Calcium/calmodulin-dependent protein kinase II causes atrial structural remodeling associated with atrial fibrillation and heart failure.

ABSTRACT:

Background

Atrial fibrillation (AF) is sustained by reentrant mechanisms that depend, in part, on atrial structural remodeling. Increased Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) activity occurs in persistent AF. A general consensus has been that electrophysiological actions of CaMKII must be the contributing factor, but electrical remodeling in AF differs considerably with electrophysiological effects of CaMKII. CaMKII has been associated with structural remodeling in several tissues, but not the cardiac atria. The role of CaMKII in sustaining AF remains undefined.

Objective

The purpose of this study was to assess the effects of CaMKII on AF-related structural remodeling.

Methods

We evaluated the objective in a porcine AF-heart failure model us

SUBMITTER: Liu Z 

PROVIDER: S-EPMC6800146 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature