Why the study?
Dietary consumption of ω-3 fatty acids is correlated with reduced cardiovascular events, but its effect on AF vulnerability and related mechanisms needed investigation in a canine model.
Does dietary fish oil reduce atrial fibrillation vulnerability in a canine model of rapid atrial pacing-induced AF?
Does dietary fish oil reduce atrial fibrillation vulnerability in a canine model of rapid atrial pacing-induced AF?
Dietary omega-3 fatty acids reduced atrial fibrillation vulnerability, electrical remodeling, ER stress, and inflammation in a canine model of rapid atrial pacing-induced AF.
ω-3 supplementation may attenuate AF vulnerability in canine models; leaves open translation to human AF prevention.
Background: It is known that dietary consumption of ω-3 fatty acids is correlated with a reduced incidence of cardiovascular events. Here, we investigated the effect of dietary ω-3 fatty acids on atrial fibrillation (AF) vulnerability in a canine model of AF and explored the related mechanisms. Methods: 24 male beagle dogs (weight, 8-10 kg) were randomly divided into four groups: (a) sham-operated group (normal chow), (b) AF group ( AF with normal chow), (c) AF+FO (AF and chow supplemented with fish oil (FO, 0.6 g ω-3 PUFA/kg/day)), (d) FO (chow supplemented with FO). Daily oral administration FO was initiated 1 week before surgery and continued throughout the study period. Results: Dietary FO significantly reversed atrial electric remodeling post rapid atria pacing (RAP). FO treatment also attenuated the elevated levels of biomakers for ER stress (all P<0.05 vs. AF). RAP-induced upregulation of inflammation factors IL-1β, IL-6, TNF-α in LA were significantly attenuated by FO treatment (all p<0.05 vs. AF). In addition, Masson staining revealed increased interstitial fibrosis in LA was significantly reduced in AF+FO group as compared to AF group (P<0.01). FO treatment also alleviated RAP-induced myocardial apoptosis (p<0.05). Conclusions: Dietary ω-3 fatty acids reduced RAP-induced AF vulnerability, possibly via attenuating myocardial ER stress and inflammation in this canine model of AF.
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Tu et al. (2020) studied this question.
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