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Biomedical subjects

S N Tereshchenko

Publications and source records attributed to S N Tereshchenko.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Polymorphism of vascular angiotensin II receptor gene and cardiovascular disorders].

AIM: To study polymorphism of the gene of vascular angiotensin II receptor. MATERIALS AND METHODS: Polymorphism that consists in variability of adenine (A) and cytosine (C) residues at position 1166 of the gene for vascular angiotensin II receptor (AT1R) was analyzed in a Moscow population (n = 98) and three groups of affected patients with myocardial infarction (n = 32, MI), left ventricular hypertrophy (LVH, n = 38) and essential hypertension (EH, n = 178). Polymorphic region of the AT1R gene was amplified using the polymerase chain reaction (PCR) and genomic DNAs from human whole blood as template. PCR products were electrophoresied in a gel after digestion with BstDEI restriction nuclease. Significance of differences in distribution of both allele and genotype frequencies at the population sample and in affected patients were estimated via exact Fisher's test. RESULTS: A significant decrease in the frequency of the A genotype was detected in all the three affected groups compared to healthy controls. Besides, the frequency of the A allele was significantly decreased in EH group with a corresponding increase in the frequency of both the AC genotype and the C allele. CONCLUSION: The A1166C polymorphism of the AT1R gene is associated with EH, MI and LVH in a Moscow population. The association is stronger with EH. The A allele and the AA genotype protect against development of disorders at early onset while the other genotypes and the C-allele are risk factors. A protective role of the AA genotype is more significant than predisposition action of the CC homozygote.

Alleles↗
PubMed2000

[Level of blood uric acid in patients with postinfarction heart failure].

AIM: To evaluate uric acid (UA) levels in patients with postinfarction chronic cardiac failure (CCF) and to investigate correlation between accumulation of uric acid, CCF severity and some other parameters. MATERIAL AND METHODS: UA levels were determined with enzyme immunoassay and acid-base status of capillary and venous blood was studied in 120 men 35-78 years of age (mean age 46.3 +/- 1.8 years) with CCF of NYHA functional class (FC) I-IV. CCF was caused by Q-wave myocardial infarction in all the patients. RESULTS: It was found that a close direct relationship exists between FC of CCF and UA content (r = 0.735, p < 0.001), FC of CCF and creatinine levels (r = 0.648, p < 0.001). Analysis of acid-base condition shows the existence of compensated gas acidosis in CCF patients. Acid-base changes were more prominent in FC III and IV. FC and gas acidosis directly correlated. CONCLUSION: In CCF there is a pathogenetic relation between high uric acid and hypoxia. However, further studies are necessary of the causes of UC rise in CCF and its influence on the severity of circulatory insufficiency.

Acid-Base Equilibrium↗
PubMed1999

[Clinico-statistical analysis of chronic cardiac failure].

AIM: To analyse epidemiologically chronic heart failure (CHF) according to 1996 records for patients admitted to therapeutic and cardiological departments of Moscow city hospital N 64. MATERIALS AND METHODS: An individual sheet has been developed for computer. The statistical processing has been conducted according to Access 97 program. It has covered 4019 case histories for 1996. 1232 patients were hospitalized for chronic cardiac failure this making 30.6% of all the hospitalizations. RESULTS: CHF was encounted in 60.9% of females and 39.1% of males. It was due to: ischemic heart disease (63.7%, with myocardial infarction in 73%), hypertension (17.5%), valvular disease (13.7%), dilated cardiomyopathy (3.7%), myocarditides and perocarditis (1.4%). Age groups 30-39 years, 40-49, 50-59, 60-69, 70-79, 80-89, 90-99 consisted of 0.6, 4, 11, 35.2, 31.4, 16.9, 0.6% of patients respectively. Females prevailed in the oldest age groups. The time from CHF diagnosis was 2, 3, 4, 5, 6, 7, 8, 9 and > 10 years in 26, 10.9, 4, 5.7, 0.9, 1.4, 1.7, 0.6 and 4% of patients, respectively. 72.9% of patients were admitted to hospital once a year. 19.7%, 5.2%, 0.9%, 0.6%, 0.9% of patients were hospitalized 2, 3, 4, 5 and more than 6 times, respectively. CHF was responsible for 50(27.8%) lethal outcomes of 180. Lethality resulted from cardiovascular insufficiency (50%), thromboembolism (30%), pneumonia (10%). CONCLUSION: CHF is a frequent cause of hospitalizations. Development of CHF, lethality, age groups distribution are closely associated with the patients' gender.

