In a large-animal model of dyssynchronous heart failure, increased lateral wall workload leads to hypertrophy and metabolic homogenization, but ultimately results in energy starvation and systolic dysfunction.
Experimental DHF is characterised by non-fibrotic, dilated LV without signs of oxidative stress. Workload increase in the lateral wall leads to hypertrophy and EMID, homogenizing metabolic profiles between wall segments. However, the ventricle enters energy starvation and systolic dysfunction.
Dietl et al. (Thu,) studied this question.