Do High Levels of n-3 Polyunsaturated Fatty Acids in Cell Membranes Increase the Risk of Postoperative Atrial Fibrillation?

Abstract

Objectives: Postoperative atrial fibrillation (POAF) has been associated with an inflammatory response to the surgical procedure. n-3 long-chain polyunsaturated fatty acids (LC-PUFA) have been proposed for the prevention of POAF. We investigated the relationship between the plasma concentration of inflammatory mediators, levels of n-3 LC-PUFA in red blood cell (RBC) membrane lipids, and the risk of POAF after coronary artery bypass grafting (CABG). Methods: A total of 125 patients who underwent CABG were studied. Inflammatory mediators in plasma and the content of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in RBC membranes were assessed. Results: Sixty-two patients (49.6%) developed POAF. The POAF group had higher RBC levels of total n-3 LC-PUFA and DHA than did patients remaining in sinus rhythm (p < 0.05). Of the inflammatory mediators, only postoperative interleukin-6 levels differed, being higher in the POAF group (p < 0.05). Inflammatory mediators were not independent predictors of POAF by multivariable logistic regression analysis. Higher levels of DHA and total n-3 LC-PUFA in RBC membranes, measured immediately prior to CABG and on postoperative day 3, were linearly associated with an increased risk of POAF (p < 0.05). Conclusions: Our findings suggest that inflammatory mediators are not associated with the occurrence of POAF. Interestingly, high n-3 LC-PUFA levels in RBC membranes appear to increase the risk of POAF.

Immunomodulation by dietary long chain omega-3 fatty acids and the potential for adverse health outcomes

“…A Danish cohort study supports the observation from the Japanese study; the Danish cohort study reported a monotonic, negative, dose-response trend for DHA, EPA and DPA and atrial fibrillation [45]. In fact, higher levels of DHA and total LCω-3PUFA in RBC membranes, measured immediately prior to coronary artery bypass grafting and on postoperative day 3, were linearly associated with an increased risk of postoperative AF [46]. These findings contradict the widely held view that LCω-3PUFA exposure decreases risk of ventricular arrhythmias, as well as the prevention and treatment of AF [47].…”

The role of the right atrium in development of postoperative atrial fibrillation: A speckle tracking echocardiography study

“…The development of atrial fibrillation (AF) after cardiac surgery has been associated with poor cardiac outcome . Several variables, including inflammatory mediators, age, or left ventricular (LV) function, have been shown to be involved in the development of post‐operative atrial fibrillation (POAF) . Sympathetic system activation may also be associated with POAF development, which has been reported to be reduced by the use of beta‐blockers before the procedure.…”

Do Omega-3 Polyunsaturated Fatty Acids Prevent Atrial Fibrillation?

“…In this open-label, prospective, randomized clinical trial, the use of PUFAs was associated with a 65% reduction of postoperative AF. Subsequently, multiple smaller trials evaluated the role of perioperative supplementation with PUFAs and the effect of this on postoperative AF, but the results were far from convincing [5,8,9,10]. Recently, Mozaffarian et al [12] studied 1,516 patients scheduled for cardiac surgery, the largest trial to date.…”

“…In a recent issue of Cardiology , Bjorgvinsdottir et al [5 ]have assessed the effects of PUFAs on postoperative AF. In this elegant study, the investigators quantified PUFAs in the cell membrane of red blood cells (RBC) and also quantified certain surrogate inflammatory markers (IL-1β, IL-6, IL-8, IL-12, IL-18, IF-γ, TNF-α, TNF-β, MIP-1α, IL-10, TGF-β and hs-CRP).…”

“…PUFAs have been shown to affect gap-junction protein (connexin-40) and to attenuate adverse remodeling of atrial tissue [6]. Genetic predisposition may account for the increased incidence of postoperative AF observed in the study [5]. The bioavailability of PUFAs varies, and it may take days to weeks to achieve steady-state plasma levels and even longer to achieve stable RBC membrane levels.…”