Circulating Monocyte Subsets and Transcatheter Aortic Valve Replacement

Int J Mol Sci. 2022 May 10;23(10):5303. doi: 10.3390/ijms23105303.

Abstract

Transcatheter aortic valve replacement (TAVR), as an alternative to open heart surgery, has revolutionized the treatment of severe aortic valve stenosis (AVS), the most common valvular disorder in the elderly. AVS is now considered a form of atherosclerosis and, like the latter, partly of inflammatory origin. Patients with high-grade AVS have a highly disturbed blood flow associated with high levels of shear stress. The immediate reopening of the valve during TAVR leads to a sudden restoration of a normal blood flow hemodynamic. Despite its good prognosis for patients, TAVR remains associated with bleeding or thrombotic postprocedural complications, involving mechanisms that are still poorly understood. Many studies report the close link between blood coagulation and inflammation, termed thromboinflammation, including monocytes as a major actor. The TAVR procedure represents a unique opportunity to study the influence of shear stress on human monocytes, key mediators of inflammation and hemostasis processes. The purpose of this study was to conduct a review of the literature to provide a comprehensive overview of the impact of TAVR on monocyte phenotype and subset repartition and the association of these parameters with the clinical outcomes of patients with severe AVS who underwent TAVR.

Keywords: aortic valve stenosis; inflammation; monocyte subsets; monocytes; shear stress; thromboinflammation; transcatheter aortic valve replacement.

Publication types

  • Review

MeSH terms

  • Aged
  • Aortic Valve Stenosis* / etiology
  • Heart Valve Prosthesis*
  • Humans
  • Inflammation / etiology
  • Monocytes
  • Thrombosis* / etiology
  • Transcatheter Aortic Valve Replacement* / adverse effects
  • Transcatheter Aortic Valve Replacement* / methods

Grants and funding

B.S. is supported by grants from the Fondation Leducq convention 16CVD01 “Defining and targeting epigenetic pathways in monocytes and macrophages that contribute to cardiovascular disease”, the European Genomic Institute for Diabetes (EGID, ANR-10-LABX-0046) and is a recipient of an Advanced ERC Grant (694717).