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1.
Mongolian Medical Sciences ; : 52-59, 2017.
Article in English | WPRIM | ID: wpr-975633

ABSTRACT

@#Article deals with age-related hypogonadism in men as an interdisciplinary problem. Current definition, prevalence, analyzes the relationship between age and the incidents of hypogonadism were shown. The detailed overview of clinical studies, meta analysis of causal link of androgen deficiency and erectile dysfunction, ischemic heart disease, arterial hypertension, dyslipidemia, and diabetes mellitus was presented. To date was found the relationship between metabolic syndrome and androgen deficiency. Low level of testosterone is closely connected with low libido as well as insulin resistance, abdominal obesity, dyslipidemia. Insulin resistance and hyperinsulinemia are noticed in patients with hypogonadism in comparison with obese and normal-weight patients. Therefore, metabolic risk factors are the connecting link of cardiovascular diseases and androgen deficiency. Meta-analysis of clinical trials of the effects of testosterone replacement therapy and safety of long term use was presented in the article. The article discusses the importance of a unified approach to the diagnosis and treatment of androgen-deficient conditions and cardiovascular disease.

2.
Mongolian Medical Sciences ; : 35-38, 2014.
Article in English | WPRIM | ID: wpr-975693

ABSTRACT

Background: Atrial septal defect (ASD) repair surgery is the most common open heart surgery. In last5 years, a total of 729 patients underwent in open heart surgery, whereas 561 patients (76.95%) hadcongenital heart disease (CHD), its 284 patients (50.6%) had ASD.Objective: To describe approach of cardiopulmonary bypass (CPB) in surgery of common ASD.Methods: We analyzed condition and process of CPB in ASD repair surgery (Department ofCardiovascular Surgery, Shastin Central Hospital of Mongolia) in 118 patients who had undergonegenetic testing in Research Center of Leipzig and Halle, Germany and Mongolian Academy of MedicalSciences. This has been found to be adequate for the routine open heart case, flow rates of 2.6-3.5 l/m2/min. The perfusionist should record the flow rate, arterial blood pressure, gas flow rate, temperature andtime regularly every 5, 10, 20, 30 minutes during bypass or when one of these parameters in changed.The beginning of bypass an activated clothing time (ACT) may be performed at the pump side to determineanticoagulation status. With clotting times below 300 sec additional heparin should be administrateddepending on the stage of the operative procedure.Results: The process of extracorporeal circulation of ASD repair surgery was observed in 118 patientswho underwent in genetic testing. There were 32.2% (38) males and 67.8% (80) females. Mean agewere 22.3±12.9 and mean body weight were 70kg. O2 consumption was 240 ml/min and CO2 productionwas 196 ml/min. In the beginning of surgery mean blood pressure were 92±5 mmHg and 58 mmHg afterthe dissection of major vessels. It is associated with a decrease of venous return to heart and cardiacoutput. After 30 minutes of CPB, blood pressure was 63 mmHg. During CPB, metabolic acidosis isalways a result of inadequate perfusion. Although the acid-base status may be immediately correctedby the administration of bicarbonate the abnormal process leading to the metabolic acidosis is notcorrected until perfusion becomes adequate. The best corrective measure is therefore to take whateversteps necessary in order to increase perfusion.Conclusion:1. Perfusion measurement of the chosen cases was measured in the level of international expertise.2. Hemodynamic aberrations were observed in the beginning of CPB, which demonstrates arequirement for increasing the pump flow rate of the machine (2.6-3.5 l/m2/min).3. Due to the fact that ASD repair surgery lasts for short period, CPB can be done in 320C of bodytemperature. Hence there is no need of hemoconcentration.

