Trans-fatty acids and sudden cardiac death
Section snippets
Sudden cardiac death
Sudden cardiac death (SCD) or out-of-hospital cardiac arrest accounts for approximately 300,000 deaths in the United States annually and 50% of cardiac mortality. Because the survival rate is at best 20% and SCD can happen as a first manifestation of heart disease, prevention of SCD is essential to public health. There is growing evidence that dietary and cell membrane n − 3 polyunsaturated fatty acids (PUFAs) decrease the risk of ventricular fibrillation and the risk of SCD [1]. Less is known of
The cardiac arrest blood study
We recently reported the results of a population-based case–control study of cell membrane TFA and out-of-hospital cardiac arrest [2]. The study was conducted in the greater Seattle area in the US, in collaboration with the Seattle and King County (Washington) Emergency Medical System. Briefly, the cases were patients with incident out-of-hospital cardiac arrest, attended by paramedics during 1988–1999 (n = 179), and whose cardiac arrest was not attributable to a non-cardiac cause. To minimize
Limitations
Studies of association cannot demonstrate cause and effect and we cannot exclude the possibility of residual confounding by a factor we did not assess, such as a dietary factor, or by confounders that were assessed incompletely. However, the association was strong and independent of multiple risk factors.
The levels of trans-18:2 in RBC membranes are small and difficult to estimate precisely. However, we measured trans-18:2 levels in cases and their matched controls in the same runs to minimize
Reproducibility
There are no other studies of cell membrane TFA and SCD. In a small case–control study of n − 3 PUFAs and sudden death nested in the Physicians’ Health Study, mean blood levels of total TFA, trans-18:1 and trans-18:2 at baseline did not differ between cases and controls [3]. However, analyses that would have taken into account the matching factors, including smoking, and other risk factors were not presented for TFA. In addition, if there were changes in the TFA content of foods during the long
Mechanisms
Possible mechanisms by which trans-18:2 might influence the risk of SCD are unknown. In contrast to n − 3 PUFAs, the possibility that trans-18:2 might influence the risk of ventricular fibrillation, has not been tested. Documented effects of TFA on blood lipids and inflammation markers, would not explain different associations of trans-18:1 and trans-18:2 with SCD.
Specificity of outcome
We have provided evidence that PUFAs in plasma phospholipids, a biomarker related to cell membrane fatty acids, are associated with fatal ischemic heart disease but not with non-fatal myocardial infarction [4]. In a case–control study nested in the Cardiovascular Health Study, both long-chain n − 3 PUFAs and α-linolenic acid were not associated with non-fatal myocardial infarction (OR of 1.0 for both). In addition, we observed no associations of trans-18:2, trans-18:1 and trans-16:1 levels with
Origin of dietary trans-18:2
Trans-18:2 fatty acids originate from the diet, with the possible exception of 9 cis-, 12 trans-18:2 which, in theory at least, might derive from 12 trans-18:1 by endogenous action of the Δ9 desaturase. Trans-18:2 fatty acids are found in small amounts in dairy products, partially hydrogenated oils, and non-hydrogenated refined oils. To what extend the different sources of dietary trans-18:2 contribute to cell membrane levels likely varies with study populations and with trends in food
Conclusion
Prevention of SCD is essential given that it can occur as a first manifestation of heart disease. We presented evidence that higher levels of trans-18:2 in RBC cell membranes, but not trans-18:1, are associated with higher risk of out-of-hospital cardiac arrest. While further studies are needed to understand the effects of trans-18:2, it would be prudent to already limit dietary intake of trans-18:2.
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