scholarly journals Assessment of calcium antagonist therapy protective effect on the thickness of the intima-media complex in patients with arterial hypertension

2021 ◽  
Vol 10 (2) ◽  
pp. 54-57
Author(s):  
N. I. Morozova ◽  
T. A. Mulerova
Keyword(s):  
Calcium Antagonist ◽  
Arterial Hypertension ◽  
Calcium Antagonists ◽  
Vascular Wall ◽  
Mthfr Gene ◽  
Point Of View ◽  
Enos Gene ◽  
Polymerase Chain ◽  
Atherosclerotic Process ◽  
Agt Gene

Aim. To evaluate the connection of calcium antagonist (amlodipine) therapy with the dynamics of the intima-media complex thickness in patients with arterial hypertension (AH), depending on genetic polymorphism.Methods. The study included representatives of the indigenous nationality (the Shors) – 901 people, of which a group of 367 people with hypertension was identified. The prospective stage of observation included 234 people who did not receive antihypertensive therapy. Based on the prescription of calcium antagonists, patients with hypertension were divided into two groups. Gene polymorphism was tested by polymerase chain reaction.Results. In the Shor cohort, the regression of the intima-media complex thickness of the carotid arteries was observed more often in hypertensive patients who received calcium antagonists if to compare them with those who did not take the drug [OR = 2.30]. In addition, the decrease in the atherosclerotic process is associated with the genotype carriage: I/I of the ACE gene [OR = 9.42], T/C of the AGT gene [OR = 3.52], 4b/4b and 4b/4a of the eNOS gene [OR = 2.26 and OR = 3.75], C/C of the MTHFR gene [OR = 2.62].Conclusion. Pharmacogenetic aspects are valuable from the point of view of an individual approach and obtaining the most pronounced pharmacological response in order to slow down the processes of vascular wall remodeling in patients with hypertension. 

scholarly journals The high expression of elastases, observed in apelin deficient mice, could contribute to premature wear of elastic fibers and vascular stiffness.

2021 ◽  
Author(s):  
Beatrice Romier ◽  
Cedric Dray ◽  
Amandine Wahart ◽  
Thinhinane Hocine ◽  
Laetitia Vanalderwiert ◽  
...  
Keyword(s):  
Arterial Hypertension ◽  
Protective Factor ◽  
Vascular Wall ◽  
Point Of View ◽  
Vascular Stiffness ◽  
Elastic Fibers ◽  
Metabolic Markers ◽  
Beneficial Effects ◽  
Vascular Point ◽  
Anatomical Parameters

Abstract Vascular stiffness is often the main cause of arterial hypertension and its complications including atherosclerosis, observed during obesity. However, the mechanisms leading to this rigidity or the preventing factors are misknown. We hypothesized that apelin, known for its beneficial effects on lipid, inflammatory, and vascular metabolism, could be a protective factor against vascular stiffness. We used mice deficient for the apelin gene (KO-APL) and compared with wild-type mice (WT) at the level of metabolic markers and inflammations of white adipose tissue (WAT), as well as aortic functional and anatomical parameters. KO-APL mice developed an inflammation associated with significant remodeling of WAT, in particular with the protease expressions such as neutrophil elastase or cathepsin S. From a vascular point of view, these same elastases are involved in the fragmentation of elastic fibers, explaining the increase in vascular velocity of pulse wave and arterial hypertension. Interestingly, univariate correlation analysis showed that the inflammation markers and protease expression of WAT were associated with remodeling of the vascular wall. Our results suggest that the modifications induced by the absence of apelin particularly in WAT, could facilitate the expression of elastases and the rupture of elastic fibers, necessary to maintain elastance. This discovery is fundamental because the synthesis of elastic fibers stops as of adolescence and is not renewed during the entire life of human. The preservation of these fibers is therefore critical in maintaining vascular homeostasis. Thus, Apelin could be an interesting therapeutic route to protect the premature wear of elastic fibers.

scholarly journals Hyperhomocysteinemia, C-677T polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene, and chronic arterial hypertension in pregnant women

2012 ◽  
Vol 11 (1) ◽  
pp. 41-44
Author(s):  
V. S. Chulkov ◽  
N. K. Vereina ◽  
S. P. Sinitsyn
Keyword(s):  
Arterial Hypertension ◽  
Pregnant Women ◽  
Intrauterine Growth Restriction ◽  
Methylenetetrahydrofolate Reductase ◽  
Mthfr Gene ◽  
Intrauterine Growth ◽  
Immunoenzymatic Method ◽  
Group I ◽  
Polymerase Chain ◽  
Complicated Pregnancy

