New opportunities for identifying the risk of cardiovascular events in young people: the role of familial hypercholesterolemia

A search was made for publications on modern methods for determining cardiovascular risk in young people with positive family history for early cardiovascular events. The use of various screening options allows timely identification of patients with heterozygous familial hypercholesterolemia who have a high cardiovascular risk. The most effective method is cascade screening. Cardiovascular risk assessment systems that include a family history of early cardiovascular events and lipid profiles in individuals under 40 years of age provide prevention of atherosclerosis. In the diagnosis of risk, the lipoprotein (a) is of particular clinical importance, elevated concentrations of which are associated with a high risk of vascular damage and an unfavorable course of atherosclerosis

ВЫЯВЛЕНИЕ И ДИСПАНСЕРНОЕ НАБЛЮДЕНИЕ ДЕТЕЙ С СИНДРОМОМ УДЛИНЕННОГО ИНТЕРВАЛА QT

Aim To assess the diagnostic accuracy of long QT syndrome in children and to estimate the results of the follow-up.Methods High-risk groups of children with bradycardia less than the second percentile and/or a family history of sudden death syndrome, and children with syncope diagnosed with the ECG testing were included in the study. All patients underwent routine medical examination, molecular genetic testing and were followed-up for 3,5–10 years.Results The majority of children haves transient corrected QT prolongation secondary to therapy, requiring ECG monitoring. High-risk group screening reports higher rates of idiopathic LQTS. ECG testing shows its efficiency among asymptomatic children with a normal heart rate. Patients present with syncope at the outpatient settings require the exclusion of a wide range of diseases, both congenital and acquired heart disease. The clinical status of the examined patients does not always correspond to the known LQTS variants. Molecular genetic analysis provides relevant information on the genetic heterogeneity of the disease, including new mutations, both pathological and beneficial ones.Conclusion Regardless of the presence or absence of molecular genetic confirmation of LQTS, beta blocker therapy in some cases combined with implanted cardioverterdefibrillator prevents the development of the adverse events in the long-term period and ensures normal emotional, intellectual and physical development.Цель Изучить эффективность диагностики синдрома удлиненного интервала QT (СУИQT) у детей и результаты наблюдения детей по данным катамнеза.Материалы и методы Проведено обследование детей двух групп риска – новорожденных с брадикардией менее 2 перцентиля и семейным анамнезом внезапной смерти, и детей с синкопе с помощью ЭКГ-скрининга, комплексного обследования выделенных групп, и наблюдение детей в течение 3,5–10 лет .Результаты Установлено, что в периоде новорожденности значительная часть детей имеет преходящее вторичное удлинение корригированного QT, что требует ЭКГ-контроля после лечения. Обследование детей из групп риска имеет большую вероятность выявления пациентов с идиопатическим СУИQT, тогда как у бессимптомных детей с нормальной частотой сердечного ритма выявление больных возможно только при проведении ЭКГ-скрининга. У пациентов с синкопе на амбулаторном этапе обследования необходимо исключение широкого спектра заболеваний, включая врожденные и приобретенные болезни сердца. Клинический статус наблюдаемых больных не всегда соответствует известным вариантам СУИQT.Заключение Независимо от наличия или отсутствия молекулярно-генетического подтверждения диагноза терапия бета-адреноблокаторами, и в ряде случаев ее сочетание в комбинации с имплантированным кардиовертером-дефибриллятором обеспечивает в течение длительного времени клиническую стабильность пациентов, удовлетворительные темпы эмоционального, интеллектуального и физического развития, предотвращает развитие сердечных событий с неблагоприятным исходом

