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D A Zateĭshchikov

Publications and source records attributed to D A Zateĭshchikov.

At least 19 recordsLinked to original sources
PubMed2006

[Polymorphism of genes of factors of hemostasis in patients with early development of ischemic heart disease.].

The review is devoted to analysis of data, related to contribution of genetic peculiarities of the hemostasis system to early development of ischemic heart disease (IHD). Information is presented on polymorphisms of tissue factor, coagulation factors VII, V, prothrombin, thrombomodulin, fibrinogen, thrombin activated fibrinolysis inhibitor, tissue plasminogen activator inhibitor, platelet membrane glycoproteines Ia, Iba, IIIa in patients with early development of IHD. Contradictoriness of existing data on effects of genetic heterogeneity of factors of hemostasis on risk of development of IHD at young age and necessity of further investigations in this area are underlined.

Coronary Artery Disease↗
PubMed2005

[Measurement of arterial stiffness and its clinical value].

Noninvasive method of assessment of arterial stiffness by means of measurement of velocity of pulse wave propagation in presented in the review. Mechanical properties of arterial wall and pathogenesis of arterial remodeling are described. Correlation of pulse wave velocity with some clinical, laboratory and other parameters is shown. Studies demonstrating clinical significance, prognostic value of the method, possible indications for the given investigation are also presented. Most part of works has been devoted to the study of arterial stiffness in hypertension, ischemic heart disease, atherosclerosis, diabetes. Elevation of arterial stiffness is associated with increases of number of vascular events, cardiovascular and total mortality. This association is most pronounced in elderly and senile persons. Thus the method allows to detect additional risk group in population. The review contains data on comparative analysis of efficacy of different groups of drugs in relation to arterial stiffness, possible mechanisms of influence effect. It is concluded that measurement of arterial stiffness is indicated in states, accompanied with changes of arterial properties, for assessment of dynamics of the process, efficacy of therapy and prognosis.

Adolescent↗
PubMed2005

[Antioxidant properties of statins].

Statins block expression of protein subunits of Gi-proteins (p22phox and gp91phox) which determine oxidase activity of NADPH oxidases and expression of GTP-ase (NADPH activator). This leads to suppression of activity of prooxidant enzyme systems (NADPH oxidase, xanthine oxidase, oxidase activity of endothelial NO-synthase) and diminishment of production of most aggressive free radicals -- superoxide anion and peroxinitrite. Hyperproduction of these radicals is associated with lowering of nitric oxide (NO) level and augmented NO destruction, the state of oxidative stress and endothelial dysfunction. Statins increase expression of enzymes with antioxidant properties (catalases, paroxonases), augment resistance of low density lipoproteins to oxidation, decrease take up of oxidized low density lipoproteins by monocytes and differentiation of monocytes into macrophages at the account of suppression of cellular scavenger receptor CD36 gene expression. Thus statins are powerful antioxidants.

Animals↗
PubMed2005

[Individual sensitivity to antihypertensive drugs: genetic aspects].

Effective blood pressure lowering is essential for prevention of complications of arterial hypertension. Most current guidelines indicate diuretics, beta-blockers, angiotensin converting enzyme inhibitors, calcium channel blockers and angiotensin receptor blockers as main antihypertensive drugs. Genetic polymorphisms underlie pathophysiology of diseases and can affect efficacy of therapy. Method of investigation of pharmacogenetic interrelationships is based on analysis of genes encoding enzymes responsible for metabolism and transport of drugs as well as genes encoding main targets of drug action (receptors). Those polymorphic genes that encode elements of the system of metabolism, adsorption, transport, elimination of drugs, and main receptor systems are considered to be main gene-candidates for pharmacogenetic studies. Some drugs have well known genotypes determining efficacy of therapy as for instance alpha-adducin gene for diuretics. Data on other classes of drugs (e.g. calcium channel blockers) are scanty. Existing information on pharmacogenetic properties of antihypertensive drugs is presented in this review.

