Up-regulation of CXC chemokine receptor 4 expression in chronic atrial fibrillation patients with mitral valve disease may be attenuated by renin-angiotensin system blockers

J Int Med Res. 2009 Jul-Aug;37(4):1145-51. doi: 10.1177/147323000903700419.

Abstract

This study characterized CXC chemokine receptor 4 (CXCR4) expression in patients with mitral valve disease and chronic atrial fibrillation (AF). Forty-eight patients with chronic AF formed two groups based on whether they were treated with or without renin-angiotensin system (RAS) blockers (AF + RAS group; n = 25, or AF - RAS group; n = 23). The controls comprised 17 mitral valve disease patients with sinus rhythm (SR group). CXCR4 mRNA and protein levels in the left atria were significantly higher in the AF - RAS and AF + RAS groups than in the SR group. CXCR4 expression was significantly lower in the AF + RAS group than the AF - RAS group. More CD34(+) cells expressed CXCR4 in the AF - RAS and AF + RAS groups than in the SR group. Angiotensin II, collagen I and left atrial diameter significantly positively correlated with CXCR4 expression in the AF - RAS group. These results suggest that CXCR4 expression is up-regulated in chronic AF patients with mitral valve disease, is associated with atrial remodelling, and that these effects are attenuated by RAS blockers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Angiotensin II / antagonists & inhibitors
  • Angiotensin II / metabolism
  • Angiotensin II Type 1 Receptor Blockers / therapeutic use*
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Atrial Fibrillation / drug therapy*
  • Atrial Fibrillation / metabolism
  • Collagen / genetics
  • Collagen / metabolism
  • Female
  • Gene Expression / drug effects
  • Heart Atria / drug effects
  • Heart Atria / metabolism
  • Humans
  • Male
  • Mitral Valve / drug effects
  • Mitral Valve / metabolism
  • Mitral Valve / pathology
  • Mitral Valve Insufficiency / drug therapy*
  • Mitral Valve Insufficiency / metabolism
  • Mitral Valve Insufficiency / pathology
  • RNA, Messenger / metabolism
  • Receptors, CXCR4 / drug effects*
  • Receptors, CXCR4 / genetics
  • Receptors, CXCR4 / metabolism
  • Up-Regulation / drug effects*
  • Up-Regulation / genetics

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Angiotensin-Converting Enzyme Inhibitors
  • RNA, Messenger
  • Receptors, CXCR4
  • Angiotensin II
  • Collagen