Effects of left ventricular assist device on heart failure patients: A bioinformatics analysis

Abstract

With the acceleration of demographic aging, heart failure has become a global public health issue. Left ventricular assist device (LVAD) provides a therapeutic option serving as a bridge to transplantation or destination treatment for end‐stage heart failure. However, neither the molecular mechanism nor the gene expression profile of LVAD pathophysiology is well understood. Microarray dataset (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21610) was retrieved from the online database of the gene expression omnibus (GEO). Differentially expressed genes (DEGs) between microarrays obtained before and after LVAD therapy were analyzed using GEO2R. Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis were carried out, followed by protein–protein interaction (PPI) network construction, which was further visualized by the Cytoscape software. Finally, a target gene‐microRNA (miRNA) network was built using the NetworkAnalyst to predict potential miRNA interactions. A total of 36 upregulated DEGs and 14 downregulated DEGs were screened out. Five hub genes with the highest degree of connectivity were identified, including CCL2, CX3CR1, CD163, TLR7, and SERPINE1. CCL2 was identified as the most outstanding hub gene which is specially regulated by miR‐124, miR‐141, and miR‐495. Our study indicates that CCL2 is crucial to the LVAD pathophysiology. The identified hub genes may be involved in cardiac inflammatory responses, remodeling, and the chemokine signaling pathway. These DEGs, pathways, hub genes, miRNAs are valuable for further investigations. This study provides a better understanding of the gene expression profile in LVAD pathophysiology.

Pulsatility protects the endothelial glycocalyx during extracorporeal membrane oxygenation

“…42,43 In addition to hemodynamics, pulsatility improves hemocompatibility, prevents bleeding complications, avoids von Willebrand Factor deficiency, and reduces systemic inflammation in these devices. 36,44 In fact, in those COVID-19 patients with severe respiratory failure, ECMO typically lasts for weeks or even months, thus a device providing more effective microcirculatory perfusion is optimal. Besides the i-Cor system, other recently reported pulsatile flow generators included the Medos Deltastream DP3 system (Medos Medizintechnik AG, USA) 45 and the K-Beat system by Inamori's group.…”

Pulsatility Protects the Endothelial Function During Extracorporeal Membrane Oxygenation

“…In patients with long-term mechanical circulatory support, the pulsatility is associated both with the left ventricular contractivity and the pump itself [39,40]. In addition to hemodynamics, pulsatility in these devices seems to improve hemocompatibility, prevent bleeding complications, avoid von Willebrand Factor de ciency, and reduce systemic in ammation [31,41].…”

Left ventricular assist device bioinformatics identify possible hubgenes and regulatory networks involved in the myocardium of patients with left ventricular assist device

“…The protein-protein interaction (PPI) network was predicted using the internet database Search Tool for the Retrieval of Interacting Genes (STRING, version 10.0). 5 The STRING database was used to build a PPI network of DEGs in this investigation, and interaction with a combined score > 0.4 was considered statistically significant. The…”

“…Therefore, the study aims to evaluate the changes in gene expression profile in myocardial tissue pre-LVAD and post-LVAD, identify potential hubgenes and the associated signaling pathways involved via comprehensive bioinformatic analysis. Although our study is not the first to use bioinformatics analysis to investigate the effects of LVAD on HFrEF patients ( 5 ), we offer an extension to the field by using a larger Gene Expression Omnibus (GEO) dataset, with a larger sample size, and a range of targets for prospective studies, to hopefully investigate impediments for the molecular mechanisms that are involved in post-LVAD pathophysiology.…”