Structural and Histochemical Changes in Rat Parietal Cortex Neurons during Biliary Drainage

brain, parietal cortex, neurons, structure and metabolism, bile loss.The aim of the study reported here was to assess structural and metabolic changes in rat parietal cortex neurons during complete external bile drainage. Quantitative histochemical and electron microscopic methods were used. The findings showed that drainage of bile from the body led to gradual increases in the numbers of hyperchromic pyknotic neurons and ghost cells, death and reductions in the numbers of neurons, and increases in the number of glial cells in all layers of the parietal cortex. There was a gradual decrease in neuron size, with loss of sphericity (elongation). The cytoplasm showed decreases in succinate dehydrogenase, NADH, NADPH, and glucose-6-phosphate dehydrogenases, and decreases in RNA content, though these changes were accompanied by activation of lactate dehydrogenase and acid phosphatase. Nuclei and organelles (mitochondria, endoplasmic reticulum, Golgi complexes) underwent destructive changes, which were accompanied by increase in the numbers and sizes of lysosomes and phagosomes. Some neurons showed activation of the nuclear apparatus and increases in the relative content of free ribosomes. Thus, loss of bile from the body induced progressive increases in structural and metabolic changes in parietal cortex neurons, leading to the death of some and compensatory changes in others

Bile loss damages the cerebellar Purkinje cells in rats

cerebellum, Purkinje cells, structure, cytochemistry, loss of bileAim: The aim of the study was the estimation of the structural and metabolic changes in cerebellar Purkinje cells of rats during the complete outside bile abduction. Material and methods: Experiments were performed on male Wistar rats weighing 200-250 g. In 26 rats the fistula of the common bile duct was made and all the bile secreted by the liver was collected through a plastic tube into the outside glass bile container. 20 animals of the control group underwent sham operation (no removal of bile). On the 1th, 3th, and 5th days after the operation the animals of the control and experimental groups were decapitated and cerebellum cortex samples were collected for histology and cytochemistry. Results: The loss of bile induced the gradual increase in structural and metabolic abnormalities of Purkinje cells resulting in severe, irreversible disturbances and even death of some of them. The gradual decrease in Purkinje cells size, the loss of their sphericity and elongation, followed by inhibition of succinate-, NADH-, glucose-6-phosphate-dehydrogenases and the activation of lactate dehydrogenase and the marker enzyme of lysosomes acid phosphatase were revealed. All the changes reflect the ratio of the processes of damage and adaptation in the affected neurons in bile absence in the body. Conclusion: Total loss of bile (on the 1st, 3rd, and 5th days) induces the gradual increase in structural and metabolic disturbances in cerebellum Purkinje cells and death of some of them

Metabolic changes in rat brain histaminergic neurons during subhepatic cholestasis

brain, histaminergic neurons, histochemistry, subhepatic cholestasis.The aim of the present work was to assess metabolic changes in histaminergic neurons in the rat brain during subhepatic cholestasis. Studies were performed on male Wistar rats using quantitative histochemical methods. The results showed that in cholestasis, histaminergic neurons in the rat hypothalamus developed significant changes in succinate dehydrogenase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase activity, in NADH and NADPH, and in acid phosphatase and monoamine oxidase B. These changes depended on the duration of cholestasis and had a dynamic, wave-like nature. The changes were apparent after five days of cholestasis, reached a maximum at 10-20 days, decreased at 45 days, and completely disappeared at 90 days

Structural-metabolic changes in histaminergic neurons of the rat hypothalamus in conditions of loss of bile

brain, histaminergic neurons, morphometry, histochemistry, bile.The aim of the present work was to evaluate structural and metabolic changes in histaminergic neurons in hypothalamic nucleus E2 in rats in conditions of complete external drainage of bile. Studies were performed on male Wistar rats (n = 45). Controls consisted of animals subjected to sham surgery with preservation of physiological bile flow throughout the experiment. Quantitative histological and histochemical methods were used. Serial frontal cryostat sections cut from the posterior hypothalamus were used for detection of the activity of the following enzymes: monoamine oxidase B, succinate dehydrogenase. NADH dehydrogenase, NADPH dehydrogenase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase, and acid phosphatase. Morphological studies of histaminergic neurons were performed on preparations stained with thionine. These studies showed that complete external drainage of bile led to transient size reductions and rounding of cell perikarya. Metabolic changes were seen within a day of bile loss and subsequently progressed. All energy metabolic pathways were suppressed and acid phosphatase activity was increased on day 5