Lack of association of CCR gene polymorphisms and left ventricular hypertrophy in essential hypertension

ABSTRACT

Left ventricular hypertrophy (LVH) is a major determinant of heart damage. Scientific evidence put in mind ofs the influence of genetic factors, on the contrary these have yet to be completely clarified. This application of mind investigates a possible relationship between LVH and sum of two units chemokine receptor (CCR) gene polymorphisms: CCR5?”32 and CCR264I. Essential hypertensive out-patients (n=118 grade I-II, age 27-54) were recruited from the Catholic University Hypertension midmost point For each subject, clinical data upon office blood pressure and M-mode/2D echocardiography were assembleed Statistical analysis did not exhibit a significant association between the CCR polymorphisms and LVH in the investigation population.

KEY WORDS: Genes, CCR Hypertension.

Hypertrophy left ventricular.

Polymorphisms (genetic).

Introduction

Left ventricular hypertrophy (LVH) is a major determinant of heart damage, is individual of the most important complications of essential hypertension (EH) and is associated with an increased risk of cardiovascular morbidity and mortality.1-3 Similar to EH LVH appears to have a variety of determinants, including haemodynamic and non-haemodynamic factors, with an underlying genetic predisposition. Age, sex body mass index (BMI), vital fluid pressure (BP), growth factors, neurohormones, cytokines and environmental factors may all contribute to generate the cascade of molecular changes and the increase in protein synthesis that lead to LVH45

However, these factors single partly explain LVH variability in the population. popular evidence suggests that the number of human cardiac myocytes is genetically determined and that myocardial architecture is erected on the basis of genotype, on the other hand the degree of growth in small room size should be determined by the agency of other stimuli.6

Familial studies have documented the genetic predisposition of LVH in EH and the introduction of molecular genetic technology has allowed the evaluation of the association of separate gene with EH and LVH on the contrary this has produced conflicting results7

New studies focusing upon the role of chronic inflammation in the pathogenesis of cardiovascular damage present to view a relationship between LVH and a certain number of mediators of the inflammatory response89 Among the different gene polymorphisms associated with EH that may have a character in LVH are those at the chemokine receptors.10-13

Chemokine receptor (CCR) gene collection of laws for a subgroup of G-protein-coupled receptors involved in the modulation of the immune rejoinder The presence of an inflammatory reply appears to play a character in the development of hypertension [i]or[/i] part of to the other mechanisms involving vascular hypertrophy and macrophage infiltration, as shown by dint of different epidemiological studies and in vivo observation in animal models14-17

In order to evaluate the influence of CCR gene in the disentanglement of LVH, this study aims to analyse the consequence of CCR5?”32 and CCR264I in a assemblage of essential hypertensive patients.

Materials and methods

Essential hypertensive out-patients (n=118: male 90 female 28; stage I-II, age range 27-54) were recruited using the following inclusion criteria: diagnosis of EH based upon careful clinical examination and routine laboratory studies, according to international guidelines;18 age range 20 to 60 years; and not previously treated with antihypertensive remedys Exclusion criteria were: evidence of coronary, valvular or primary myocardial disease; cerebrovascular accident; malignant hypertension or secondary form of hypertension; and diabetes.

All patients underwent office BP measurement and echocardiography. life-current pressure was measured using a hermes sphygmomanometer. Three readings were taken above a 10-minute period and systolic BP (SBP) and diastolic BP (DBP) were taken as the mean of the three measurements. vital current pressure measurement was performed after five minutes' ease in a quiet environment, with the patient in a sitting position.

A M-mode/2D echocardiography (HP Sonos 1000) was performed with patients in a partial left decubitus position, using 25-mHz traducers upon light-sensitive paper at 50 mm/sec Left ventricular measurements were made according to the Penn Convention.19,20 extremity diastolic measurements of interventricular septal thickness (IVS), left ventricular internal dimension (LVID) and posterior wall thickness (PWT) were taken, following the Penn Convention protocol, to measure left ventricular mass (LVM) This was calculated by the agency of a simple anatomically validated formula: LVM = 104 ([IVS +LVID + PWT]^sup 3^ LVID)^sup 3^ - 136 To minimise the impact of variation in material part size on LVM, it was indexed (LVMI) for material substance surface area (BSA). An LVMI cut-off value of 134 g/m^sup 2^ was single outed for the detection of LVH in men and a value of 110 g/m^sup 2^ in women sways comprised patients with normal LVM and structure

After obtaining informed assent a blood sample (4 mL) was bring togethered and genomic DNA was isolated from peripheral life-blood cells using standard methodology based upon sodium dodecyl sulphate (SDS)/proteinase K lysis and phenol/chloroform extraction.21 CCR2 and CCR5 genotypes were determined through a polymerase chain reaction (PCR) technique described previously.22