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

BACKGROUND Fish oil reduces the incidence of sudden cardiac death in postmyocardial infarction patients. Triggered activity is the principal mechanism of arrhythmogenesis under these conditions. OBJECTIVE The purpose of this study was to test whether dietary fish oil in pigs inhibits Ca2+ overload-induced triggered activity. METHODS Pigs were fed a diet of fish oil or sunflower oil for 8 weeks. Ventricular myocytes (omega 3: 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. RESULTS Dietary fish oil reduced the incidence of triggered action potentials and delayed after depotarizations compared to control (9.1% in omega 3 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 (Delta APD(90): 23.2 +/- 8.5 ms in omega 3 and 107.4 +/- 15.9 in control, P <.05). omega 3 myocytes displayed decreased sarcoplasmic reticulum Ca2+ content, reduced L-type Ca2+ current (I-Ca,(L)), and less recruitment of the Na+/Ca2+ exchange current (I-NCX) in response to norepinephrine compared to control. In the absence of norepinephrine, the slow component of the delayed rectifier current (I-Ks) was larger in omega 3 myocytes. In the presence of norepinephrine, I-Ks increased to the same level in omega 3 and control myocytes. CONCLUSION Dietary 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.