title: Relations of biomarkers representing distinct biological pathways to left ventricular geometry.
abstract: BACKGROUND
  Several biological pathways are activated concomitantly during left ventricular (LV) remodeling. However, the relative contribution of circulating biomarkers representing these distinct pathways to LV geometry is unclear.
  
  
  RESULTS
  We evaluated 2119 Framingham Offspring Study participants (mean age, 57 years; 57% women) who underwent measurements of biomarkers of inflammation (C-reactive protein), hemostasis (fibrinogen and plasminogen activator inhibitor-1), neurohormonal activation (B-type natriuretic peptide), and renin-angiotensin-aldosterone system (aldosterone and renin modeled as a ratio [ARR]) and echocardiography at a routine examination. LV geometry was defined on the basis of sex-specific distributions of LV mass (LVM) and relative wall thickness (RWT): normal (LVM and RWT <80th percentile), concentric remodeling (LVM <80th percentile but RWT >or=80th percentile), eccentric hypertrophy (LVM >or=80th percentile but RWT <80th percentile), and concentric hypertrophy (LVM and RWT >or=80th percentile). We related the biomarker panel to LV geometry using polytomous logistic regression adjusting for clinical covariates and used backwards elimination to identify a parsimonious set of biomarkers associated with LV geometry. Modeled individually, C-reactive protein, fibrinogen, plasminogen activator inhibitor-1, and ARR were related to LV geometry (P<0.01). In multivariable analyses, the biomarker panel was significantly related to altered LV geometry (P<0.0001). On backwards elimination, logARR alone was significantly and positively associated with eccentric (odds ratio per SD increment, 1.20; 95% confidence interval, 1.05 to 1.37) and concentric LV hypertrophy (odds ratio per SD increment, 1.29; 95% confidence interval, 1.06 to 1.58).
  
  
  CONCLUSIONS
  Our cross-sectional observations on a large community-based sample identified ARR as a key correlate of concentric and eccentric LV hypertrophy, consistent with a major role for the renin-angiotensin-aldosterone system in LV remodeling.
authors.affiliation: Framingham Heart Study, 73 Mount Wayte Ave, Framingham, MA 01702-5803, USA.
authors.forename: Raghava S
authors.initials: RS
authors.lastname: Velagaleti
authors.forename: Philimon
authors.initials: P
authors.lastname: Gona
authors.forename: Daniel
authors.initials: D
authors.lastname: Levy
authors.forename: Jayashri
authors.initials: J
authors.lastname: Aragam
authors.forename: Martin G
authors.initials: MG
authors.lastname: Larson
authors.forename: Geoffrey H
authors.initials: GH
authors.lastname: Tofler
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Lieb
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Wang
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
mesh_terms: D000450:Aldosterone / Q000097:blood; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D006332:Cardiomegaly / Q000000981:diagnostic imaging / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D005337:Fibrin / Q000378:metabolism; D006352:Heart Ventricles / Q000033:anatomy & histology*; D006801:Humans; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D012044:Regression Analysis; D012084:Renin-Angiotensin System / Q000502:physiology; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone; D005337:Fibrin; D002097:C-Reactive Protein