Abstract 18779: Baroreflex Activation Therapy Rapidly Improves Hemodynamics and Maintains End Organ function in Volume Load Induced Heart Failure
Background: Arterial baroreflex tightly controls sympathetic nerve activity (SNA) and stabilizes hemodynamics. Baroreflex controlled SNA dynamically regulates not only vascular resistance or cardiac afterload, but also stressed blood volume, thus cardiac preload. It is also well known that acute heart failure (AHF) excessively activates SNA which in turn induces central volume shift and worsens hemodynamics (e.g. pulmonary edema). Thus, we hypothesized that electrical baroreflex activation (BA) immediately inhibits excessive SNA and improves hemodynamics while maintaining end-organ function.
Methods: In 8 Sprague-Dawley rats, we created myocardial infarction to impair left ventricular (LV) systolic function. We attached electrodes to the unilateral aortic depressor nerve and stimulated by 5±2V (10Hz) for BA. We infused donated blood (15 ml/kg) to induce AHF and simultaneously measured parameters of SNA, hemodynamics, renal artery flow (RF) and urine flow (UF) for 30 minutes (CTL). After removing blood to restore the baseline condition, we re-infused volume with BA and compared those parameters with or without BA.
Results: Volume infusion in CTL increased AP, while BA significantly reduced SNA (-27.7±15.0%, p<0.01) and AP (CTL: 123±15, BA: 110±10 mmHg, p<0.01). BA markedly suppressed the increase in LV filling pressure (CTL: 42±7, BA: 33±7 mmHg, p<0.05) indicating the improvement of pulmonary edema. Furthermore, BA increased CO (CTL: 75±40, BA: 82±40 ml/min/kg, p<0.05), while did not affect RF (CTL: 15±2, BA: 16±3 ml/min/kg, p=n.s.) or UF (CTL: 2.3±0.3, BA: 2.3±0.2 ml/kg/30min, p=n.s.) despite the decreases in AP (see Figure).
Conclusions: In impaired LV systolic function, volume loading markedly deteriorates hemodynamics and induces AHF. BA immediately inhibits SNA and significantly improves pulmonary edema without compromising hemodynamics. Baroreflex activation therapy may serve as a new therapeutic strategy for AHF.
Author Disclosures: Y. Oga: None. T. Sakamoto: None. K. Saku: None. T. Tohyama: None. T. Nishikawa: None. T. Kishi: None. H. Tsutsui: None. K. Sunagawa: None.
- © 2016 by American Heart Association, Inc.