Key result
In subjects with normal LVEF, left ventricular hypertrophy was associated with reduced longitudinal volume accommodation and enhanced radial volume accommodation compared to controls.
Observational (n=20)
In patients with LVH and normal LVEF, impaired longitudinal diastolic filling is compensated by increased radial volume accommodation to maintain overall filling volume.
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Altered LV filling in hypertrophy with preserved EF is hypothesis-generating; leaves open prospective validation before clinical adoption.
Cardiac output maintenance is so fundamental that, when regional systolic function is impaired, as during ischemia, nonischemic 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 left ventricular ejection fraction (LVEF) subjects (10 with LVH, 10 without LVH), 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), whereas 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 pathophysiological subsets is warranted.
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Riordan et al. (2007) conducted an observational in Left ventricular hypertrophy (n=20). Left ventricular hypertrophy vs. Controls without left ventricular hypertrophy was evaluated on Percent of E-wave volume accommodated radially and longitudinally (p=<0.01). In subjects with normal LVEF, left ventricular hypertrophy was associated with reduced longitudinal volume accommodation and enhanced radial volume accommodation compared to controls.
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