Left ventricular (LV) longitudinal function is mechanically coupled to the elasticity of the
ascending aorta (AA). The pathophysiologic link between a stiff AA and reduced longitudinal strain
and the subsequent deterioration in longitudinal LV systolic function is likely relevant in heart failure
with preserved ejection fraction (HFpEF). The proposed therapeutic effect of freeing the LV apex and
allowing for LV inverse longitudinal shortening was studied in silico utilizing the Living Left Heart
Human Model (Dassault Systémes Simulia Corporation). LV function was evaluated in a model
with (A) an elastic AA, (B) a stiff AA, and (C) a stiff AA with a free LV apex. The cardiac model
simulation demonstrated that freeing the apex caused inverse LV longitudinal shortening that could
abolish the deleterious mechanical effect of a stiff AA on LV function. A stiff AA and impairment of
the LV longitudinal strain are common in patients with HFpEF. The hypothesis-generating model
strongly suggests that freeing the apex and inverse longitudinal shortening may improve LV function
in HFpEF patients with a stiff AA.