressure drops at the guide sheath tip with increasing papaverine dose. pFFR changes following 20, 30, and 40 mg of papaverine were 0.87±0.10, 0.84±0.10, and 0.84±0.10, respectively (P<0.001). Although not significantly different, pFFR decreased more in several patients at 30 mg of papaverine than at 20 mg. The pFFR at 40 mg of papaverine was almost similar to that at 30 mg of papaverine. The necessary papaverine dose was not changed according to sex and number of run-off vessels. The contralateral femoral crossover approach is useful in FFR measurement for SFA lesions, and maximal hyperemia is induced by 30 mg of papaverine.
    Journal of atherosclerosis and thrombosis 08/2015; DOI:10.5551/jat.30957
  • Source

    Journal of atherosclerosis and thrombosis 03/2015; 22(7). DOI:10.5551/jat.ED007
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Our previous "J-BENEFIT (Japan BEzafibrate cliNical EFfectIveness and Tolerability)" study demonstrated that bezafibrate improves blood lipid profiles and glucose control in dyslipidemic patients with diabetes. However, bezafibrate did not significantly improve low-density lipoprotein cholesterol (LDL-C), although some patients showed decreases while others showed increases in the LDL-C levels. Therefore, a subgroup analysis of the J-BENEFIT study was conducted to identify factors influencing the bezafibrate-induced changes in the LDL-C levels. Methods: Of the 3,316 patients in the J-BENEFIT study, 2,116 not treated with other lipid-lowering drugs were enrolled in the current study, and the effects of 24-week treatment with bezafibrate on the LDL-C levels were analyzed. A reduction in the LDL-C level of ≥ 25% occurred in 253 patients, and a logistic-regression analysis was used to identify factors associated with this improvement. Results: Among the 2,116 overall patients, bezafibrate treatment significantly increased the LDL-C levels from 123.9±36.7 to 125.7±31.3 mg/dL. The subanalysis showed that the treatment responses varied according to the baseline LDL-C level, with significant decreases in the ≥ 160 and ≥ 140-<160 mg/dL groups, no significant decrease in the ≥ 120-<140 mg/dL group and a significant increase in the <120 mg/dL group. A multivariate logistic-regression analysis of the data for the patients with an LDL-C of ≥ 25% identified a female sex, the use of anti-hypertensive and hypoglycemic agents and a high baseline LDL-C level to be significant determinants of the LDL-C response to bezafibrate. Conclusions: Our results showed that treatment with bezafibrate improves the LDL-C levels and lipid profiles in dyslipidemic diabetic patients, especially women, subjects co-treated with anti-hypertensive or hypoglycemic agents and those with high baseline LDL-C levels.
    Journal of atherosclerosis and thrombosis 03/2015; 22(7). DOI:10.5551/jat.27425
  • Source

    Journal of atherosclerosis and thrombosis 03/2015; 22(6). DOI:10.5551/jat.ED008
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Angiotensin Ⅱ(Ang Ⅱ) produces reactive oxygen species (ROS), thus contributing to the development of cardiac hypertrophy and subsequent heart failure, and stimulates the expression of monocyte chemoattractant protein-1 (MCP-1). In addition, Toll-like receptor 4 (TLR4) is involved in the upregulation of MCP-1. In order to clarify whether TLR4 is involved in the onset of cardiac dysfunction caused by Ang Ⅱ stimulation, we investigated the effects of TLR4 on oxidative stress, the MCP-1 expression and cardiac dysfunction in mice with Ang Ⅱ-induced hypertension. Methods: TLR4-deficient (Tlr4(lps-d)) and wild-type (WT) mice were randomized into groups treated with Ang Ⅱ, norepinephrine (NE) or a subdepressor dose of the Ang Ⅱreceptor blocker irbesartan (IRB) and Ang Ⅱ for two weeks. Results: Ang Ⅱ and NE similarly increased systolic blood pressure in all drug-treated groups compared to that observed in the control group among both WT and Tlr4(lps-d) mice (p<0.05). In the WT mice, Ang Ⅱ induced cardiac hypertrophy as well as vascular remodeling and perivascular fibrosis of the intramyocardial arteries and monocyte/macrophage infiltration in the heart (p<0.05). Furthermore, Ang Ⅱ treatment decreased the left ventricular diastolic function and resulted in a greater left ventricular end-systolic dimension (p<0.05) in addition to producing a five-fold increase in the NADPH oxidase activity, ROS content and MCP-1 expression (p<0.05). In contrast, the Tlr4(lps-d) mice showed little effects of Ang Ⅱ on these indices. In the WT mice, IRB treatment reversed these changes compared to that seen in the mice treated with Ang Ⅱ alone. NE produced little effect on any of the indices in either the WT or Tlr4(lps-d) mice. Conclusions: TLR4 may be involved in the processes underlying the increased oxidative stress, selectively activated MCP-1 expression and cardiac hypertrophy and dysfunction seen in cases of Ang Ⅱ- induced hypertension.
    Journal of atherosclerosis and thrombosis 03/2015; 22(8). DOI:10.5551/jat.27292
  • Source
    Koh Ono ·

