TTN and familial dilated cardiomyopathy: Therefore, we conclude that length-dependent activation is depressed in DCM, and the mechanisms involve (1) reduced thin filament cooperative activation (and ensuing reduction of cross-bridge formation upon lattice reduction), and (2) titin’s isoform switching, i.e., from N2B isoform to N2BA isoform, and the resultant reduction of titin’s modulation of interfilament lattice spacing.