Adrenergic beta-Antagonists↗
PubMed2005

[Associations of hemostasis factors genes with early development of ischemic heart disease and manifestation of myocardial infarction in young age].

AIM: To study polymorphisms of genes of factors of the system of hemostasis in young patients with ischemic heart disease (IHD). MATERIAL: Two groups of patients participated in the study: patients with first manifestation of IHD at the age < or = 50 years (men) or < or = 55 years (women) (n=158), and patients with first IHD manifestation at the age > or = 70 years (n=92). METHODS: We studied polymorphic markers of genes encoding clotting factors V (F5) and VII (F7), subunit IIIa of platelet integrin (ITGB3), beta-chain of fibrinogen (FGB) and tissue plasminogen activator type 1 (PLANH1). RESULTS: After separation of a subgroup of patients with MI without preceding angina we revealed significant differences in distribution of frequencies of genotypes of polymorphic marker C(-426)T of factor V gene: genotype TT was significantly more frequent in young (14.9%) than in old (2%) patients (p=0.008). Multifactorial logistic regression revealed independent association of early IHD with smoking (OR 6.112 [2.567-14.552]; p<0.001) and presence of genotype TT of C(-426)T polymorphic marker of F5 gene (OR=9.410 [1.074-82.459]; p=0.043). CONCLUSION: Thus we obtained data on the presence of independent association between IHD risk and manifestation of MI in young age with genotype TT of polymorphic marker C(-426)T of F5 gene as well as with traditional risk factors of IHD.

Adult↗
PubMed2004

[Detection and morphofunctional predictors of left auricular thrombosis in patients with atrial fibrillation].

Atrial fibrillation significantly worsens quality and duration of patient's life because of frequent development of thromboembolic complications. The main cause of these complications is formation of intracardiac thrombosis. Prevalence of left atrial thrombosis in patients with atrial fibrillation varies from 8 to 24%. About 90% of thromboses are localized in left auricle. This paper contains review of different methods of detection of left auricular thrombosis. Main structural and functional predictors of thrombosis and possibilities of modern techniques of their visualization are also described. Different methods of echocardiography first of all transesophageal echocardiography are at present foremost in assessment of structural and functional predictors of thrombosis development. With the help of transesophageal echocardiography it is possible to accomplish functional monitoring of the state of left auricle during treatment with different drugs and/or after cardioversion. Detection of risk factors of left auricular thrombosis is an important clinical task because it allows to select a group of high risk patients in which long-term therapy with anticoagulants is indicated.

Anticoagulants↗
PubMed2004

[Association of polymorphic marker A1/A2 of gene ITGB3 with coronary artery disease and myocardial infarction].

The distributions of the alleles and genotypes of polymorphic marker A1/A2 of gene ITGB3 encoding the beta3 subunit of integrin alphaIIbbeta3 in groups of patients with coronary artery disease (CAD), including those who have had myocardial infarction (MI), and in the control group have been compared. Analysis using Fisher's test has not revealed significant differences between these groups with respect to the distributions of the alleles and genotypes of polymorphic marker A1/A2 of gene ITGB3. This indicates that this polymorphic marker is not associated with either CAD or MI in the Moscow population.

Case-Control Studies↗
PubMed2004

[Association of polymorphic marker G(-455)A of gene FGB with coronary artery disease].

Patients with coronary artery disease (CAD), including those who have had myocardial infarction (MI), and control subjects have been compared with respect to the distributions of the alleles and genotypes of polymorphic marker G(-455)A of gene FGB encoding the fibrinogen beta-chain. The groups studied do not differ significantly with respect to the distributions of G(-455)A alleles and genotypes. This indicates that this marker is not associated with CAD in the Moscow population. Allele A of the G(-455)A polymorphic marker has been found to be associated with an increased fibrinogen content of blood plasma in women with CAD.

Alleles↗
PubMed2004

[Genetic Predictors of Unfavorable Course in High Risk Patients With Ischemic Heart Disease. Data of Follow-up for Two Years.].