    Journal of atherosclerosis and thrombosis 02/2015; 22(4). DOI:10.5551/jat.ED006
  • Source

    Journal of atherosclerosis and thrombosis 02/2015; 22(3). DOI:10.5551/jat.ED009
  • Source

    Journal of atherosclerosis and thrombosis 02/2015; 22(7). DOI:10.5551/jat.ED005
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Chronic kidney disease (CKD) is known to frequently cause cardiovascular events. However, it is unclear how renal dysfunction affects the vascular response. We herein studied the effects of renal dysfunction on the aortic behavior in adenine-fed mice, investigating mechanisms underlying the occurrence of cardiovascular events in CKD patients. Methods: Biochemical analyses of the plasma creatinine, blood urea nitrogen (BUN) and glucose levels and measurements of the blood pressure were performed using C57BL/6 mice fed with and without an adenine-containing diet. The relaxing effects of acetylcholine (ACh) or sodium nitropurusside (SNP) and effects of NO synthase (NOS) inhibitors on the contractions induced by phenylephrine (PE) were measured in endothelium-intact aortas obtained from both mice. Results: The mice fed 0.25% adenine for four weeks showed greater plasma creatinine and BUN concentrations than the control mice, suggesting that adenine-fed mice are a useful CKD model. Furthermore, ACh relaxed the PE-stimulated, endothelium-intact aortas, the effect of which was less potent in the adenine-fed mice than in the control mice. In contrast, the degree of SNP-induced relaxation of the aortas was the same in the adenine-fed mice and control mice. The α1-adrenergic agonist, PE, induced more potent absolute tension of the endothelium-intact aortas in the CKD model mice than in the control mice, while the NOS inhibitors, N-nitro-L-arginine (LNA) and asymmetric dimethylarginine (ADMA) enhanced the contraction effects of PE in both mice. Conclusions: The findings of this study indicate that spontaneous and stimulated NO release from the endothelium is decreased in the CKD model mouse aorta. The NO-mediated correlation between renal and elastic arterial endothelial dysfunction is suggested to be a cause of cardiovascular events in patients with CKD.
    Journal of atherosclerosis and thrombosis 02/2015; 22(8). DOI:10.5551/jat.28191
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In the recent issue of the Journal of Atherosclerosis and Thrombosis, Wang et al. assessed the relationship between the red cell distribution width (RDW) and acute myocardial infarction (AMI). However, assessing all parameters affecting the RDW, determining the optimum RDW cut-off value for predicting the prognosis of coronary artery disease (CAD), excluding metabolic comorbidities affecting the RDW values and identifying the specific range for the WBC count within the exclusion criteria would provide more reliable results and improve the credibility of the entire article in this study population.
    Journal of atherosclerosis and thrombosis 02/2015; 22(2). DOI:10.5551/jat.27573
  • Source

    Journal of atherosclerosis and thrombosis 02/2015; 22(3). DOI:10.5551/jat.ED004
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aim: The current study investigated how prevalent the absence of a prior history of intermittent claudication would be in patients with critical limb ischemia (CLI) and examined the associated clinical features. Methods: We used a database of 559 Japanese CLI patients participating in a multicenter prospective study. A history of intermittent claudication prior to CLI onset was surveyed at registration. The 95% confidence interval (CI) of its prevalence was calculated using the Clopper-Pearson method. Logistic regression analysis was performed to assess the association between the clinical features and the absence of preceding intermittent claudication. Results: The study subjects were 73±10 years old and 67% were male. Tissue loss occurred in 82% of this population. The prevalence of the absence of prior intermittent claudication was 50% [95% CI: 46-55%]. In multivariate logistic regression analysis, a non-ambulatory status, diabetes mellitus, and regular dialysis were significantly and independently associated with the lack of a prior history of intermittent claudication (all p<0.05). Indeed, the presence of these features was associated with a higher prevalence of the lack of the history. Regular dialysis, but not non-ambulatory status or diabetes mellitus, lost its statistical significance after further adjustment for the presence of isolated infrapopliteal lesions, whereas the presence of isolated infrapopliteal lesions itself was significantly associated with a lack of prior intermittent claudication. Conclusions: The absence of a prior history of intermittent claudication was prevalent in CLI patients. Patients with a non-ambulatory status, diabetes mellitus, and regular dialysis were more likely to lack a prior history of intermittent claudication.
    Journal of atherosclerosis and thrombosis 02/2015; 22(7). DOI:10.5551/jat.28217