title: Insulin resistance and plasma triglyceride level are differently related to cardiac hypertrophy and arterial stiffening in hypertensive subjects.
abstract: OBJECTIVE
  The frequent association between the type 2 diabetes mellitus and cardio-vascular diseases suggests that metabolic factors may contribute to cardio-vascular remodeling. The aim of our study was to examine the relationships between left ventricular posterior wall thickness (LVPWT), pulse wave velocity (PWV), and the metabolic abnormalities of insulin resistance syndrome, in hypertensive patients.
  
  
  METHODS
  In 227 consecutive hypertensives, we examined the relationships between LVPWT, PWV, and metabolic factors: plasma glucose, insulin, total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides levels as well as the homeostasis model assessment of insulin resistance (HOMA). The Pearson correlation coefficient and multiple regression analysis (including age, gender, body mass index, and 24-hour systolic blood pressure) were used as statistical tests.
  
  
  RESULTS
  In univariate analysis, glucose, HDL-cholesterol, and triglycerides levels were related to LVPWT (r = 0.19, p < 0.05; r = -0.26, p < 0.001; r = 0.31, p < 0.001, respectively); all metabolic variables, except HDL-cholesterol, correlated to PWV (plasma glucose r = 0.25, p < 0.001; total cholesterol r = 0.22, p < 0.01; triglycerides r = 0.20, p < 0.01; insulin r = 0.19, p < 0.01; HOMA r = 0.27; p < 0.001). In the multivariate model, plasma triglycerides remained correlated with LVPWT (beta = 0.19, p < 0.02) independently of systolic blood pressure, plasma aldosterone, and normetanephrine. Only HOMA and insulin level remained associated with PWV (beta = 0.14; beta = 0.13 respectively, p < 0.05).
  
  
  CONCLUSIONS
  These data suggest that among typical metabolic abnormalities of insulin resistance syndrome, plasma triglycerides, and insulin as well as degree of insulin resistance may contribute to cardiac hypertrophy and arterial stiffening independently of hemodynamic and hormonal factors.
authors.affiliation: Service de Cardiologie, Hospices Civils de Lyon, France. liliana.legedz@univ-lyon1.fr
authors.forename: Liliana
authors.initials: L
authors.lastname: Legedz
authors.forename: Giampiero
authors.initials: G
authors.lastname: Bricca
authors.forename: Pierre
authors.initials: P
authors.lastname: Lantelme
authors.forename: Marie-Odile
authors.initials: MO
authors.lastname: Rial
authors.forename: Pierre
authors.initials: P
authors.lastname: Champomier
authors.forename: Madeleine
authors.initials: M
authors.lastname: Vincent
authors.forename: Hugues
authors.initials: H
authors.lastname: Milon
mesh_terms: D001158:Arteries / Q000503:physiopathology*; D001786:Blood Glucose; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology*; D008076:Cholesterol, HDL / Q000097:blood; D004548:Elasticity; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow; D013577:Syndrome; D014280:Triglycerides / Q000097:blood*; D020257:Ventricular Remodeling
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D007328:Insulin; D014280:Triglycerides