The Relationship between Angiotensin-II Type 1 Receptor Gene Polymorphism and Repolarization Parameters after a First Anterior Acute Myocardial Infarction

Öztürk, Önder; Öztürk, Ünal; Nergiz, Şebnem; Karahan, Mehmet

doi:10.4070/kcj.2016.46.6.791

Cited by 8 publications

(4 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The renin-angiotensin system is crucial regulating blood pressure and the development of CAD. Studies have found that polymorphisms in renin-angiotensin system-related genes, including AGT rs4762 ( 20 ), AGTR1 rs5186 ( 21 ), AGTR2 rs11091046 ( 22 ), KLK1 rs5517 ( 23 ), ACE rs1799752 ( 24 ), as well as ACE2 rs4646142 and rs1978124 ( 25 ), were associated with the risk of MI . The ACE gene insert/delete (I/D, rs1799752) polymorphism is the most extensively studied.…”

Section: Single-omics Approachesmentioning

confidence: 99%

From multi-omics approaches to personalized medicine in myocardial infarction

Zhan,

Tang,

et al. 2023

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Myocardial infarction (MI) is a prevalent cardiovascular disease characterized by myocardial necrosis resulting from coronary artery ischemia and hypoxia, which can lead to severe complications such as arrhythmia, cardiac rupture, heart failure, and sudden death. Despite being a research hotspot, the etiological mechanism of MI remains unclear. The emergence and widespread use of omics technologies, including genomics, transcriptomics, proteomics, metabolomics, and other omics, have provided new opportunities for exploring the molecular mechanism of MI and identifying a large number of disease biomarkers. However, a single-omics approach has limitations in understanding the complex biological pathways of diseases. The multi-omics approach can reveal the interaction network among molecules at various levels and overcome the limitations of the single-omics approaches. This review focuses on the omics studies of MI, including genomics, epigenomics, transcriptomics, proteomics, metabolomics, and other omics. The exploration extended into the domain of multi-omics integrative analysis, accompanied by a compilation of diverse online resources, databases, and tools conducive to these investigations. Additionally, we discussed the role and prospects of multi-omics approaches in personalized medicine, highlighting the potential for improving diagnosis, treatment, and prognosis of MI.

show abstract

Section: Single-omics Approachesmentioning

confidence: 99%

From multi-omics approaches to personalized medicine in myocardial infarction

Zhan,

Tang,

et al. 2023

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…Проведенные генетические исследования показали взаимосвязь генотипа СС гена AGTR1(A1166C) с толщиной задней стенки ЛЖ, межжелудочковой перегородки (МЖП) и ИММЛЖ в общей популяции (Jin Y. и соавт., 2012), а у пациентов с коронарной болезнью сердца генотипы АС и СС были ассоциированы с конечно-диастолическим и конечно-систолическими размерами и фракцией выброса ЛЖ (Mishra A. и соавт., 2015) [35,36]. Также была установлена взаимосвязь АС и СС генотипов гена AGTR1 (A1166C) с повышенным риском реполяризационных нарушений при ЭКГ (длительность и дисперсия интервала QT) у пациентов с острым инфарктом миокарда передней стенки ЛЖ (Ozturk O. и соавт., 2016) и CC генотипа -с увеличением риска развития жизнеугрожающих аритмий у пациентов с хронической сердечной недостаточностью [37,38]. Синергичное влияние генетического полиморфизма генов AGTR1 и CYP11B2 на развитие ГЛЖ может быть обусловлено тем, что альдостерон потенциирует гипертрофические эффекты ангиотензина II [39].…”

Section: на следующую на первую на предыдущую к содержаниюunclassified

Прогнозирование Риска Развития Гипертрофии Левого Желудочка При Артериальной Гипертензии С Учетом Полиморфизма Генов Ренин-Ангиотензинальдостероновой Системы

