Garg · The Journal of nutrition 2021 · prospective cohort study · n=6229

Plasma ω-3 and ω-6 PUFA Concentrations and Risk of Atrial Fibrillation: The Multi-Ethnic Study of Atherosclerosis.

Cited 14 times in the scientific literature.

Level 3 - non-randomized controlled study

Prospective cohort study with multivariable-adjusted survival analysis

PubMed 33693794 · doi:10.1093/jn/nxab016 · record verified 2026-08-30

What was done

Researchers analyzed data from 6,229 participants in the Multi-Ethnic Study of Atherosclerosis (mean age 62 years; 53% female; 39% White, 27% Black, 22% Hispanic, 12% Chinese American) who were free of atrial fibrillation (AF) at baseline. Plasma phospholipid omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) were quantified at baseline using gas chromatography. Incident AF was tracked through hospital discharge records and Medicare claims using ICD-9 codes over a median follow-up of 12.9 years. Multivariable Cox proportional hazards regression models evaluated associations between PUFA levels and incident AF.

What was found

Over follow-up, 813 participants (13%) developed AF. Each higher SD increment in arachidonic acid (AA; 20:4n-6) was associated with an 11% reduced risk of incident AF (HR: 0.89; 95% CI: 0.82, 0.96). Total n-6 PUFA concentrations were also associated with lower risk (HR per SD increment: 0.93; 95% CI: 0.87, 1.00). Overall, individual n-3 PUFAs showed no significant association with AF risk. In subgroup analyses, higher circulating DHA (22:6n-3) and EPA (20:5n-3) were associated with decreased AF risk in Black participants, and higher DHA in Hispanic participants, but no significant associations were observed in White or Chinese American participants.

Why it matters

This study evaluates circulating fatty acid biomarkers in a diverse multi-ethnic cohort, linking higher omega-6 PUFAs (specifically arachidonic acid) to lower AF risk and highlighting potential racial/ethnic variations in the associations for omega-3 PUFAs.

Limits

Incident AF was ascertained via hospital discharge and Medicare claims codes, which may miss subclinical or outpatient paroxysmal cases. Plasma PUFAs were measured at a single baseline time point, potentially failing to capture long-term changes. The observational nature precludes causal inference and leaves risk of residual confounding.

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