It has been shown in animals and probably in humans, that n-3 polyunsaturat
ed fatty acids (PUFAs) are antiarrhythmic. We report recent studies on the
antiarrhythmic actions of PUFAs. The PUFAs stabilize the electrical activit
y of isolated cardiac myocytes by modulating sarcolemmal ion channels, so t
hat a stronger electrical stimulus is required to elicit an action potentia
l and the refractory period is markedly prolonged. Inhibition of voltage-de
pendent sodium currents, which initiate action potentials in excitable tiss
ues, and of the L-type calcium currents, which initiate release of sarcopla
smic calcium stores that increase cytosolic free calcium concentrations and
activate the contractile proteins in myocytes, appear at present to be the
probable major antiarrhythmic mechanism of the PUFAs.