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Insulin resistance and plasma triglyceride level are differently related to cardiac hypertrophy and arterial stiffening in hypertensive subjects

Authors Liliana Legedz, Giampiero Bricca, Pierre Lantelme, Marie-Odile Rial, Pierre Champomier, Madeleine Vincent, Hugues Milon

Published 15 December 2006 Volume 2006:2(4) Pages 485—490

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Liliana Legedz1, Giampiero Bricca2, Pierre Lantelme1, Marie-Odile Rial1, Pierre Champomier1, Madeleine Vincent3, Hugues Milon1

1Service de Cardiologie, Hospices Civils de Lyon, France; 2EA 3740 Génomique Fonctionnelle dans l’athéro-thrombose, Université Lyon I, Faculté de Médecine Laënnec, Lyon, France; 3Laboratoire des Explorations Fonctionnelles Endocriniennes et Métaboliques, Université Lyon I, Faculté de Médecine Rockefeller, Lyon, France

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 (β = 0.19, p < 0.02) independently of systolic blood pressure, plasma aldosterone, and normetanephrine. Only HOMA and insulin level remained associated with PWV (β = 0.14; β = 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.

Keywords: cardiac hypertrophy, arterial stiffness, insulin resistance

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