Abstract 1087: Potential Mechanisms of Beneficial Effects of Omega-3 Polyunsaturated Fatty Acids on Atrial Fibrillation
Background: Dietary n-3 poly unsaturated fatty acids (PUFAs) appear to reduce the prevalence of atrial fibrillation (AF), but little is known about potential mechanisms. We assessed the effect of PUFAs on 2 discrete experimental AF substrates:
CHF-associated structural remodeling induced by ventricular tachypacing (VTP, 240 bpm x 2 wks); and
electrical remodeling induced by atrial tachypacing (ATP, 400 bpm x 1 wk; with AV block and 80 bpm ventricular pacing to control rate).
Methods: Thirty three mongrel dogs were allocated to 5 groups; 1) ATP dogs (n=6), 2) ATP+PUFA dogs (n=6), 3) VTP dogs (n=10), 4) VTP+PUFA dogs (n=6), and 5) sham operated dogs (n=5). PUFAs were administrated orally (5 g/day) for 2 wks before starting ATP or VTP, and continued throughout the ATP or VTP period. Phase-delay conduction analysis was based on 240 electrode epicardial mapping.
Results: During 2 wks of pretreatment, PUFAs did not affect atrial ERP or duration of burst pacing-induced AF (DAF) in any group. ATP alone shortened ERP (from 139±7 at baseline to 102±8 ms at 1-wk ATP, **P<0.01, BCL 300 ms) and increased DAF (from 8±4 at baseline to 969±373 s at 1-wk ATP**). PUFAs did not alter ATP effects on ERP or DAF, which averaged 95±8 ms and 903±401 s respectively after 1 wk-ATP in ATP+PUFA dogs. VTP alone increased DAF (from 31±7 s in sham dogs to 923±245 s in VTP dogs**), phase delay range reflecting slow conduction zones (P5–95, 1.1±0.1 in sham dogs vs 2.4±0.2 ms/mm VTP dogs**), and the conduction heterogeneity index (P5–95/P50, 0.9±0.02 sham dogs vs 1.5±0.1 VTP dogs, *p<0.05). PUFAs suppressed VTP-induced increases in DAF (to 367±289 s*), P5–95(1.5±0.04 ms/mm*), and P5–95/P50 (1.0±0.01**). LV end diastolic pressure (LVEDP), left (LAP) and right (RAP) atrial pressure increased in VTP dogs (13±1, 12±1, 10±1 mm Hg, respectively, vs 5±1**, 4±1**, 4±1** mm Hg in sham dogs), effects significantly attenuated by PUFAs (LVEDP: 9±1, LAP: 7±1, RAP: 5±1 mm Hg).
Conclusion: PUFAs suppress CHF-induced atrial structural remodeling and AF promotion, but do not affect tachycardia-induced electrical remodeling. Beneficial effects of PUFAs on structural remodeling may account for their clinical anti-AF action. Closer examination of potential benefits of PUFAs for CHF and associated AF may be warranted.