3.
Mongolian Medical Sciences ; : 18-24, 2014.
Article in English | WPRIM | ID: wpr-975488

ABSTRACT

BACKGROUND:Congenital heart defects (CHD) turn out to be the leading cause of infant mortality in their first yearafter infectious diseases. Per 1,000 infants, born with CHD, about 19-75 failed to survive. It revealsthe fact that CHD is a major cause of childhood mortality in worldwide. Beyond the progress ofmedicine and surgery, the cause of CHD is not fully defined. The majority of studies reveal that CHDis triggered by many factors, such as the genetic and environmental factors.Based on the evidences of the sequence of the human genome and advances in moleculartechnology, genetic factors play a major role. Per 100 newborninfants, they’re found one child, bornwith a CHD is concerned as a highly frequent incident for birth anomaly. Only 0.5% of these congenitaldefects enable to be inherited in accordance with Mendel’s genetic laws, which is associated withthe change and mutation of a single gene. Many found that most congenital anomalies dependupon mutation or change in multiple genes and other relevant factors. As a result of the progressivedevelopment of molecular biology in the past 20 years discovered a range of genes involved in fetusformation, development, growth and control of processes. In our country case, corrective surgeryfor CHD dominates among all cardiovascular surgery in Mongolia. Particularly, for all incidents donesome corrective surgery of congenital heart defects, atrial septal defect operation occupies 42.44%,in other word it is a substantial part of the CHDoperation (D.Tsegeenjav, 2009). Molecular geneticsstudy of infant born with heart defects and simultaneous anomaly of other organ system researchstill has not been done for Mongolian population. In many cases the diagnosis of CHD is delayeduntil their adulthood, which is a research gap to address without further delay and the finding mustbe applied in practice in the near future.GOAL:The aim of the research is to conduct a molecular genetic study of children, born with CHD andcombined abnormalities of other organs and systems, identify gene lesion, location and characteristicsof mutations, pathogenetic mechanism of congenital defects and anomalies among the Mongolianpopulation.RESULT:For this study, there are 118 patients, with congenital heart disease, received surgical treatmentin the cardiovascular department of III central state hospital named P.N. Shastin, involved afterconfirmed diagnosis through objective and instrumental investigations (ECG, Fluoroscopy, EchoKG).The 118 healthy family members of patients sampled as a control group. According to the diagnosisof patients with congenital heart defect, such as atrial septal defects-95 (81.2% ± 3.6), ventricularseptal defects-17 (14.5% ± 3.3), patent ductusarteriosus- 2 (1.7± 0 .0%) have combined severedefects - 4 (3.3% ± 1.0). Out of 118 patients with congenital heart defects, 32.2% (38 patients)was male, whereas women accounted for 67.8% (80 patients) with average age of 22, 3 ± 12.9(minimum 1.0 year, maximum 51 year). These comprised 42.4% in 1-17 years old (average age10 ± 5.27) and 57.6% in 18-51 years old (average age 31 ± 9.54). The 33.9% ± 4.4 (40 patients) of operated patients responded the questionnaire that they have a hereditary heart defect. Shortnessof breath, heart pain, and recurrent pneumonia were the main complaints of patients with CHDthat significantly authentic to statistical probability. From the taken 118 blood samples, 95 werediagnosed ASD, in 7 diagnosed VSD, in 2 diagnosed PDA, in 4 diagnosed combined defects. Forthe 95 samples, we decided to examine the ASD associated GATA4, TBX5gene. It draws attentionto the fact that 81.2% of all congenital heart defects found only ASD. To examine the ASD genes inthe sample, the following changes have occurred. The study found 8 variants of mutations formingASD. It includes on exon 1 Gly 93 Ala (c.278G> C), on exon 1 P163S (c.487C>T).CONCLUSIONS:1. Patients with ASD alone occupy 81,2% of all heart defects in our study.2. For the samples of ASD, the study found 8 different mutations of GATA4.3. In the sample of blood not found TBX5 gene mutation.4. In the samples, one patient with dextrocardiasitusinvertus was combined with congenital heartdefects found E359Xfs (c.1075delG) deletion variation on exon3.

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