Павлова¹,

Ogurtsova²,

Денисевич³

et al. 2021

Кардиология В Беларуси

View full text Add to dashboard Cite

Цель. Определить клинико-генетические факторы риска прогрессирования гипертрофии левого желудочка (ГЛЖ) с учетом полиморфизма генов ренин-ангиотензин-альдостероновой системы (РААС) по данным проспективного пятилетнего наблюдения пациентов с эссенциальной артериальной гипертензией (АГ). Материалы и методы. Клинико-инструментальное обследование выполнено у 155 пациентов с АГ, из них 82 мужчины и 73 женщины (средний возраст 54,5±9,4 года). Признаки ГЛЖ оценивались при эхокардиографии (ЭхоКГ) с расчетом индекса массы миокарда левого желудочка (ИММЛЖ). Генотипирование полиморфных локусов генов ренин-ангиотензин-альдостероновой системы (РААС), I/D ангиотензинпревращающего фермента (АСЕ), М235Т ангиотензиногена (AGT), G83A ренина (REN), C(-344)T альдостеронсинтазы (СYP11B2), A1166C рецепторов кангиотензину II 1-го типа (AGTR1) и 2-го типа C3123A (AGTR2) проводилось методом полимеразной цепной реакции. Результаты. Прогрессирование ГЛЖ по результатам повторной ЭхоКГ через 5 лет наблюдалось у 46 человек (29,7%), у 67 пациентов ИММЛЖ оставался в пределах нормативных значений и у 42 - отмечалось его снижение до нормативных величин. В многофакторной регрессионной модели прогнозирования предикторами прогрессирования ГЛЖ в течение 5 лет являлись: носительство мутантного ТТ генотипа гена AGT (ОШ=3,79; 95% ДИ 1,39-10,33; р=0,009), нерегулярное антигипертензивное лечение (ОШ=3,45; 95% ДИ 1,41-8,33; р=0,006), биаллельные сочетания полиморфизма A1166C гена AGTR1 (С аллель) и C(-344)Т) гена CYP11B2 (СТ/ТТ генотипы) (ОШ=1,53; 95% ДИ 1,05-2,23; р=0,028), более высокая степень АГ у носителей ААгенотипа гена AGTR2 (ОШ=1,58; 95% ДИ 1,07-2,33; р=0,022). Точность прогноза прогрессирования ГЛЖ у пациентов с АГ по разработанной многофакторной модели составила 73% при общей безошибочности модели 71%. Заключение. Прогрессирование ГЛЖ в течение 5 лет у пациентов с АГ обусловлено влиянием полиморфизма генов РААС - AGT (М235Т), AGTR1 (A1166C), CYP11B2 (C(-344)T), AGTR2 (С3123А) и их взаимодействиями в сочетании с нерегулярным лечением и степенью заболевания. Purpose. To determine the clinical and genetic risk factors of progression of left ventricular hypertrophy (LVH), taking into account the polymorphism of the genes of the renin-angiotensin- aldosterone system (RAAS), according to the data of a prospective five-year follow-up of patients with essential arterial hypertension (AH). Materials and methods. Clinical and instrumental examination was performed in 155 patients with hypertension, including 82 men and 73 women (average age - 54.5±9.4 years). The signs of LVH were assessed with the help of echocardiography with calculation of the left ventricular myocardial mass index (LVMI). Genotyping of polymorphic loci of the genes of the renin-angiotensin-aldosterone system (RAAS), I/D angiotensin converting enzyme (ACE), М235Т angiotensinogen (AGT), renin G83A (REN), C(-344)T aldosterone BC2 receptors) (CYP1166) II type 1 (AGTR1) and type 2 C3123A (AGTR2) was carried out with polymerase chain reaction. Results. The progression of LVH according to the results of repeated echocardiographic examination in 5 years was observed in 46 patients (29.7%); in 67 patients, LVMI remained within the normative values; in 42 patients, it decreased to the normative values. In the multivariate regression model, the predictors of LVH progression during 5 years were the following: mutant TT genotype of the AGT gene (OR=3.79; 95% CI 1.39-10.33; p=0.009), irregular antihypertensive treatment (OR=3.45; 95% CI 1.41-8.33; p=0.006), biallelic combinations of the polymorphism A1166C of the AGTR1 gene (C allele) and C (-344) T) of the CYP11B2 gene (CT/TT genotypes) (OR=1.53; 95% CI 1.05-2.23; p=0.028), a higher degree of AH in the carriers of the AA genotype of the AGTR2 gene (OR=1.58; 95% CI 1.07- 2.33; p=0.022). The accuracy of prediction of the LVH progression in patients with hypertension according to the multivariate model was 73%, while the infallibility was 71%. Conclusion. The progression of LVH within 5 years in patients with AH is caused by the influence of the polymorphism of the RAAS genes - AGT (M235T), AGTR1 (A1166C), CYP11B2 (C(-344)T), AGTR2 (C3123A) and their interactions in combination with irregular treatment and the degree of the disease.

