Abstract

The distribution of the T29C TGFβ1 gene polymorphism was analyzed in 198 hypertensives with left ventricular hypertrophy (LVH) and in 235 hypertensives without LVH. Circulating TGFβ1 levels, procollagen type III levels, microalbuminuria, and left ventricular geometry and function were evaluated in all the hypertensives with LVH subgrouped according to T29C TGFβ1 gene polymorphism. Circulating TGFβ1 was evaluated by ELISA technique, procollagen type III by a specific radioimmunoassay, microalbuminuria by radioimmunoassay, and left ventricular geometry and function by echocardiography. All groups were comparable for gender, age, and sex. Regarding T29C TGFβ1 gene polymorphism, prevalence of TC or CC genotypes was significantly (P < .05) higher in hypertensives with LVH than hypertensives without LVH TC and CC LVH hypertensives were characterized by a higher prevalence of subjects with microalbuminuria (P < .05 TC and CC versus TT), by increased levels of TGFβ1, procollagen type III, urinary albumin excretion, LVM, LVM/h2.7, and lower values of left ventricular ejection fraction (P < .05 TC and CC versus TT). Our data suggest that T29C TGFβ1 gene polymorphism was associated with clinical characteristics adequate to recognize a subset of LVH hypertensives with a higher severity of hypertension.

Highlights

  • Hypertension represents the most common powerful risk factor for cardiovascular morbidity and mortality [1]

  • To our knowledge this is the first study to investigate the impact of Transforming growth factor β1 (TGFβ1) Leu → Pro at codon 10 polymorphism on left ventricular geometry and function in hypertensive patients

  • Our data indicate a higher prevalence of TC and CC Leu10 → Pro polymorphism in hypertensives with left ventricular hypertrophy (LVH) than hypertensives without LVH, associated to some unfavorable clinical characteristics of hypertension

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Summary

Introduction

Hypertension represents the most common powerful risk factor for cardiovascular morbidity and mortality [1]. High blood pressure is associated with adverse morphological and functional changes in the cardiovascular and renal system, including left ventricular hypertrophy (LVH), microalbuminuria and progressive renal and heart disease. The disproportional accumulation of fibrous tissue is the major characteristic of the adverse structural remodelling of cardiac tissue in hypertensives promoting systolic and diastolic dysfunction [2,3,4,5]. Transforming growth factor β1 (TGFβ1) is a multifunctional cytokine and its gene has been found in position. The reduction in circulating TGFβ1 through a block of the renin-angiotensin system (RAS) was reported to be associated with an improvement of renal function and a reversion in LVH [8, 9]. Recent experimental data indicate that blockade of the TGFβ, through a novel orally specific inhibitor of the TGFβ receptor 1, results in significant improvement of deleterious cardiac remodelling after infarction [10]

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