The effect of omecamtiv mecarbil on the regulatory state of the cardiac thick filament

This thesis aims at describing the molecular mechanisms responsible for the regulation of contraction in the heart with particular interest toward the definition of the mechanism by which the putative inotropic agent omecamtiv mecarbil (OM) influences the activation of the thick, myosin-containing filament and the mechanical output of the cardiac muscle gaining specific credit for its application to dilated cardiomyopathy therapy.