Abstract 17240: Ventricular Unloading and Improved Oxygen Delivery With LVAD Support Correlates With an Increase in Angiogenesis and TIE-1 Expression
Background: Ventricular unloading with the use of a left ventricular device (LVAD) is used for patients with advanced heart failure. The use of LVAD has been reported to lead to myocardial recovery in some patients, indicating that some degree of cardiomyocyte functional recovery and/or regeneration can be induced by decreasing the external load and improving oxygen delivery. This study is aimed to determine the cellular response of failing human hearts to mechanical unloading and its relationship to angiogenesis.
Methods: Pre- and post-LVAD heart tissue samples were collected from 13 patients at the time of VAD implant and heart transplantation. Six patients had ischemic cardiomyopathy and seven patients had nonischemic cardiomyopathy. All had no histologic evidence of active myocarditis. The average duration of LVAD support was 10 months. Hemodynamic data and Echo measurements before LVAD implant were compared to measurements pre- explant. H&E and CD31 immunostaining was perfored. The capillary density was measured by Image software and analyzed by using the Wilcoxon signed rank sum test. mRNA levels of several angiogeneic factors were measured by quantitative RT-PCR.
Results: There was improvement in Wedge pressure, mean Pulmonary artery pressure and in cardiac index and statistically increased capillary density after LVAD support. Angiogenic factor TIE mRNA level was significantly up-regulated and correlated with improved angiogenesis. mRNA levels of VEGF, VEGFR-2, IGF-1, RIPK-1 were not statistically significantly altered.
Conclusion: A Significant positive effects on the vascular architecture of human hearts was observed by the unloading and improved cardiac index post LVAD. This is partly due to increased TIE up-regulation and may have a potential role in recovery post LVAD. Proangiogenic therapy to promote recovery can be a therapeutic option that is synergistic with LVAD support and should be evaluated in clinical trial.
Author Disclosures: E.A. Hamad: None. N. Jhala: None. T. Vasiliadis: None. K. Amer: None. R. Alvarez: None. Y. Toyoda: None. H. Wang: None.
- © 2016 by American Heart Association, Inc.