Abstract 20142: Impaired Intraventricular Blood Transport in Hypertrophic Cardiomyopathy
Intraventricular blood flow patterns in the healthy left ventricle (LV) are determined by the large vortices that develop during diastole. These vortices have been proposed to enhance blood mixing and filling. Patients with hypertrophic cardiomyopathy (HCM) show concentric remodeled LVs with large wall-flow friction that impairs vortex formation. We aimed to assess whether the absence of vortex-mediated flow may alter blood transport and mixing in the LV, facilitating blood stasis and thrombogenesis in HCM.
Two-dimensional flow velocity fields from color Doppler echocardiographic sequences were obtained in 20 patients with HCM and 20 matched control healthy volunteers (LV mass (g): 441±135 vs 127±37, p<0.05; LV sphericity: 0.36±009 vs 0.51±0.06, p<0.005). Using the advection equation for the residence time, TR , we tracked the blood transport barriers which couple filling and ejection: 1- Direct flow (VDF; flow entering and leaving the LV in the same cycle) 2- Retained inflow (VRI; flow entering the LV ventricle not exiting in the same cycle), 3- Delayed ejection (VDE; flow exiting the LV that entered in a previous cycle), and 4- Residual volume (VRV; flow not entering the LV before the previous cycle which remains in the LV even after the following cycle). Additionally, we quantify the TR of the blood after 8 beats to assess in-vivo the location and extent of the stasis regions inside the LV in both groups.
HCM group showed significantly larger VDF (0.35±0.11% vs 0.25±0.09%, p=0.006) and lower VRI and VDE (0.11±0.06% vs 0.18±0.07%, p=0.008, and 0.18±0.05% vs 0.23±0.06%, p=0.04) than the control group. Kinetic energy of these regions also showed differences between groups (Kin(VDF): 22.6 ±15.2mJ/m vs 14.6±6.7mJ/m, p=0.04, Kin(VRI): 3.7 ±4.8mJ/m vs 9.1±7.5mJ/m, p=0.01, and Kin(VDE): 7.7 ±3.7mJ/m vs 15.9±13.6 mJ/m, p=0.01). HCM patients showed larger blood apical regions with high TR in contact with the LV wall (aggregate variable C= from 2.1±0.9s to 0.7±0.8s vs 1.3±0.6s to 0.2±0.2s, p<0.05 for all regions with TR> 1 to 6s).
Flow transport within the LV is impaired in HCM. In turn, abnormal transport generates regions of blood stasis near the apex that may contribute to the increased thromboembolic risk of HCM.
Author Disclosures: C. Fernandez-Aviles: None. P. Martinez-Legazpi: None. L. Rossini: None. C. Pérez del Villar: None. Y. Benito: None. A. Delgado-Montero: None. A. Gonzalez-Mansilla: None. F. Fernandez-Aviles: None. J. del Alamo: None. J. Bermejo: None. R. Yotti: None.
- © 2016 by American Heart Association, Inc.