Abstract 19811: Asynchronous Flow Modulation Prevents Endothelial Cell Anti-Oxidant Response Seen Following Continuous Flow Ventricular Assist Device Support
Introduction: Ventricular assist devices (VADs) are now standard therapy for patients with advanced heart failure that are poorly responsive to medical therapy. Due to advantages such as compact size, reliability, energy efficiency, installation and operation, continuous flow VADs (CF-VADs) are widely preferred over pulsatile flow VADs. However CF-VAD support results in non-physiological flow with diminished pulsatility, which is believed to contribute to adverse events in patients including gastrointestinal (GI) bleeding, hemorrhagic strokes, arteriovenous malformations, and compromised end-organ function. Using an endothelial cell culture model (ECCM) we previously demonstrated that human aortic endothelial cells (HAECs) subject to conditions seen following CF-VAD support elicits a strong anti-oxidant response in comparison to normal pulsatile flow.
Hypothesis: We hypothesized that “Artificial flow modulation generated via rapid changes in pump speed can inhibit the anti-oxidant response seen with diminished pulsatility”
Methods: To validate our hypothesis that artificial pulsatility will minimize or inhibit endothelial anti-oxidant response, we subjected HAECs to normal pulsatile flow, CF-VAD flow and 2 different type of flow modulation approaches (Asynchronous: 40 bpm, 45 mmHg PP and Synchronous: 80 bpm, 20 mmHg PP) and evaluated expression of anti-oxidant genes.
Results: Our results (Fig. 1) suggest that asynchronous flow modulation applied at a lower frequency but with higher pulse pressure completely inhibits the anti-oxidant response seen with CF-VAD support. In stark contrast, synchronous flow modulation did not affect anti-oxidant gene expression which remained at levels seen with CF-VAD support.
Conclusions: Preliminary evaluation of flow modulation approaches suggest that asynchronous rather than synchronous flow modulation may provide better outcomes as evidenced by the inhibition of the anti-oxidant response.
Author Disclosures: G. Shanmugam: None. P.K. Patibandla: None. T.A. Haglund: None. G.A. Giridharan: None. N.S. Rajasekaran: None. P. Sethu: None.
- © 2016 by American Heart Association, Inc.