title: Elucidation of spatially distinct compensatory mechanisms in diastole: radial compensation for impaired longitudinal filling in left ventricular hypertrophy.
abstract: 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.
authors.affiliation: Department of Biomedical Engineering, School of Engineering and Applied Science, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: Matt M
authors.initials: MM
authors.lastname: Riordan
authors.forename: Sándor J
authors.initials: SJ
authors.lastname: Kovács
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D000368:Aged; D001794:Blood Pressure; D016022:Case-Control Studies; D003971:Diastole; D015150:Echocardiography, Doppler; D004699:Endocardium / Q000000981:diagnostic imaging / Q000503:physiopathology; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D008955:Models, Cardiovascular; D013318:Stroke Volume; D013997:Time Factors; D016277:Ventricular Function, Left