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Intake of total trans, trans-18:1 and trans-18:2 fatty acids and risk of sudden cardiac death in women

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2009

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Elsevier
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Chiuve, Stephanie E., Eric B. Rimm, JoAnn E. Manson, William Whang, Dariush Mozaffarian, Meir J. Stampfer, Walter C. Willett, and Christine M. Albert. 2009. “Intake of Total Trans, Trans-18:1, and Trans-18:2 Fatty Acids and Risk of Sudden Cardiac Death in Women.” American Heart Journal 158 (5): 761–67. https://doi.org/10.1016/j.ahj.2009.08.015.

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Background Total intake of trans fat is associated with coronary heart disease (CHD), and recent reports in primarily male populations suggest that blood levels of specific trans isomers may have different effects on risk, particularly risk of sudden cardiac death (SCD).Methods We prospectively examined the association between dietary intake of trans fat and SCD among 86,762 women from the Nurses' Health Study. Coronary heart disease risk factors, including diet and lifestyle factors, were updated via questionnaires every 2 to 4 years, beginning in 1980.Results Over 26 years, we documented 317 SCD events. In the primary analysis, we found no significant association between intake of total trans fat, trans-18:1, or trans-18:2 isomers and risk of SCD. Compared to the lowest quintile of intake, the relative risk (95% CI) of SCD in the highest quintile was 1.28 (0.82-2.00) for total trans, 1.08 (0.64-1.83) for trans-18:1, and 1.19 (0.76-1.88) for trans-18:2. In a secondary prespecified analysis, total trans fat was significantly related to SCD among women who reported a diagnosis of CHID before SCD (relative risk 3.24, 95% Cl 1.42-7.40 for the highest vs lowest quintile, P trend = .01); however, the test for interaction was not significant (P =. 11).Conclusions In this large prospective cohort of women, neither dietary intake of trans fat nor the individual trans isomers, trans-18:1 and trans-18:2, were significantly associated with risk of SCD. However, trans fat intake may be associated with SCD risk among women with CHID, suggesting that trans fat intake may play a greater role in SCD risk among those with clinically manifest atherosclerosis. (Am Heart J 2009; 158:761-7.)

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