Do alterations in intercellular coupling play a role in cardiac contractile dysfunction?

Myocardial stunning and hibernation have been subjects of intense laboratory and clinical investigations to elucidate mechanisms responsible for contractile dysfunction after transient ischemia or chronic hypoperfusion. Considerable evidence has implicated the generation of oxygen-derived free radicals and derangements in myocardial energy metabolism and excitation-contraction coupling as major contributors to the pathogenesis of myocardial stunning and hibernation. Despite enormous progress in this area, however, our understanding of the cellular pathophysiology of contractile dysfunction in ischemic heart disease remains incomplete.