G-6A Polymorphism of the Angiotensinogen Gene and Its Association With Left Ventricular Mass in Asymptomatic Young Adults from a Biethnic CommunityThe Bogalusa Heart Study

Patel, Dharmendrakumar A.; Li, Shengxu; Chen, Wei; Srinivasan, Sathanur R.; Boerwinkle, Eric; Berenson, Gerald S.

doi:10.1016/j.amjhyper.2005.05.031

Cited by 13 publications

(10 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The authors made a conclusion that particular background including age, gender and ethnical factors can lead to this genotype impacting LVH development. Correlation between the A allele and LVH was also confirmed by an American study, showing differences between ethnical groups too [24]. Our study also revealed prevalence of the A allele in patients below 50 years old with LVH (50% vs 46%), but distinctions were insignificant.…”

Section: Clinical and Genetic Factors Of Left Ventricular Hypertrophysupporting

confidence: 70%

“…Авторы сделали вывод о том, что данный генотип оказывает влияние на раз-витие ГЛЖ в определенных условиях и зависит от воз-раста, пола, этнических факторов. В американском исследовании также была подтверждена взаимосвязь между А аллелем и ГЛЖ, причем также выявлены от-личия в этнических группах [24]. В нашем исследова-нии при анализе возрастной группы пациентов до 50 лет также обнаружено преобладание аллеля А у больных с ГЛЖ (50% против 46%), однако различие не было ста-тистически значимым.…”

Section: Clinical and Genetic Factors Of Left Ventricular Hypertrophyunclassified

See 1 more Smart Citation

Association of Clinical and Genetic Factors With Left Ventricle Hypertrophy in Arterial Hypertension

Kuznetsova

Gavrilov²,

Rebrikov

et al. 2010

Racionalʹnaâ farmakoterapiâ v kardiologii

View full text Add to dashboard Cite

Aim. To evaluate association of clinical and genetic factors with left ventricle hypertrophy (LVH) in patients with arterial hypertension (HT).Materials and methods. 672 patients with HT were involved, aged 50,6 y.o. in average, men 67%. Laboratory assays, ECG, echocardiography were performed. Control group included 184 healthy persons. Genotyping with single-nucleotide substitutions of the endothelial NO synthase (eNOS) Glu298Asp gene, the C242T of the NADPH oxidase p22phox subunit and the angiotensin 2 receptor type 1 А1166С gene was carried out using a polymerase chain reaction (PCR) with evaluating of restriction fragments length polymorphism, while with substitutions of the angiotensinogen М235Т, G(-6)A gene allele-specific PCR "in real time" was applied.Results. LVH was found in 39% of patients. It was more frequent in persons above 50 years old (OR 2,8, р<0,0001), in men (OR 1,43, p=0,035), in HT of degree 2-3 (OR 3,35, р<0,0001), HT duration more than 5 years (OR 2,52, р<0,05), in obesity (OR 1,57, р=0,005) or diabetes (OR 3,33, р<0,0001) presence. At genetic factors evaluation decrease of LVH risk was revealed in persons with the MM polymorphism of the angiotensinogen М235Т gene (OR 0,506, р=0,0187). Association of the MM genotype with LVH risk lowering was more obvious at the young age (OR 0,31, р=0,018). The A allele of the eNOS gene Glu298Asp polymorphism increased risk of LVH development when HT was diagnosed in the young age (OR 1,98, р=0,037) and in women up to 50 years old (OR 2,34, р=0,027). The T allele of the p22phox NADPH oxidase gene С242Т polymorphism correlated with LVH risk reduction in HT patients up to 50 years old (OR 0,6, p=0,01), the C allele -with increase of it (OR 1,66, р=0,01), this influence was more noticeable in women up to 50 years old (T allele -OR 0,21; C allele -OR 4,57, p=0,001). Conclusion. Hypertensive LVH correlates with age, male gender, HT degree and duration, obesity and diabetes mellitus. Genetic factors were less associated with LVH. Цель. Анализ ассоциации клинических и генетических факторов с гипертрофией левого желудочка (ГЛЖ) у пациентов с артериальной гипертонией (АГ). Материал и методы. Обследованы 672 пациента АГ, средний возраст 50,6 лет, мужчин 67%. Выполнялись лабораторные исследования, ЭКГ, эхокардиография. Группу контроля состави-ли 184 человека. Генотипирование по однонуклеотидным заменам Glu298Asp гена эндотелиальной NO синтазы, С242Т субъединицы p22phox NADPH оксидазы и А1166С гена рецептора 1 типа к ангиотензину 2 проводилось методом полимеразной цепной реакции (ПЦР) с анализом полиморфизма длины рестрикционных фрагментов, а по заменам М235Т, G(-6)A гена ангио-тензиногена с помощью аллель-специфичной ПЦР «в реальном времени». Результаты. ГЛЖ диагностирована у 39% больных, чаще в возрасте старше 50 лет (ОШ 2,8, р<0,0001), у мужчин (ОШ 1,43, р=0,035), при наличии 2-3 степени АГ (ОШ 3,35, р<0,0001), давности АГ более 5 лет (ОШ 2,52, p<0,05), при наличии ожирения (ОШ 1,57, р=0,005), сахарного диабета (ОШ 3,33, р<0,0001). При анализе генетических факто...

