Table 1. The table shows the putative mode of action of PUFA at various biological levels as they relate to mechanism of AF.

RMP=resting membrane potential, AP=action potential, Ito=transient outward potassium current, RP=refractory period, APD=action potential duration, PUFA=polyunsaturated fatty acid, AF=atrial fibrillation, RA=right atrium, LA=left atrium, PV=pulmonary vein, ERP=effective refractory period

Site of Action	Putative Antifibrillatory Action
Ion channels	Inhibition of the sodium current[61] Inhibition of calcium current[62] Enhancement of potassium currents (Ito and delayed rectifier current)[62]
Cell membrane	Hyperpolarization of RMP[63] Increases strength of the current necessary to ilicit AP[63] Reduces APD (APD at 75% repolarization) [63] Increases sarcolemmal membrane fluidity[64] Preservation of plasmalemma and mitochondrial membrane integrity[65]
Myocyte	Restoration of synchronous contraction of myocyte by PUFA[64]
Electrical properties	Prolongation of mean AF cycle length[28] Lengthening of ERPs in RA, LA and PVs[28] Lower incidence of AF initiated from PVs during ERP tesing[28] Reduced vulnerability of normal or ischemic myocardium to arrhythmias[66,67]
Neurohormonal axis	Reduction of resting heart rate[68] and association with heart rate variability prab prabably related to increased vagal activity[68] Attenuation of vascular response to angiotensin[69] Decreases inflammation and oxidative stress[39–41]