title: Soluble cell adhesion molecules in hypertensive concentric left ventricular hypertrophy.
abstract: OBJECTIVE
  Concentric left ventricular (LV) hypertrophy is an important cardiovascular risk factor. We investigated whether concentric LV hypertrophy is associated with activation of the vascular endothelium, as assessed by measurements of soluble cell adhesion molecules.
  
  
  METHODS
  E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) were measured in serum from hypertensive patients with LV hypertrophy (64 with concentric and 47 with eccentric hypertrophy) and from two matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects. Carotid artery intima-media thickness (IMT) was examined by ultrasonography and LV mass by echocardiography. Neurohormone activities of the renin-angiotensin-aldosterone system were also measured.
  
  
  RESULTS
  E-selectin levels were higher in hypertensive than in normotensive subjects (56 +/- 19 versus 49 +/- 11 ng/ml, P = 0.031). Patients with concentric LV hypertrophy had higher levels of E-selectin (61 +/- 21 versus 49 +/- 15 ng/ml, P < 0.001), ICAM-1 (273 +/- 49 versus 254 +/- 49 ng/ml, P = 0.043), VCAM-1 (591 +/- 131 versus 544 +/- 78 ng/ml, P = 0.038) and greater carotid artery IMT (0.99 +/- 0.26 versus 0.83 +/- 0.15 mm, P = 0.018) than eccentric LV hypertrophy patients. E-selectin and VCAM-1 correlated positively to LV relative wall thickness (P = 0.040 and 0.037, respectively), with a similar trend for ICAM-1 (P = 0.083). E-selectin correlated with serum aldosterone (P < 0.001), and E-selectin and ICAM-1 with plasma angiotensin converting enzyme activity (P = 0.003 and 0.036, respectively).
  
  
  CONCLUSIONS
  Increased levels of soluble cell adhesion molecules and an increased carotid artery IMT characterize concentric LV hypertrophy. This indicates perturbations at the vascular level, involving activation of the vascular endothelium in hypertensive patients with concentric LV hypertrophy.
authors.affiliation: Division of Internal Medicine, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden. karin.malmqvist@med.ds.sll.se
authors.forename: Karin
authors.initials: K
authors.lastname: Malmqvist
authors.forename: Håkan N
authors.initials: HN
authors.lastname: Wallén
authors.forename: Claes
authors.initials: C
authors.lastname: Held
authors.forename: Thomas
authors.initials: T
authors.lastname: Kahan
mesh_terms: D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000097:blood*; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications* / Q000000981:diagnostic imaging; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000150:complications* / Q000000981:diagnostic imaging; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D012995:Solubility; D014463:Ultrasonography; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D000450:Aldosterone; D007703:Peptidyl-Dipeptidase A