Abstract 17052: Wearable Vibroacoustic Transthoracic Stimulation Improves Left Ventricular Function, Remodeling and Regulates Syndecan-4 / VEGF Levels in Rats After Myocardial Infarction
Background: Heart Failure (HF) post MI remains an important cause of morbidity and mortality and leads to high healthcare expenditures. Wearable devices that address chronic medical conditions will have a positive impact on disease management and cost. Vibroacoustic Transthoracic Stimulation (VATS) is the noninvasive delivery of sonic 100 Hz stimulation by a speaker embedded in a wearable chest harness. VATS induces pulsatile shear stress on the vascular endothelium via penetrating rhythmic sound waves. Syndecan-4 is a transcriptionally regulated gene in response to increase in shear stress. It serves as a part of a mechanotransduction system and coreceptor for fibroblast growth factors (FGFs) and vascular endothelial growth factor (VEGF). We hypothesize that physical acoustic forces from VATS may induce cardioprotective effects by regulating Syndecan-4 levels, thereby affecting left ventricle (LV) remodeling and contributing to improvement in LV function after MI.
Objective: We investigated the effects of VATS on LV function, remodeling and Syndecan-4 / VEGF after chronic MI in rats.
Methods: After MI, rats (SD-300gms) were randomized to receive daily 1 hr VATS (MI-VATS) (n=5) Control (MI-C) (n=5) for 4 weeks and sham surgery group (n=5). LV pressure-volume relationships were analyzed using a conductance catheter. LV fibrosis was analyzed by digital microscopy.
Results: VATS significantly improved ejection fraction (EF), left ventricular end systolic pressure (LVESP) and dP/dtmax. VATS reduced LV fibrosis by 19% (p<0.01). Syndecan-4 and VEGF levels were higher in LV of MI-VATS rats by 21% and 16% respectively (p<0.01). Data: * p<0.01 (Sham vs. MI-C), † p<0.01 (MI-C vs MI-VATS)
Conclusions: In a rat model HF induced by chronic MI, a wearable Vibroacoustic Transthoracic Stimulator markedly improved LV function and reduced fibrosis, possibly via modulation of Syndecan-4 / VEGF expression. These findings have implications for cardiac rehabilitation post MI.
Author Disclosures: A. Uryash: None. J.A. Adams: None.
- © 2016 by American Heart Association, Inc.