Aim. To investigate the prevalence of C-677T polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene and hyperhomocysteinemia (HHC) in pregnant women with chronic arterial hypertension (CAH). Material and methods. This prospective cohort study included two groups: Group I – pregnant women with CAH (n=80), and Group II – pregnant women without AH (n=40). In all participants, homocysteine (HC) levels were assessed using immunoenzymatic method, at 9-12 weeks, 22-24 weeks, and 30-32 weeks. Genotyping of the C-677T polymorphism of MTHFR gene was performed using polymerase chain reaction. Results. In pregnant women with CAH, HC levels were higher than in women without AH, throughout the pregnancy. Group I also demonstrated higher prevalence of T allele and T/C genotype. In pregnant women with HHC, relative risk (RR) of pre-eclampsia was 3,5 (95% CI 2,0-5,6), of chronic placental insufficiency - 1,2 (95% CI 0,9-1,6), and of intrauterine growth restriction syndrome - 6,4 (95% CI 3,1-13,3). Conclusion. HCC, as well as its combination with C-677T polymorphism of MTHRF gene, could be regarded as a biomarker of complicated pregnancy in women with CAH.

scholarly journals Development of additional criteria for development of complications in patients with arterial hypertension who are carriers of the methylenetetrahydrofolate reductase gene polymorphism

2018 ◽  
pp. 196-200
Author(s):  
T. A. Degaeva ◽  
L. N. Goncharova ◽  
I. V. Sychev
Keyword(s):  
Arterial Hypertension ◽  
Methylenetetrahydrofolate Reductase ◽  
Cardiovascular Complications ◽  
Carrier State ◽  
Mthfr Gene ◽  
Reductase Gene ◽  
Primary Arterial Hypertension ◽  
Polymerase Chain ◽  
Methylenetetrahydrofolate Reductase Gene Polymorphism

The article provides data on 114 patients with stage 2 primary arterial hypertension (AH) according to the WHO classification (2008) and the development of complications associated with hemostasis violations depending on the nationality of patients (Mordva-Moksha, Russians) and polymorphism methyltetrahydrofolate reductase (MTHFR) gene carrier state. Polymorphic genotypes were identified using polymerase chain reaction (PCR) along with traditional clinical and instrumental studies. The analysis of MTHFR gene polymorphic genotypes carriage showed a significant predominance of intermediate genotypes (88% – CT genotype at position 677, 66% – AC genotype at position 1298) regardless of nationality of patients with AH. The carriage of “unfavourable” TT genotypes of MTHFR gene at position 677 prevails in men of the Mordva-Moksha (20%) as compared with the patients of Russian nationality. During a 3-year follow-up, 12% of patients with AH (6.9% of MordvaMoksha and 5.1% of Russian) suffered acute myocardial infarction (MI) or acute cerebrovascular accident (ACVA). Cardiovascular complications (MI/ACVA) developed 1.5 times more often in Mordva patients than in patients with AH of Russian nationality. IM occurred 3 times more often in Mordva-Moksha men than in patients with AH of Russian nationality. The Mordva-Moksha men with AH, who were carriers of the “unfavourable” TT genotypes of MTHFR gene at position 677, developed a complication in the form of MI in 100% cases.

scholarly journals Clinical and genetic factors determining target lesions of patients with arterial hypertension among Mountain Shoria population

2017 ◽  
Vol 14 (3) ◽  
pp. 42-50
Author(s):  
T A Mulerova
Keyword(s):  
Arterial Hypertension ◽  
Protective Effect ◽  
Ethnic Group ◽  
Russian Federation ◽  
Mthfr Gene ◽  
Ace Gene ◽  
Indigenous Ethnic Group ◽  
The Russian Federation ◽  
High Level ◽  
Agt Gene

