Journal of Atherosclerosis and Thrombosis
Online ISSN : 1880-3873
Print ISSN : 1340-3478
ISSN-L : 1340-3478
Volume 20 , Issue 9
Showing 1-5 articles out of 5 articles from the selected issue
Committee Report
  • Ozkan Gungor, Fatih Kircelli, Luminita Voroneanu, Adrian Covic, Ercan ...
    2013 Volume 20 Issue 9 Pages 698-707
    Published: 2013
    Released: September 24, 2013
    [Advance publication] Released: August 02, 2013
    Cardiovascular disease constitutes the major cause of mortality in patients with chronic kidney disease. Arterial stiffness is an important contributor to the occurrence and progression of cardiovascular disease. Various risk factors, including altered hormone levels, have been suggested to be associated with arterial stiffness. Based on the background that chronic kidney disease predisposes individuals to a wide range of hormonal changes, we herein review the available data on the association between arterial stiffness and hormones in patients with chronic kidney disease and summarize the data for the general population.
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Original Article
  • Maki Miyamoto-Sasaki, Tomoyuki Yasuda, Tomoko Monguchi, Hideto Nakajim ...
    2013 Volume 20 Issue 9 Pages 708-716
    Published: 2013
    Released: September 24, 2013
    [Advance publication] Released: June 05, 2013
    Aim: Although statins increase the plasma concentration of high-density lipoprotein cholesterol (HDL-C), it has not been elucidated whether the increased HDL particles possess normal antiatherosclerotic properties. Pitavastatin functions to increase the plasma HDL-C level and decrease the lowdensity lipoprotein cholesterol (LDL-C) level. In the present study, we sought to examine the qualitative changes in HDL during pitavastatin treatment.
    Methods: A total of 30 patients with dyslipidemia were treated with 2 mg of pitavastatin for four weeks. The cholesterol efflux capacity and activities of the antioxidative enzymes paraoxonase-1 (PON-1) and platelet-activating factor acetylhydrolase (PAF-AH) were evaluated using polyethethylene glycol-treated HDL fractions before and after pitavastatin treatment.
    Results: Pitavastatin treatment decreased the serum LDL-C level by 39% and increased the serum HDL-C level by 9% (p<0.05). In addition, pitavastatin increased the phospholipid content of HDL by 7.8% (p<0.05). The pitavastatin-induced increase in the HDL-C level coincided with an increase in the cholesterol efflux capacity of the isolated HDL fraction of 8.6% (p<0.05). The post-pitavastatin treatment activity of HDL-associated PON-1 (paraoxonase and arylesterase) was increased by 9% (p<0.05) and 11% (p0.05), respectively, while the HDL-associated PAF-AH activity was not affected by pitavastatin.
    Conclusions: In addition to its LDL-C-lowering effects, pitavastatin elevates the HDL-C level and enhances the cholesterol efflux capacity and antioxidative properties of HDL. Pitavastatin therefore increases the amount of functional HDL without attenuating HDL quality.
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  • Tsuyoshi Nozue, Kazuki Fukui, Shingo Yamamoto, Tomoyuki Kunishima, Shi ...
    2013 Volume 20 Issue 9 Pages 717-725
    Published: 2013
    Released: September 24, 2013
    [Advance publication] Released: June 08, 2013
    Aim: The TRUTH trial demonstrated that 8-month statin therapy alters the composition of coronary artery plaque using virtual histology (VH)-intravascular ultrasound (IVUS). The extended TRUTH study was conducted to evaluate the relationship between changes in coronary atherosclerosis and mid-term clinical outcomes and identify the factors associated with cardiovascular events.
    Methods: Of 164 patients with angina pectoris who participated in the TRUTH trial, 119 subjects with analyzable IVUS data at both enrollment and the 8-month follow-up were enrolled and observed for at least two years. The primary end point was the time to first occurrence of cardiovascular composite events, including cardiovascular death, nonfatal myocardial infarction, nonfatal cerebral infarction, unstable angina and ischemic-driven revascularization, except for target lesion revascularization.
    Results: The frequency of reaching the primary end point was 13% (16/119), with a mean follow-up period of 41.9±9.4 months. Although plaque regression and changes in plaque composition were not associated with future cardiovascular events, the serum high-sensitivity C-reactive protein (hs-CRP) levels at the start of the extended TRUTH study were significantly higher in the event group than in the event-free group (1.43 mg/L vs. 0.58 mg/L, p=0.01). A multivariate logistic regression analysis showed that the hs-CRP level was an independent significant predictor of cardiovascular events (odds ratio: 1.69; 95% confidence interval: 1.14-2.50, p=0.01).
    Conclusions: Coronary artery plaque regression and changes in plaque composition during statin therapy do not predict future cardiovascular events in patients with angina pectoris. Instead, the serum hs-CRP level can be used as a predictor of cardiovascular events.
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  • Mitsuyoshi Takahara, Osamu Iida, Yoshimitsu Soga, Keisuke Hirano, Teru ...
    2013 Volume 20 Issue 9 Pages 726-732
    Published: 2013
    Released: September 24, 2013
    [Advance publication] Released: June 06, 2013
    Aim: We investigated whether any seasonal variation is observed in the incidence, severity and prognosis of critical limb ischemia (CLI) requiring endovascular therapy.
    Methods: We analyzed a multicenter database of 1,568 consecutive CLI cases undergoing primary endovascular therapy for infrainguinal lesions between July 2004 and June 2011. The monthly incidence was assessed according to the cumulative number of cases in each month, using a simple moving average. The data were fitted to a nonlinear regression model with a cosine function. The monthly proportion of cases in each Rutherford classification among the overall CLI population was assessed using a multinomial logistic regression model. The monthly risk of major amputation was evaluated using a Cox proportional hazard regression model.
    Results: Significant seasonal variation was observed in the incidence of CLI (p<0.01). It was higher in the period from winter to spring, with a peak in March, and lower in the period from summer to autumn, with a trough in September; the fold difference between the peak and trough was 2.2. The seasonal variation was more markedly observed in the cases with a more severe Rutherford class. The proportion of cases in each Rutherford class among the overall CLI population also exhibited significant seasonal variation (p<0.01). In addition, the risk of major amputation demonstrated significant seasonal variation (p=0.03); however, the statistical significance was lost following adjustment for the Rutherford classification (p=0.10).
    Conclusions: Seasonal variation is observed in the incidence and severity of CLI. The seasonality of the limb prognosis is likely explained by that of the CLI severity.
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