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Background Heart failure with preserved ejection fraction (HFPEF) involves failure of cardiovascular reserve in multiple domains. In HFPEF animal models, dietary sodium restriction improves ventricular and vascular stiffness and function. We hypothesized that the sodium-restricted Dietary Approaches to Stop Hypertension diet (DASH/SRD) would improve left ventricular diastolic function, arterial elastance, and ventricular-arterial (V-A) coupling in hypertensive HFPEF. Methods and Results Thirteen patients with treated hypertension and compensated HFPEF consumed the DASH/SRD (target sodium 50 mmol/2100 kcal) for 21 days. We measured baseline and post-DASH/SRD brachial and central BP (via radial arterial tonometry), and cardiovascular function with echocardiographic measures (all previously invasively validated). Diastolic function was quantified via the Parametrized Diastolic Filling formalism, which yields relaxation/viscoelastic (c) and passive/stiffness (k) constants through analysis of Doppler mitral inflow velocity (E-wave) contours. Effective arterial elastance (Ea) end-systolic elastance (Ees), and V-A coupling (defined as the ratio Ees:Ea) were determined using previously published techniques. Wilcoxon matched-pairs tests were used for pre-post comparisons. The DASH/SRD reduced clinic and 24-hour brachial systolic pressure (155±35 to 138±30 and 130±16 to 123±18 mmHg, both p=.02) and central end-systolic pressure trended lower (116±18 to 111±16 mmHg, p=.12). In conjunction, diastolic function improved (c, 24.3±5.3 to 22.7±8.1 s−1;p=.03; k, 252±115 to 170±37 s−1;p=.03), Ea decreased (2.0±0.4 to 1.7±0.4 mmHg/ml;p=.007), and V-A coupling improved (Ees:Ea, 1.5±0.3 to 1.7±0.4;p=.04). Conclusions In hypertensive HFPEF patients, the sodium-restricted DASH diet was associated with favorable changes in ventricular diastolic function, arterial elastance, and V-A coupling.

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During early rapid filling, blood aspirated by the left ventricle (LV) generates an asymmetric toroidal vortex whose development has been quantified using vortex formation time (VFT), a dimensionless index defined by the length-to-diameter ratio of the aspirated (equivalent cylindrical) fluid column. Since LV wall motion generates the atrioventricular pressure gradient resulting in the early transmitral flow (Doppler E-wave) and associated vortex formation, we hypothesized that the causal relation between VFT and diastolic function (DF), parametrized by stiffness, relaxation, and load, can be elucidated via kinematic modeling. Gharib et al. (Gharib M, Rambod E, Kheradvar A, Sahn DJ, Dabiri JO. Proc Natl Acad Sci USA 103: 6305-6308, 2006) approximated E-wave shape as a triangle and calculated VFT(Gharib) as triangle (E-wave) area (cm) divided by peak (Doppler M-mode derived) mitral orifice diameter (cm). We used a validated kinematic model of filling for the E-wave as a function of time, parametrized by stiffness, viscoelasticity, and load. To calculate VFT(kinematic), we computed the curvilinear E-wave area (using the kinematic model) and divided it by peak effective orifice diameter. The derived VFT-to-LV early rapid filling relation predicts VFT to be a function of peak E-wave-to-peak mitral annular tissue velocity (Doppler E'-wave) ratio as (E/E')(3/2). Validation utilized 262 cardiac cycles of simultaneous echocardiographic high-fidelity hemodynamic data from 12 subjects. VFT(Gharib) and VFT(kinematic) were calculated for each subject and were well-correlated (R(2) = 0.66). In accordance with prediction, VFT(kinematic) to (E/E')(3/2) relationship was validated (R(2) = 0.63). We conclude that VFT(kinematic) is a DF index computable in terms of global kinematic filling parameters of stiffness, viscoelasticity, and load. Validation of the fluid mechanics-to-chamber kinematics relation unites previously unassociated DF assessment methods and elucidates the mechanistic basis of the strong correlation between VFT and (E/E')(3/2).