Abstract 11663: The Features of Hypertensive Heart Failure With Preserved Ejection Fraction Assessed by 3-Dimensional Speckle Tracking Echocardiography With Novel Software
Background: Left ventricular (LV) pressure overload causes hypertrophy (LVH), which leads to reduced LV relaxation and compliance and results in heat failure with preserved ejection fraction (HFpEF). The transition from compensatory remodeling to myocardial failure is not fully understood. We developed novel 3-dimensional speckle tracking echocardiography (3D-STE) with high volume rates that allows measurement of LV peak strain during systole and strain rate (SR) during isovolumic relaxation (SR-IVR), as indices of LV contractility and relaxation, respectively.
Methods: We measured LV peak strain and LV SR-IVR by novel 3D-STE in HTN patients with preserved EF>50% (n=107, age 69±7) and controls (n=60, age 69±9). HTN patients was divided into 5 groups (A: normal geometry, n=25; B: concentric remodeling, n=20; C: concentric LVH, n=24; D: eccentric LVH, n=21; and E: HFpEF, n=17).We estimated LV stiffness as diastolic stress / radial strain. LV stress was calculated as radius x pressure / thickness. Pulmonary capillary wedge pressure (PCW) was estimated as 10.7 - 12.4 x log [left atrial (LA) active emptying function / minimum LA volume], as we previously reported.
Results: Among 6 groups, LV radial SR-IVR in HFpEF was lowest and this group had elevation of E/e’ and PCWP. LV stiffness was highest in HFpEF. Although LVEF in HFpEF remained >50%, LVEF in HFpEF decreased in association with increased systolic stress compared with HTN with LVH despite no difference in LV strain.
Conclusions: The underlying pathophysiology of HFpEF was diastolic dysfunction such as decreased relaxation and increased stiffness, but LVEF in HFpEF was also reduced (within the normal range), and this was associated with increased systolic stress. Thus, HFpEF was caused mainly by increased stiffness but may be partially caused by reduced EF that is subject to loading conditions. It is important to reduce systolic stress and stiffness in HTN to prevent transition from compensatory remodeling to HFpEF.
Author Disclosures: N. Sato: None. M. Kawasaki: None. M.R. Zile: None. R. Tanaka: None. S. Minatoguchi: None. T. Watanabe: None. K. Ono: None. M. Saeki: None. M. Nagaya: None. N. Onishi: None. K. Amano: None. T. Kojima: None. S. Warita: None. M. Iwama: None. T. Noda: None. H. Sato: None. S. Watanabe: None. H. Houle: None. S. Minatoguchi: None.
- © 2014 by American Heart Association, Inc.