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Volume 156, Issue 6, Pages 1117-1123 (December 2008)


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Omega-6 and trans fatty acids in blood cell membranes: A risk factor for acute coronary syndromes?

Robert C. Block, MD, MPHaCorresponding Author Informationemail address, William S. Harris, PhDbc, Kimberly J. Reid, MSb, John A. Spertus, MD, MPHbc

Received 6 May 2008; accepted 19 July 2008. published online 15 October 2008.

Background

Although fatty acid intake has been associated with risk of coronary disease events, the association between blood omega-6 and trans fatty acids (FAs) at the time of an acute coronary syndrome (ACS) is unknown.

Methods

The relationship of blood FA composition to ACS was analyzed in 768 incident cases and 768 controls (matched on age, sex, and race).

Results

Compared to controls, ACS cases' blood cell membrane content of linoleic acid was 13% lower (P < .0001); arachidonic acid was 3.6% higher (P < .001); the trans isomer of oleic acid was 13.3% higher (P < .0001); and the trans-trans isomer of linoleic acid was 13.3% higher (P = .003). In multivariable analyses, a 1-SD decrease in linoleic acid was associated with >3 times the odds for being a case (odds ratio [OR] 3.23, 95% confidence interval [CI] 2.63-4.17). The relationship of arachidonic acid to ACS was U shaped; compared to the first quartile of arachidonic acid, the ORs for case status in the second, third, and fourth quartiles were 0.73 (95% CI 0.47-1.13), 0.65 (95% CI 0.41-1.04), and 2.32 (95% CI 1.39-3.90), respectively. The OR for a 1-SD increase in trans oleic acid was 1.24 (95% CI 1.06-1.45), and for trans-trans linoleic acid, 1.1 (95% CI 0.93-1.30). All associations were independent of membrane omega-3 FA content.

Conclusions

High blood levels of linoleic acid but low levels of trans oleic acid are inversely associated with ACS. The relationship of arachidonic acid to ACS appears more complex.

a Department of Community and Preventive Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY

b Division of Cardiovascular Research, Saint Luke's Mid America Heart Institute

c Department of Medicine, University of Missouri-Kansas City, Kansas City, MO

Corresponding Author InformationReprint requests: Robert C. Block, MD, MPH, Division of Epidemiology, Department of Community and Preventive Medicine, University of Rochester School of Medicine and Dentistry, Box 644, 601 Elmwood Avenue, Rochester, NY 14642.

 This study received funding from the following sources: (1) The Saint Luke's Hospital Foundation, Kansas City, MO; (2) grant KL2 RR 024136 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and the NIH Roadmap for Medical Research. The contents of this study are solely the responsibility of the authors and do not necessarily represent the official view of the NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/. Information on Re-engineering the Clinical Research Enterprise can be obtained from http://nihroadmap.nih.gov/clinicalresearch/overview-translational.asp.

PII: S0002-8703(08)00647-9

doi:10.1016/j.ahj.2008.07.014


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