Inhibition of Elevated Ca²⁺/Calmodulin-Dependent Protein Kinase II Improves Contractility in Human Failing Myocardium

Abstract

The present study shows for the first time that CaMKII inhibition acutely improves contractility in human HF where CaMKIIδ expression is increased. The mechanism proposed consists of a reduced SR Ca(2+) leak and consequently increased SR Ca(2+) load. Thus, CaMKII inhibition appears to be a possible therapeutic option for patients with HF and merits further investigation.