show abstract

“…Angiotensin II is the most potent vasoconstrictive and inflammatory component of the RAAS. Most of its pressor, inflammatory, and proliferative actions are regulated by AT1R which is expressed in the myocardium [8].…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphism of Angiotensin II Type 1 Receptors and Their Effect on the Clinical Outcome of Captopril Treatment in Arab Iraqi Patients with Acute Coronary Syndrome (Mid Euphrates)

et al. 2019

View full text Add to dashboard Cite

Genetic variation in the angiotensin II type 1 receptor (AT1R) has an important effect on the outcome of acute coronary syndrome (ACS) initiated treatment with captopril. This study aims to investigate the impact of genetic polymorphism of AT1R (rs5186 and rs275651) on the ACS outcome in Iraqi patients treated with captopril. A total of 250 Iraqi individuals with ACS were included in this case-control study and they were divided into two study groups; Study group 1 included 125 participants who were prescribed captopril, 25 mg twice daily and study group 2 included 125 participants who received no captopril as part of their ACS treatment (control study). The AT1R gene (rs5186) CC genotype was found to be associated with ST-elevation myocardial infarction (STEMI) (Odd's ratio (O.R) = 1.2, P = 0.7), while AC was associated with Non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) (O.R = 1.2, P = 0.8). AC genotype is more prone to have Percutaneous coronary intervention (PCI) after ACS attack (O.R = 1.2, P = 0.6). CC genotype had a risk to get less improvement (O.R = 1.6, P = 0.5), so might require higher doses of captopril during acute coronary insult. The AT1R gene (rs275651) AA genotype was associated with UA (O.R = 1.3, P = 0.9). AA and AT genotypes were more prone to have PCI after ACS attack (O.R = 3.9 P = 0.2, O.R = 3.5, P = 0.3 respectively) and thus requiring higher doses of captopril. We conclude that the AT1R rs5186, rs275651 genetic polymorphisms might partially affect the clinical outcome of ACS patients treated with captopril and might have captopril resistance which requires higher doses.

show abstract

The Relationship between Angiotensin-II Type 1 Receptor Gene Polymorphism and Repolarization Parameters after a First Anterior Acute Myocardial Infarction

Cited by 8 publications

References 23 publications

From multi-omics approaches to personalized medicine in myocardial infarction

From multi-omics approaches to personalized medicine in myocardial infarction

Прогнозирование Риска Развития Гипертрофии Левого Желудочка При Артериальной Гипертензии С Учетом Полиморфизма Генов Ренин-Ангиотензинальдостероновой Системы

Genetic Polymorphism of Angiotensin II Type 1 Receptors and Their Effect on the Clinical Outcome of Captopril Treatment in Arab Iraqi Patients with Acute Coronary Syndrome (Mid Euphrates)

Contact Info

Product

Resources

About