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Am J Cardiovasc Drugs. 2017 Oct;17(5):409-420. doi: 10.1007/s40256-017-0238-z.

The Ratio of Eicosapentaenoic Acid (EPA) to Arachidonic Acid may be a Residual Risk Marker in Stable Coronary Artery Disease Patients Receiving Treatment with Statin Following EPA Therapy.

Author information

1
Department of Health Planning Center, Nihon University Hospital, 1-6 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8309, Japan. tani.shigemasa@nihon-u.ac.jp.
2
Department of Cardiology, Nihon University Hospital, Tokyo, Japan. tani.shigemasa@nihon-u.ac.jp.
3
Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. tani.shigemasa@nihon-u.ac.jp.
4
Department of Cardiology, Nihon University Hospital, Tokyo, Japan.
5
Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.

Abstract

BACKGROUND:

We investigated the relationship between the eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio and non-high-density lipoprotein cholesterol (non-HDL-C) level, a major residual risk of coronary artery disease (CAD), in statin-treated CAD patients following EPA therapy.

METHODS:

We conducted a 6-month, prospective, randomized clinical trial to investigate the effect of the additional administration of EPA on the EPA/AA ratio and the serum non-HDL-C level in stable CAD patients receiving statin treatment. We assigned CAD patients already receiving statin therapy to an EPA group (1800 mg/day; n = 50) or a control group (n = 50).

RESULTS:

A significant reduction in the serum non-HDL-C level was observed in the EPA group, compared with the control group (-9.7 vs. -1.2%, p = 0.01). A multiple-regression analysis with adjustments for coronary risk factors revealed that achieved EPA/AA ratio was more reliable as an independent and significant predictor of a reduction in the non-HDL-C level at a 6-month follow-up examination (β = -0.324, p = 0.033) than the absolute change in the EPA/AA ratio. Interestingly, significant negative correlations were found between the baseline levels and the absolute change values of both non-HDL-C and triglyceride-rich lipoproteins, both markers of residual risk of CAD, indicating that patients with a higher baseline residual risk achieved a greater reduction.

CONCLUSION:

The present results suggest that the achieved EPA/AA ratio, but not the absolute change in EPA/AA ratio, following EPA therapy might be a useful marker for the risk stratification of CAD among statin-treated patients with a high non-HDL-C level.

CLINICAL TRIAL REGISTRATION:

UMIN ( http://www.umin.ac.jp/ ) Study ID: UMIN000010452.

PMID:
28634822
DOI:
10.1007/s40256-017-0238-z
[Indexed for MEDLINE]

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