“…The embryonic heart, the main driver of hemodynamic loads, acutely adapts passive ventricular properties and contractile function in response to altered loads (Keller, 2001; Tobita et al, 2002; Shi et al, 2013), and proceeds to undergo abnormal growth and morphogenesis that later result in cardiac defects (Harh et al, 1973; Clark et al, 1989; Hogers et al, 1997; Sedmera et al, 1999; Tobita and Keller, 2000). Studies have shown that mechanical stresses and strains in the myocardium regulate ventricular growth and remodeling, and trigger endothelial cell organization and signaling (Fisher et al, 2001; Hove et al, 2003; Van Der Heiden et al, 2006), as well as changes in geometry and passive properties to offset the effects of altered wall stresses and/or strain (Omens, 1998).…”