title: Differential associations between soluble cellular adhesion molecules and atherosclerosis in the Dallas Heart Study: a distinct role for soluble endothelial cell-selective adhesion molecule.
abstract: OBJECTIVE
  Endothelial cell-selective adhesion molecule (ESAM) is a junctional-type cellular adhesion molecule (CAM) that is uniquely expressed in vascular endothelium and activated platelets and mediates neutrophil and monocyte diapedesis across the endothelium. Given its role in endothelial pathobiology, we hypothesized that soluble ESAM (sESAM) would be independently associated with atherosclerosis and vascular stiffness.
  
  
  RESULTS
  We measured sESAM, soluble intercellular adhesion molecule (sICAM)-1, and soluble vascular cell adhesion molecule (sVCAM)-1 in 3222 subjects participating in the Dallas Heart Study, a probability-based population sample. Coronary artery calcium (CAC) was measured by electron beam computed tomography, and abdominal aortic wall thickness (AWT), aortic plaque burden (APB), and aortic compliance (AC) by MRI. Increasing levels of sESAM were associated with all major cardiovascular risk factors as well as with inflammatory markers such as monocyte chemoattractant protein-1, but only weakly correlated with sICAM-1 and sVCAM-1. In multivariate analyses, sESAM was independently associated with prevalent CAC (OR 1.2 per SD increase, 95% CI 1.1 to 1.3; P=0.005), AWT (P=0.035), and AC (P=0.006), but not APB (P=0.15). In contrast, no independent associations were observed between sICAM-1 or sVCAM-1 and any of the atherosclerosis phenotypes.
  
  
  CONCLUSIONS
  In this first reported clinical study of sESAM in humans, sESAM levels were independently associated with CAC, AWT, and AC, whereas sICAM-1 and sVCAM-1 were not. These findings support a unique role of this cellular adhesion molecule in atherosclerosis and suggest the need for further exploration of sESAM as a predictive biomarker and potential mediator of atherosclerosis.
authors.affiliation: Division of Cardiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9047, USA. anand.rohatgi@utsouthwestern.edu
authors.forename: Anand
authors.initials: A
authors.lastname: Rohatgi
authors.forename: Andrew W
authors.initials: AW
authors.lastname: Owens
authors.forename: Amit
authors.initials: A
authors.lastname: Khera
authors.forename: Colby R
authors.initials: CR
authors.lastname: Ayers
authors.forename: Kamakki
authors.initials: K
authors.lastname: Banks
authors.forename: Sandeep R
authors.initials: SR
authors.lastname: Das
authors.forename: Jarett D
authors.initials: JD
authors.lastname: Berry
authors.forename: Darren K
authors.initials: DK
authors.lastname: McGuire
authors.forename: James A
authors.initials: JA
authors.lastname: de Lemos
mesh_terms: D000328:Adult; D000368:Aged; D001011:Aorta / Q000502:physiology; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology*; D002118:Calcium / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood / Q000502:physiology*; D003187:Compliance; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012307:Risk Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015815:Cell Adhesion Molecules; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002118:Calcium