Adult↗
PubMed1999

[Polymorphism of GPIIIA platelet glycoprotein gene PIA1/A2 compared to plasma hemostasis in myocardial infarction patients].

AIM: To investigate gene PIA1/A2 polymorphism and some parameters of plasma hemostasis in postmyocardial infarction (PMI) patients with chronic cardiac failure (CCF). MATERIALS AND METHODS: A total of 58 PMI patients with CCF, pulmonary artery thromboembolism (PATE), phlebothrombosis (PT) were examined. The age of the patients ranged from 24 to 84 years. Polymorphism of platelet glycoprotein GPIIIa gene was assessed according to the standard PCR-RFLP. RESULTS: Occurrence of genotypes PIA1/A2, PIA1/A2 was 70.8 and 29.2%, respectively; of allele PIA1 and PIA2 84.5 and 15.5%, respectively. In PMI patients genotype PIA1/A1 occurred in 71.7% of cases, genotype PIA1/A2--in 28.3%. Incidence of alleles was: 84.0% (PIA1), 16.0% (PIA2). PATE patients had genotype PIA1/A1, PT patients had distribution of the genotypes 50.0% and 50.0%, respectively. In patients who had suffered MI at the age under 45 years prevalence of the genotypes was 63.2% PIA1A1, 36.8% PIA1A2, of alleles 83.6% PIA1, 16.4% PIA2. In patients with a history of MI at the age over 50 the incidence of the genotypes and alleles was, respectively, 75.0% PIA1A1, 25.0% PIA1A2, 87.7% PIA1, 12.3% PIA2. Patients with genotype PIA1/A2 had a significantly higher fibrinogen than PIA1A1. Concentration of soluble fibrin monomeric complex was higher in patients with genotype PIA1/A2 reflecting activation of intravascular clotting. AT-III decrease by 5.4% indicated lower anticoagulant activity in patients with genotype PIA1A2. CONCLUSION: In patients with MI at the age under 45 years gene PIA1A2 and allel PIA2 occurred more frequently than in patients who had MI at older age. Allele PIA2 was associated with the risk of MI onset at young age. It is suggested that patients with genotype PIA1/A2 are at higher risk of thrombotic conditions, of coronary artery thrombosis in particular, than patients with genotype PIA1/A1.

Adult↗
PubMed1998

[Plasma hemostasis and biochemical indices in trimetazidine treatment of patients with chronic heart failure].

AIM: This study of trimetasidine effects on plasmic hemostasis and blood biochemistry in patients with chronic heart failure (CCF) of NYHA functional class II-III. MATERIALS AND METHODS: This study enrolled 30 patients (24 males and 6 females) aged 40-72 years with class II-III CCF, postinfarction cardiosclerosis and ejection fraction under 40%. Previously the patients received perindopril (the inhibitor of angiotensin converting enzyme) in daily dose 2-4 mg, on-demand digoxin and diuretics. Trimetasidine was given in a daily dose 60 mg for 6 months. Before and after the treatment the patients' blood was examined for: levels of factors VII and X of antithrombin III coagulation, soluble fibrinomonomeric complexes (SFMC), fibrinogen, glucose, uric acid, creatinines, total cholesterol, high density lipoprotein, triglycerides, AST, ALT, LDH, acid phosphotase, gamma-GT, sodium, potassium, activated partial thrombin time. RESULTS: Initially, the patients had a 23.9% increase in the levels of factors VII and X, a 14.3% decrease of antithrombin III, 29.8 and 227.6% rise in concentrations of fibrinogen and SFMC, respectively, compared to controls. Aftertreatment values of fibrinogen, factors VII and X, SFMC fell by 21.1, 17 and 35.5%, respectively. The thrombin time arose by 17.9% (p > 0.05). Insignificant inhibition was registered in the activity of acid phosphotase and gamma-GT. Glucose, AST, ALT, LDH levels remained unchanged. Plasma creatinine tended to lowering. Total cholesterol insignificantly increased at high levels of HDL cholesterol (p > 0.05) and reduced levels of triglycerides (p > 0.05). CONCLUSIONS: Trimetasidine therapy, given after conventional treatment with diuretics, digoxin, inhibitor of angiotensin-converting enzyme, aspirin has a beneficial effect in patients with circulatory deficiency through improving hemostatic and biochemical parameters.

Acid Phosphatase↗
PubMed1997

[The polymorphism of the angiotensin-converting enzyme gene in patients with hypertension, left ventricular hypertrophy and the development of a myocardial infarct at a young age. Preliminary report].