Objective. To establish associations between clinical and genetic risk factors and target lesions (heart, blood vessels, kidneys) of patients with arterial hypertension (AH) among the population of Mountain Shoria, depending on ethnicity. Matherials and methods. A clinical and epidemiological study of compactly living population in the remote areas of the Mountain Shoria was carried out. This middle altitude region is located in the south of Western Siberia. 1409 people were examined (901 representatives of the indigenous ethnic group - the Shors, 508 representatives of the non-indigenous ethnic group - 90% of them being Caucasian). The diagnosis of AH was set in accordance with the recommendations of the Society of Cardiology of the Russian Federation / Medical Society of the Russian Federation on the Problem of Arterial Hypertension, 2010. Assessment of the structural and functional state of the cardiac muscle and duplex scanning of brachiocephalic arteries among the patients with AH was made by echocardiography. A photometric method was used to examine the urinary albumin concentration level. The polymorphisms of the genes ACE (I/D, rs4340), АGT (c.803T>C, rs699), AGTR1 (А1166С, rs5186), ADRB1 (с.145A>G, Ser49Gly, rs1801252), ADRA2B (I/D, rs28365031), MTHFR (c.677С>Т, Ala222Val, rs1801133) and NOS3 (VNTR, 4b/4a) were tested by the PCR method. Results. Among the members of the indigenous ethnic group left ventricle hypertrophy (LVH) correlated with the AG progression features (extent and duration), smoking, genotypes I/D of the ACE gene among men and T/T and C/T of the MTHFR gene; increased intima-media complex thickness (IMT) correlated with the AG progression features (duration), male sex, age, genotypes T/C of the AGT gene and C/T of the MTHFR gene; high level of albuminuria (AU) correlated with the AG progression features (extent and duration), lipid disorders (hypoalphacholesterolemia, hypertriglyceridemia, hyperbetacholesterolemia), genotypes D/D and I/D of the ACE gene, D/D of the ADRA2B gene and the C/T of the MTHFR gene among 18-64-year-olds. Genotype T/C of the AGT gene had a protective effect on LVH, genotypes G/G and A/G of the ADRB1 gene had protective effects on IMT and AU levels. In the nonindigenous ethnic group LVH correlated with the AG progression features (duration), hypertriglyceridemia, abdominal obesity, genotypes D/D of the ACE gene, 4b/4a and 4a/4a of the NOS3 gene; increased IMT correlated with the AG progression features (duration), age and genotypes T/C and C/C of the AGT gene; AU high level correlated with the AG progression features (extent and duration), obesity, abdominal including, genotypes C/C of the AGTR1 gene, D/D of the ADRA2B gene and T/T of the MTHFR gene. Genotype I/D of the ADRA2B gene had protective effect on IMT. Conclusion. The study demonstrated the importance of the ethnogenetic mechanisms in the multifactorial pathology development. The problem requires further research, also identification of people with AH and target lesions is needed for monitoring during the prophylactic medical examination of the population.

scholarly journals Subclinical atherosclerosis: The benefits of calcium antagonists

2012 ◽  
Vol 18 (2) ◽  
pp. 118-125
Author(s):  
O. M. Drapkina ◽  
O. N. Korneeva ◽  
N. V. Mankova
Keyword(s):  
Calcium Antagonists ◽  
Subclinical Atherosclerosis ◽  
Vascular Wall ◽  
Routine Clinical Practice ◽  
Atherosclerosis Progression ◽  
Non Invasive ◽  
Atherosclerotic Lesions ◽  
Invasive Method ◽  
Atherosclerotic Process ◽  
Suitable Marker

Recently the research has been focused on the earlier stages of the atherosclerotic process, i.e. subclinical atherosclerosis. Endothelial dysfunction is a suitable marker of subclinical atherosclerosis. In routine clinical practice, ultrasonography is the most useful and accessible non-invasive method for diagnosis of subclinical atherosclerosis. Carotid intimai media thickness (IMT) was shown to be predictive for the risk of cardiovascular events. Furthermore, vascular stiffness can be a helpful marker for assessment of the vascular wall state and blood flow. Calcium antagonists (CA) seem to be promising for the prevention of subclinical atherosclerosis progression, and amlodipine has the priority due to the metabolic neutralilty, vasodilation effect and favourable effects on renal hemodynamics. The data on IMT assessement showed that amlodipine slows down the development of atherosclerotic lesions in hypertensive patients.

Model Characterization of Pulmonary Arterial Hypertension: Analysis of Lung Pathology with Respect to Human Disease

2020 ◽  
Author(s):  
◽  
Eptisam lambu
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Human Disease ◽  
Vascular Remodeling ◽  
Vascular Wall ◽  
Lung Pathology ◽  
Pulmonary Arterial ◽  
Lung Pathogenesis ◽  
Arterial Endothelial Cells

Pulmonary arterial hypertension (PAH) is a rare multifactorial disease characterized by abnormal high blood pressure in the pulmonary artery, or increased pulmonary vascular resistance (PVR), caused by obstruction in the small arteries of the lung. Increased PVR is also thought to be caused by abnormal vascular remodeling, due to thickening of the pulmonary vascular wall resulting from significant hypertrophy of pulmonary arterial smooth-muscle cells (PASMCs) and increased proliferation/impaired apoptosis of pulmonary arterial endothelial cells (PAECs). Herein, we investigated the mechanisms and explored molecular pathways mediating the lung pathogenesis in two PAH rat models: Monocrotaline (MCT) and Sugen5416/Hypoxia (SuHx). We analyzed these disease models to determine where the vasculature shows the most severe PAH pathology and which model best recapitulates the human disease. We investigated the role vascular remodeling, hypoxia, cell proliferation, apoptosis, DNA damage and inflammation play in the pathogenesis of PAH. Neither model recapitulated all features of the human disease, however each model presented with some of the pathology seen in PAH patients.

