Abstract

Many studies in the past 50 years have shown that dietary lipids can modulate the progression of coronary artery disease, heart failure, and cardiac arrhythmogenesis. Polyunsaturated fatty acids (PUFAs) are small biologically active lipid molecules that serve as a substrate for metabolic activity, cellular signals, and as precursors for signaling molecules such as prostaglandins, leukotrienes, etc. Small structural changes between PUFAs, especially with respect to chain length and the number and position of double bonds have a significant impact on their biological activities. 1 PUFAs can modulate ion channel activity, cardiac myocyte contractility and Ca 2+ cycling, and cell survival in response to ischemia or mechanical stress. Epidemiologic evidence suggests that dietary consumption of fatty fish (salmon, sardines, and herring) lowers the risk of incident atrial fibrillation (AF). 2 Fish oil contains a complex mix of x3-PUFA, x6-PUFA, x9-PUFA, and other lipids and antioxidant molecules. The most abundant long chain x3PUFAs in fatty fish are eicosapentaenoic acid (EPA, 20 carbon) and docosahexaenoic acid (DHA, 22 carbon). 1 In an attempt to identify which components of fish oil confer benefi ti n AF prevention, additional studies have sought to separately evaluate the impact of EPA and DHA on risk of AF. In 2 such studies, consumption of DHA, but not EPA was associated with lower risk of AF. 3,4 It is thus plausible that dietary consumption of DHA has a meaningful impact on AF risk. While fish are the most concentrated natural source of EPA and DHA, a-linolenic acid (ALA) is the most abundant plant based x3-PUFA. Can dietary consumption of ALA, an abundant, sustainable and inexpensive x3-PUFA, lower the risk of AF in the same manner that consumption of fish and DHA appear to do? In this issue of the JAHA, Fretts and colleagues 5 directly address this important question. They use an epidemiologic approach to assess the relationship between plasma ALA levels, dietary ALA consumption, and AF risk. In their study of 2899 subjects (65 years or older at study entry), there were 707 cases of incident AF during a 15 to 16 year (nearly 30 000 person-years) follow-up. No relationship was detected between plasma ALA and incident AF after correcting for age, sex, and a variety of clinical and demographic factors. Strengths of the study include the size and age of the population, and the relatively large fraction of incident AF. Their results are consistent with an epidemiologic analysis suggesting that from age 40, there is approximately a 25%

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