Dietary fish oil reduces the incidence of triggered arrhythmias in pig ventricular myocytes

BackgroundFish oil reduces the incidence of sudden cardiac death in postmyocardial infarction patients. Triggered activity is the principal mechanism of arrhythmogenesis under these conditions.ObjectiveThe purpose of this study was to test whether dietary fish oil in pigs inhibits Ca2+ overload-induced triggered activity.MethodsPigs were fed a diet of fish oil or sunflower oil for 8 weeks. Ventricular myocytes (ω3: fish oil, n = 11; control: sunflower oil, n = 8) were isolated by enzymatic dissociation and used for patch clamp studies and intracellular Ca2+ recordings. Triggered activity was induced by rapid pacing in the presence of norepinephrine.ResultsDietary fish oil reduced the incidence of triggered action potentials and delayed afterdepolarizations compared to control (9.1% in ω3 and 84.6% in control, P <.05), concomitant with a reduction in spontaneous Ca2+ release. Dietary fish oil prevented Ca2+ overload and reduced action potential prolongation in response to norepinephrine (ΔAPD90: 23.2 ± 8.5 ms in ω3 and 107.4 ± 15.9 in control, P <.05). ω3 myocytes displayed decreased sarcoplasmic reticulum Ca2+ content, reduced L-type Ca2+ current (ICa,L), and less recruitment of the Na+/Ca2+ exchange current (INCX) in response to norepinephrine compared to control. In the absence of norepinephrine, the slow component of the delayed rectifier current (IKs) was larger in ω3 myocytes. In the presence of norepinephrine, IKs increased to the same level in ω3 and control myocytes.ConclusionDietary fish oil reduces the incidence of triggered activity and prevents Ca2+ overload and AP prolongation in response to norepinephrine. Fish oil may prevent arrhythmias in patients with heart failure.