Prognostic value of clinical parameters and polymorphisms of apo-B, apo-E, LPL, , PPARA, PPARG2 genes was studied in 154 patients with acute unstable angina. Duration of follow-up was 2 years. Diabetes (OR 3.29, 1.28-8.50, p=0.014), history of stroke (OR 6.11, 1.21-31.00, p=0.029), changes of terminal part of ventricular complex on ECG, recorded during acute phase of ischemic heart disease (OR 2.19, 1.01-4.57, p=0.046), and genotype II of polymorphic marker ID of apoB gene (OR 2.20, 1.06-4.57, p=0.027) were independent predictors of unfavorable course of ischemic heart disease. Thus genetic factors play a role not only in formation of coronary atherosclerosis but determine the course of ischemic heart disease.

Angina, Unstable↗
PubMed2003

[Polymorphic markers I/D and G7831A of angiotensin-I-converting enzyme gene and left ventricular hypertrophy in patients with essential hypertension].

AIM: To elucidate possible association of angiotensin-I-converting enzyme (ACE) gene polymorphic markers I/D and G7831A with left ventricular hypertrophy (LVH) in patients with essential hypertension. MATERIAL: Patients with essential hypertension (n=123, 37 with and 86 without LVH, mean age 59.15+/-1.19 years). METHODS: Left ventricular (LV) mass was determined echocardiographically by Devereux method. Alleles and genotypes of ACE gene polymorphic markers were identified by polymerase chain reaction. RESULTS AND CONCLUSION: There was no association between I/D marker of ACE gene and LVH. Carriers of A allele compared with carriers of G allele of G7831A marker had significantly higher LV mass (284.1+/-10.20 g, and 248.5+/-14.42 g, respectively, p=0.033) and LV mass index (151.7+/-5.23 g/m2 and 131.0+/-6.74 g/m2, respectively; p=0.02). Among patients with LVH frequency of A allele was significantly higher than among patients without LVH (0.401 and 0.230, respectively; p=0.0065, OR=2.116 [1.197-3.7481]). Using binary logistic regression model we have found that presence of LVH was linked with age, sex and maximal systolic blood pressure (BP). Such factors as smoking, maximal diastolic BP, ordinary systolic and diastolic BP, duration of hypertension, coronary artery disease and diabetes were not related to LV mass index. Using multifactorial logistic regression model we have found that the presence of A allele of G7831A polymorphic marker of ACE gene, age and maximal systolic BP could be considered as independent risk factors of LVH.

Age Factors↗
PubMed2003

[Hereditary factors and left ventricular hypertrophy].

Left ventricular hypertrophy (LVH) is an independent risk factor for morbidity and mortality from cardiovascular disease in men and women with hypertension and in asymptomatic subjects with normal blood pressure. In hypertensive patients it is a stronger coronary risk factor than casual blood pressure readings. Correlation between levels of high blood pressure, duration of hypertension and left ventricular mass is poor. Epidemiological studies suggest that left ventricular hypertrophy may be influenced by genetic factors. In our review we present study groups of genes contributing to the development of left ventricular hypertrophy: 1) genes that encode components of hormonal pathways, 2) genes of key sympathetic and parasympathetic receptors, 3) genes that modify intracellular ion homeostasis, 4) genes that modify energy metabolism, 5) genes that modify motor unit composition and regulation. Angiotensinogen gene, angiotensin-converting enzyme gene, angiotensin receptor type 1 gene, aldosterone synthase gene, nitric oxide synthase gene, type A natriuretic peptide receptor gene, beta(2)-adrenergic receptor gene, G-protein beta(3) subunit gene are associated with left ventricular hypertrophy.

Angiotensinogen↗
PubMed2003

[Endothelin receptor blockers--one more agent for the treatment of pulmonary hypertension].

Data on participation of derangements of pulmonary vessel endothelial function in pathogenesis of pulmonary hypertension served as basis for therapeutic use of prostanoids, sildenafil, and endothelin(ET) receptor blockers. A first representative of the latter group - bosentan (nonselective ET-receptor antagonist) has been recently registered as an agent for the treatment of pulmonary hypertension. Bosentan and other ET receptor antagonists has been studied in several trials. Results of these trials are reviewed in this paper which also contains characteristics of main representatives of ET receptor antagonists as well as information on their tolerability and major side effects.