show abstract

Section: Clinical and Genetic Factors Of Left Ventricular Hypertrophysupporting

confidence: 70%

Section: Clinical and Genetic Factors Of Left Ventricular Hypertrophyunclassified

Association of Clinical and Genetic Factors With Left Ventricle Hypertrophy in Arterial Hypertension

Kuznetsova

Gavrilov²,

Rebrikov

et al. 2010

Racionalʹnaâ farmakoterapiâ v kardiologii

View full text Add to dashboard Cite

show abstract

“…Therefore, polymorphisms located in coding or promoter regions of AGT may be upstreaming effectors of RAS for sHF. In the previous association studies of the AGT gene with sHF, G-6A and M235T polymorphism were thought to be related with sHF [4,5]. That is because the M235T polymorphism has been found to be associated with the elevation of plasma AGT levels in some Caucasian populations and the G-6A variant is in close linkage disequilibrium with the M235T polymorphism [6].…”

Section: Introductionmentioning

confidence: 99%

Association between Genetic Polymorphisms in the Renin-Angiotensin System and Systolic Heart Failure Revised by a Propensity Score-Based Analysis

Chang

Lin

Juang³

et al. 2010

Cardiology

View full text Add to dashboard Cite

Objectives: The objective of this study is to identify possible genetic polymorphisms of the renin-angiotensin system (RAS) in systolic heart failure (sHF). Methods: A total of 509 patients were enrolled into this study. A non-parsimonious multivariable logistic regression model that incorporated potential risk factors was applied to calculate the propensity score for developing sHF. A 1:1 case-control selection process was made according to the rank of propensity. The six genetic polymorphisms of angiotensinogen (AGT), including T174M, M235T, G-6A, A-20C, G-152A, and G-217A, and angiotensin-converting enzyme (ACE) gene I/D polymorphism were typed by polymerase chain reaction and DNA sequencing technique. Results: The CC genotype at T174M was positively associated with sHF (OR 2.81, 95% CI 1.20–6.61, p = 0.018). The GG genotype at G-152A was also positively associated with the presence of sHF (OR 6.25, 95% CI 1.54–25.4, p = 0.010). OR of the ACE DD genotype for sHF, as compared with ACE II genotype, was 1.37 (p = 0.475), and OR for ID genotype compared with II genotype was 5.95 for sHF (95% CI 2.16–16.4, p = 0.001). Conclusions: The exploration of these RAS genes related to sHF may provide a more targeted and tailored treatment of sHF.

show abstract

“…There is also some, but not yet rigorous evidence for the relevance of angiotensinogen (AGT) gene to LVH level [Jeng et al, 1999;Makeeva et al, 2004;Patel et al, 2005]. However, such a link between these genetic polymorphism and LVH has not been confirmed in other populations [Fernandez, et al, 1998;Kauma et al, 1998, Shlyakhto et al, 2001.…”

Section: Left Ventricular Hypertrophy and Genetics Of Renin-angiotensmentioning

confidence: 96%

Renin--Angiotensin System Gene Polymorphism and Regression of Left Ventricular Hypertrophy in Hypertension

Shlyakhto¹,

Conrady²

2007

CPG

View full text Add to dashboard Cite

Evidence is beginning to accumulate that not only development and progression of left ventricular hypertrophy (LVH) in hypertension is genetically predisposed, but its regression during therapy has several genetic determinants. Renin-angiotensin system (RAS) is generally considered to be the major contributor to LVH development. I/D polymorphism of angiotensin-converting enzyme (ACE) gene was shown to determine plasma ACE concentrations and LVH severity in hypertension. Several studies have also documented association of angiotensin II type I receptor gene (AT1R) polymorphism (A1166C) with LVH. Impact of angiotensinogen (ATG) genetic polymorphisms (-6G/A or M235T) in LVH is not so well established. Gene-gene interactions between these genes are also described.Since pharmacogenetic approach has been introduced to testing of antihypertensive drug efficacy, the influence of RAS genetic polymorphisms on LVH regression during treatment was also analyzed in several studies. The data obtained nowadays are rather controversial. Large proportion of studies documented lower LVH regression in patients carrying D allele (or DD genotype) of ACE gene. C allele of AT1R gene is also shown to influence LVH reversal during treatment. However, major clinical studies concerning effects of different drugs on hypertensive LVH did not include genetic investigations; the existing data are obtained on rather small patient samples, do not take into account gene-environmental interactions, and need to be tested in larger trials.

show abstract

G-6A Polymorphism of the Angiotensinogen Gene and Its Association With Left Ventricular Mass in Asymptomatic Young Adults from a Biethnic CommunityThe Bogalusa Heart Study

Cited by 13 publications

References 31 publications

Association of Clinical and Genetic Factors With Left Ventricle Hypertrophy in Arterial Hypertension

Association of Clinical and Genetic Factors With Left Ventricle Hypertrophy in Arterial Hypertension

Association between Genetic Polymorphisms in the Renin-Angiotensin System and Systolic Heart Failure Revised by a Propensity Score-Based Analysis

Renin--Angiotensin System Gene Polymorphism and Regression of Left Ventricular Hypertrophy in Hypertension

Contact Info

Product

Resources

About