Cardiac output maintenance is so fundamental, that when regional systolic function is impaired, as during ischemia, non-ischemic segments compensate by becoming hypercontractile. By analogy, diastolic compensatory mechanisms that maintain filling volume must exist, but remain to be fully elucidated. Viewing filling in spatially distinct (longitudinal, radial) mechanistic terms facilitates elucidation of diastolic compensatory mechanisms. Because impairment of longitudinal (long-axis) diastolic function (DF) in left ventricular hypertrophy (LVH) is established, we hypothesized that to maintain filling volume, radial (short-axis) filling function would compensate. In 20 normal ejection fraction (LVEF) subjects (10 with LVH, 10 non-LVH controls), we analyzed longitudinal function via Doppler tissue imaging of mitral annular motion and radial function as change in short-axis endocardial dimension via M-mode. The spatial (long-axis, short-axis) endocardial LV dimensions and their changes allowed assignment of E-wave filling volume into (cylindrical geometry-based) longitudinal and radial components. Despite indistinguishable (p=0.70) E-wave velocity-time integrals (E-wave filling volume surrogate), systolic stroke volumes, and end-diastolic volumes in the LVH and control groups, longitudinal volume in absolute terms and the percent of E-wave volume accommodated longitudinally were reduced in the LVH group (p<0.05 and p<0.01, respectively) while the percent of E-wave volume accommodated radially was enhanced (p<0.01). We conclude that in normal LVEF (decreased longitudinal volume accommodation) LVH subjects vs. controls, spatially distinct compensatory mechanisms in diastole manifest as increased radial volume accommodation per unit of E-wave filling volume. Assessment of spatially distinct diastolic compensatory mechanisms in other pathophysiologic subsets is warranted.