scholarly journals Study of genes involved in angiogenesis and metabolic processes of peripheral blood lymphocytes in patients with chronic endometritis

2021 ◽  
Vol 38 (4) ◽  
pp. 25-35
Author(s):  
E. G. Kobaidze
Keyword(s):  
Clinical Manifestations ◽  
Mthfr C677t ◽  
Peripheral Blood Lymphocytes ◽  
Mthfr Gene ◽  
Reproductive Period ◽  
Enos Gene ◽  
Metabolic Processes ◽  
Chronic Endometritis ◽  
Blood Lymphocytes ◽  
Healthy Women

Objective. To study the polymorphisms of the genes involved in angiogenesis and in metabolic processes, to assess the level of lymphocytes in patients with chronic endometritis and practically healthy women of reproductive period. Materials and methods. 86 patients were examined; DNA regions of the genes eNOS 1799983 (Glu298Asp), PPARA (G2528C), ApoE rs429358 (Cys130Arg), MTHFR (C677T, A1298C) were used as primers; blood lymphocytes (CD3+, CD4+, CD8+, CD19+, CD95+) were assessed. Results. Statistically significant differences in gynecological and chronic somatic pathology were obtained in patients with chronic endometritis; they more often than practically healthy women had polymorphisms of the genes ApoE rs429358, eNOS1799983, PPARA (G2528C); patients with chronic endometritis more often had dysregulation of the immune system in the form of insufficiency of the cellular effector link of immunity and changes in the PPARA, ApoE, eNOS gene. Attention was drawn to the obtained relationships of polymorphic genes and clinical manifestations in patients with chronic endometritis, in particular, with a history of non-developing pregnancy in anamnesis, there was more often detected polymorphism of the ApoE gene, with abnormal uterine bleeding polymorphism of PPARA, with chronic inflammatory pathology of the gallbladder polymorphism of the MTHFR gene. Conclusions. The prevalence of polymorphism of the genes eNOS 1799983 (Glu298Asp), PPARA (G2528C), ApoE rs429358 (Cys130Arg), MTHFR (C677T, A1298C) was obtained in patients with chronic endometrial inflammation compared with practically healthy participants in the study. Insufficiency of the cellular effector link of immunity was revealed in the majority of patients with ChE and an association with allele C genotypes G/C and C/C of PPARA 4253778 gene, with allele C genotypes G/C and C/C of ApoE42935 gene, with allele C genotypes G/C and C/C of eNOS 1799983 gene and G/C genotype of MTHFR gene (C677T, A1298C).

scholarly journals Associations of Gene Polymorphisms and Prognosis in Highly Adherent to Treatment Patients After Myocardial Infarction

2021 ◽  
Vol 11 (5) ◽  
pp. 380-388
Author(s):  
K. G. Pereverzeva ◽  
S. S. Yakushin ◽  
A. A. Nikiforov ◽  
A. A. Novoselova
Keyword(s):  
Myocardial Infarction ◽  
Genetic Factors ◽  
Dual Antiplatelet Therapy ◽  
Adherence To Treatment ◽  
Lpl Gene ◽  
High Adherence ◽  
Cyp2c19 Gene ◽  
Polymerase Chain ◽  
One Year ◽  
Agt Gene

Aim. To evaluate the influence of genetic factors on the risk of developing a combined endpoint, during a one-year supervision of patients, who had myocardial infarction and highly adherent to drug therapy.Material and methods. The research included 250 patients with high adherence to treatment with myocardial infarction, using the method of polymerase chain reaction we determined the polymorphisms Thr174Met and Met235Thr in the AGT gene, Arg389Gly and Ser49Gly in the ADRB1 gene, Ser447Ter in the LPL gene and Leu28Pro in the APOE gene, Trp212Ter and G681A in the CYP2C19 gene, and then we evaluated their influence on the prognosis.Results. A significant influence on the risk of developing combined endpoint was noticed for the polymorphism of CYP2C19 (G681A) gene. For the GA genotype of the CYP2C19 gene (G6881A), the OR of developing an unsuccessful outcome was 1.97 (95 % CI 1.05 — 3.69) (P = 0.03). For сarrier-state of A allele the OR was 1.46 (95 % CI 1.06 — 3.64) (P = 0.03). Conclusion. The results received indicate the need for individual approach for the choice of drugs from the group of inhibitors P2Y12-receptors for dual antiplatelet therapy, and if clopidogrel is chosen it is necessary to resolve the issue of pharmacogenetic testing for CYP2C19.

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