Alterations of Sodium Channel Kinetics and Gene Expression in the Postinfarction Remodeled Myocardium

Abstract

Our findings raise the possibility that the increase in the slow component of I(Na) in post-MI remodeled myocytes is secondary to the increased expression of NaCh I. Additional studies are required to address these questions and to characterize the functional role of the NaCh I subtypes in cardiac myocytes.