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Prescription Fish Oil Fails to Prevent Recurrent Atrial Fibrillation

Authors

Alice Goodman

Chicago—Fish oil (prescription omega-3 supplements, Lovaza) failed to prevent recurrence of atrial fibrillation (AF) compared with placebo in a randomized controlled trial reported at a late-breaking clinical trials session during the AHA meeting. Limited data from small trials suggested that omega-3 polyunsaturated fatty acids might be effective in preventing recurrent AF. Since existing pharmacologic treatments are of limited value and have adverse events, the investigators decided to study omega-3 fatty acids in patients with AF. “Many patients take fish oil without proof that it works. This was an attempt to do a definitive study to find out if manufactured omega-3 is beneficial in AF. The major finding was that it didn’t work,” said Peter R. Kowey, MD, Lankenau Institute for Medical Research, Wynnewood, Pennsylvania. He emphasized that this study did not evaluate dietary fish oil, but rather fish oil supplementation. The study enrolled 663 US outpatients with confirmed symptomatic paroxysmal (n=542) or persistent (n=121) AF with no substantial structural heart disease and normal sinus rhythm at recruitment. Patients were randomized to receive 8 g/day of prescription omega-3 or placebo for the first 7 days and then 4 g/day of prescription omega-3 or placebo through week 24. At 24 weeks, in those with paroxysmal AF, 48% of the placebo patients and 52% of the omega-3 group had a recurrence of AF or atrial flutter. Looking at patients with persistent AF, 33% of the placebo group and 50% in the omega-3 group had documented AF or atrial flutter. No significant difference in recurrence was observed between the 2 treatment arms for paroxysmal AF, persistent AF, or combined AF. Secondary end points followed the same pattern. Discontinuations due to adverse events were similar between the 2 arms: 5% of placebo patients and 4% of those taking prescription omega-3. Diarrhea and nausea were the most common events leading to discontinuation, and the rates of these adverse events were similar between treatment arms. No evidence of harm was observed with omega-3. The overall incidence of treatment-emergent adverse events was similar across treatment arms: 13% and 16%, respectively. Two deaths unrelated to the study drug occurred—1 in each group. A significant decrease in mean systolic blood pressure was seen at week 24 in the omega-3 group compared with placebo (mean difference, −2.3 mm Hg; P=.05). Mean heart rate was lower at the time of first recurrence of AF or atrial flutter in the prescription group versus the placebo group. The decrease in heart rate from baseline in heart rate at week 24 was not significantly different between groups. A subgroup analysis in the paroxysmal AF group failed to show a benefit for omega-3 in any subgroup, including age, sex, race, smoking history, alcohol consumption, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use, or geographical region. Although these results do not support the common practice of taking omega-3 fatty acids to reduce symptomatic episodes of paroxysmal AF, perhaps it would be useful in select patient populations, suggested formal discussant Christine Albert, MD, of Brigham and Women’s Hospital, Boston, Massachusetts. Dr. Kowey said that a randomized trial large enough to tease out subsets of arrhythmia patients who might benefit from omega-3 was not feasible, because it would need to be huge. He also said that he doubted that a primary prevention trial would show efficacy of omega-3 in AF, since it failed as secondary prevention.

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