Antihypertensive Agents↗
PubMed2003

[Tissue plasminogen activator and plasminogen activator inhibitor gene polymorphisms: possible relation to atherosclerosis and its complications].

In the present review the dates about association of genetic variants of a plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator (tPA) with ischemic heart disease and atherosclerosis of other localization are toted. The singularities of synthesis of PAI-1 and tPA, possible paths of regulation of their activity briefly surveyed. Known polymorphisms of PAI-1 gene and tPA gene, their localization, frequencies in different ethnic groups are circumscribed. In operation the genetic influence of polymorphisms of PAI-1 gene and tPA gene on synthesis and plasma concentration of PAI-1 and tPA, including under an operation of risk factors of atherosclerosis, and as possible clinical consequences of sectional violations is featured. In the review the possible role of polymorphisms of PAI-1 gene and tPA gene in a pathogenesis of atherosclerosis, association with hazard thrombotic complications for different diseases is considered. Many clinical examinations are circumscribed which have confirmed or not confirmed a possible connection of genetic markers with development and current of ischemic heart disease and other vascular diseases. We considered that there are no enough dates to one valued estimation of possible role of polymorphisms of PAI-1 and tPA genes in pathogenesis of atherosclerosis. It is necessary to get new genetic studies in groups of patient with high risk of ischemic heart disease and atherosclerosis.

Arteriosclerosis↗
PubMed2003

[Genetic predictors of left ventricular hypertrophy: do polymorphisms of peroxisome proliferator activated nuclear receptor genes play any role?].

AIM: To assess possible associations of polymorphic markers of PPARA and PPARG2 genes with presence of left ventricular hypertrophy (LVH) in patients with hypertension. MATERIAL: Patients with hypertension (n=163, mean age 60.93+/-0.82 years) with (n=110) and without (n=53) LVH. METHODS: Echocardiography was used for evaluation of left ventricular mass and mass index and polymerase chain reaction - for identification of alleles and genotypes of polymorphic markers of ACE, NOS3, PPARA, PPARG2 genes. RESULTS AND CONCLUSION: There was no association between presence of LVH and polymorphic marker Pro12AIa. Carriers of 4a allele of a polymorphic marker ecNOS4a/4b of NOS3 gene, A allale of a polymorphic marker G7831A of ACE gene, and C allele of PPARA gene had significantly greater left ventricular myocardial mass index. Monofactorial regression analysis showed that degree of LVH was significantly related to age, duration of hypertension, maximal systolic blood pressure. No relationship was found between left ventricular mass index and smoking, maximal diastolic blood pressure, habitual systolic and diastolic blood pressure, duration of hypertension, presence of ischemic heart disease, diabetes. According to results of multifactorial analysis A allele of a polymorphic marker G7831A of ACE gene, age and maximal systolic blood pressure were while C allele of PPARA gene was not independently related to the presence of LVH.

Female↗
PubMed2003

[Peroxisome proliferator activated nuclear receptors: possible role in the development of atherosclerosis].

Peroxisome proliferator activated nuclear receptors (PPAR) belong to steroid receptors and are represented by 3 types: PPAR alpha, PPAR beta, PPAR gamma. PPAR alpha is a key regulator of fatty acid beta-oxidation, participates in development of inflammatory reaction and atherosclerosis formation. Main effects of fibrates are mediated through PPAR alpha activation. PPAR gamma plays important role in lipid metabolism, processes of cell differentiation and growth, participates in glucose utilization and mechanisms of insulin resistance. Specific activators of PPAR gamma are glytazones--a group of antidiabetic drugs. The role of PPAR beta in atherosclerosis formation has not been elucidated yet however results of some studies indicate participation of this receptor in atherosclerosis. Data of studies devoted to the role of PPARs and polymorphic markers of these receptors in the process of atherosclerosis are reviewed.

Animals↗