ALTERATIONS OF EXCITATION-CONTRACTION COUPLING IN STUNNED MYOCARDIUM AND IN FAILING MYOCARDIUM

Although both myocardial stunning and chronic heart failure are charac terized by contractile dysfunction, there are profound differences in their underlying mechanisms. Changes in cardiac contractile force can be effected by modulation of intracellular [Ca2+] or by alteration of the contractile protein response to intracellular Ca2+. New evidence s uggests that the principal lesion in the stunned myocardium resides at the level of the contractile proteins, which may be injured by protea ses activated early during reperfusion. In contrast, failing myocardiu m is known to display abnormal intracellular Ca2+ handling, indicative of dysfunction of the sarcoplasmic reticulum, Alterations of gene exp ression and isoform switching of the myofilaments also occur in failin g myocardium, consistent with an observed shift of the kinetics of cro ssbridge cycling. In conclusion, changes in both intracellular Ca2+ ho meostasis and myofilament function occur in failing myocardium, while stunned myocardium primarily reflects an uncoupling between Ca2+ and c ontractile force.