Insertion/deletion (I/D) polymorphism of angiotensin-I-converting enzyme (ACE) gene was studied by use of the polymerase chain reaction in 168 normal subjects living in Moscow region and in 70 patients: 38 with essential hypertension (EH), 9 of which survived myocardial infarction at young age, 13 with hypertrophic cardiomyopathy (HCMP) and 19 with myocardial infarction (MI). Left ventricular hypertrophy (LVH) was detected in 24 of 38 EH patients. There was a highly significant increase in the frequency of the ID genotype in EH patients compared to the controls (62.4% versus 32.7%, P < 0.01). There was a relevant decrease in the frequency of the DD genotype in EH patients in comparison with the control (20.8% versus 47.6%, P < 0.05). These results strongly suggest that the ACE gene is associated with EH. No significant differences in both allele and genotype frequencies of the ACE gene were revealed in two groups of patients with MI and with HCMP compared to the controls. Thus, no relations between the ACE gene and these disorders were observed. In hypertensives with MI the II genotype was not detected and the frequency of both D allele and DD genotype was sufficiently increased compared to normotensive patients with MI. Thus, the DD genotype in hypertensives may be a risk factor for MI. The frequency of the DD genotype was significantly increased in hypertensive patients with LVH compared to the uncomplicated hypertension (37.5% versus 7.1%, P < 0.05). Therefore, this genotype is associated with LVH in hypertensive subjects.

Adult↗
PubMed1997

[The angiotensin-converting enzyme inhibitor perindopril in the treatment of congestive heart failure].

The efficacy of perindopril in congestive heart failure (CHF) class II-III (NYHA) was studied in a trial including 37 patients (35 males and 2 females) aged 39-71 years (mean age 57.9 +/- 1.4) with postinfarction cardiosclerosis. They had CHF class II-III and ejection fraction (EF) < 45%. Perindopril was given in a single daily dose 2-4 mg for 6 months. The treatment resulted in a significant lowering of CHF class (from 2.5 +/- 0.1 to 1.7 +/- 0.1 (p < 0.01). Exercise tolerance increased from 256.2 +/- 18.6 s to 349.8 +/- 27.0 s (p < 0.05). Pump and contractile functions of the myocardium improved: stroke volume increased by 12.7%, ejection fraction by 20.5%, total peripheral vascular resistance fell by 9.7%, circulating blood volume by 9.2%. Parameters of oxygen transport to tissues and tissue respiration also changed for the better. The authors state high efficacy of perindopril in CHF patients.

Adult↗
PubMed1997

[Change of circadian pattern of arterial pressure in patients with congestive heart failure treated with perindopril, an inhibitor of angiotensin-converting enzyme (ACE)].

The 24-h profile of blood pressure (BP) was studied in 28 patients (21 males and 7 females) with congenital heart failure (CHF) of NYHA class II-III (ejection fraction < 45%). The patients were 46 to 76 years of age and had postinfarction cardiosclerosis. They had not received ACE inhibitors before. Two groups were formed basing on the presence of hypertension. Perindopril was administered in a single daily dose of 2 mg or higher if demanded to reduce symptoms of CHF and/or to normalize BP. The treatment continued for 3 months. The 24-h BP profile was assessed using portable device SpaceLabs 90207 (USA). In CHF patients with hypertension perindopril significantly lowered mean 24-h, day and night BP and its loads, reestablished two-phase circadian rhythm of AP and corrected BP variability. In CHF patients free of hypertension significant changes of the profile were not registered. It is evident that unwanted changes in the BP 24-h profile due to perindopril were absent in CHF normotensives.

Aged↗
PubMed1991

[Comparison of the clinical and hemodynamic effects of nitroglycerin, isosorbide dinitrate and isosorbide-5-mononitrate in acute myocardial infarction].

One hundred and eighty patients with acute myocardial infarction (MI) were followed up. The patients were divided into 3 groups: (1) those receiving glyceryl trinitrate (GTN) (n = 43); (2) those on isosorbide dinitrate (ISDN) (n = 66); (3) those on isosorbide-5-mononitrate (IS-5-MN) (n = 71). In all the groups, the drugs were given by long-term continuous oligovolumic infusion. Following 24 hours of administration, 66.7, 47.3, and 17.1% increases in infusion rates were required in 74.4, 72.7, and 26.8% of the patients from Groups 1, 2, and 3, respectively. All the agents produced a pronounced antianginal effect and resulted in alleviated acute left ventricular failure. The in-hospital mortality rates were 16.2, 16.7, and 12.7% in Groups 1, 2, and 3, respectively. GTN, ISDN, and IS-5-MN caused adverse effects in 4.7, 18.2, and 2.8% of the patients from Groups 1, 2, and 3, respectively.

Adult↗