In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.

The free consultation period for this content is over.

It is now only available year-round to ESC Professional Members, Fellows of the ESC, and Young combined Members

Long-term administration of eicosapentaenoic acid prevents the progress of left ventricular hypertrophy via reducing oxidative stress and advanced glycation end-products in patients with hypertension

Session Poster session 3

Speaker Akihiro Aoyama

Event : ESC Congress 2015

  • Topic : preventive cardiology
  • Sub-topic : Risk Factors and Prevention
  • Session type : Poster Session

Authors : A Aoyama (Sagamihara,JP), T Masuda (Sagamihara,JP), M Ogura (Sagamihara,JP), Y Kamada (Sagamihara,JP), S Tanaka (Sagamihara,JP), K Kamiya (Sagamihara,JP), K Nozaki (Sagamihara,JP), E Maekawa (Sagamihara,JP), M Yamaoka-Tojo (Sagamihara,JP), J Ako (Sagamihara,JP)

A. Aoyama1 , T. Masuda2 , M. Ogura2 , Y. Kamada1 , S. Tanaka1 , K. Kamiya3 , K. Nozaki3 , E. Maekawa4 , M. Yamaoka-Tojo2 , J. Ako4 , 1Kitasato University, Graduate School of Medical Sciences - Sagamihara - Japan , 2Kitasato University, School of Allied Health Sciences, Department of Rehabilitation - Sagamihara - Japan , 3Kitasato University Hospital, Department of Rehabilitation - Sagamihara - Japan , 4Kitasato University, School of Medicine, Department of Cardiovascular Medicine - Sagamihara - Japan ,

European Heart Journal ( 2015 ) 36 ( Abstract Supplement ), 473-474

Background: Elevated oxidative stress has been shown to promote the production of advanced glycation end-products (AGEs) in patients with hypertension (HT). AGEs are known to enhance left ventricular hypertrophy (LVH) via the activation of nuclear factor-kappa B in myocardium. Although eicosapentaenoic acid (EPA) reduces oxidative stress, it is unclear whether EPA inhibits the AGEs production and prevents the progress of LVH. This study aimed to investigate the effect of long-term EPA administration on LVH in HT patients.

Methods: We recruited 65 HT patients whose resting blood pressure was controlled <140/90mmHg. In crossover method, all patients were administered 1,800 mg of EPA ethyl-ester daily and antihypertensives for 10 months in the EPA(+) group and only antihypertensives for 10 months in the EPA(−) group. We measured serum concentrations of EPA and arachidonic acid (AA). Serum malondialdehyde-modified LDL-cholesterol (MDA-LDL) and plasma pentosidine were measured as parameters of oxidative stress and AGEs, respectively. Left ventricular mass index (LVMI) was assessed as a parameter of LVH. All parameters were measured before and after the observation period and compared between the two groups. We calculated the changes in pentosidine and LVMI from baselines to those measured after the observation period (Δpentosidine and ΔLVMI).

Results: EPA and EPA/AA ratio were significantly higher in the EPA(+) group than in the EPA(−) group (P<0.001, respectively). MDA-LDL, pentosidine and LVMI were significantly lower in the EPA(+) group than in the EPA(−) group (P<0.05, respectively). Δpentosidine was positively correlated with ΔLVMI (r=0.31, P<0.05).

Conclusion: Long-term administration of EPA prevented the progress of LVH via reducing oxidative stress and AGEs in HT patients.

Figure 1. Comparisons in MDA-LDL, pentosidine, and LVMI between the EPA(+) and EPA(&#x2212;) groups.

Get your access to resources

Join now
  • 1ESC Professional Members – access all ESC Congress resources 
  • 2ESC Association Members (Ivory, Silver, Gold) – access your Association’s resources
  • 3Under 40 or in training - with a Combined Membership, access all resources
Join now

Our sponsors

ESC 365 is supported by Bayer, Boehringer Ingelheim and Lilly Alliance, Bristol-Myers Squibb and Pfizer Alliance, Novartis Pharma AG and Vifor Pharma in the form of educational grants. The sponsors were not involved in the development of this platform and had no influence on its content.

logo esc

Our mission: To reduce the burden of cardiovascular disease

Who we are