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Laptev D.N.,Endocrinology Research Center | Ryabykina G.V.,Russian Cardiology Research and Production Center
Diabetes Mellitus | Year: 2013

Aim. To determine the effects of hypoglycemia on the duration of QT interval, heart rate variability (HRV) and frequency of arrhythmic events, as well as to closer investigate the factors associated with the development of various heart rhythm disorders in children and adolescents with type 1 diabetes mellitus (T1DM). Materials and methods. The study included 150 children and adolescents with T1DM at the age of 6-18 years. All participants underwent Holter monitoring and continuous glucose monitoring (CGM) for 24 hours. QTc and HRV parameters (SDNN, RMSSD, SVVR) were calculated automatically. Data was averaged for 5'-interval and juxtaposed with CGM. Patients identified with hypoglycemic events (blood glucose <3.5 mmol/L) during the day (7:00-23:00) and nighttime (23:00-7:00) were selected for further study. In these patients length of QTc and RR intervals, HRV parameters and arrhythmic events were analyzed and collated with CGM data. Results. We observed 39 episodes of nocturnal hypoglycaemia in 32 patients (21.3%) and 89 episodes of daytime hypoglycaemia in 46 patients (30.7%). Marked prolongation of QTc (hypo- vs. normoglycemia, respectively: 431 vs. 420 ms; p<0.05) and reduced HRV (hypo- vs. normoglycemia, respectively: SDNN 68 and 90 ms; RMSSD 56 and 61 ms; p <0.05) occurred during episodes of nocturnal hypoglycemia. The same pattern was observed during the day (hypo- vs. normoglycemia, respectively: SDNN 58 and 63 ms; RMSSD 32 and 36 ms; p<0.05). Eleven subjects with nocturnal hypoglycemia demonstrated either ventricular or supraventricular premature complexes. Thirty of subjects with diurnal hypoglycemia also had either ventricular or supraventricular premature complexes. Hypoglycemic episodes vs. normoglycemia were characterized by an increase in ventricular and supraventricular ectopic beats, ST segment and T-wave amplitude depression. Various rhythm abnormalities were associated with cardiovascular autonomic and peripheral neuropathy. Conclusion. During episodes of hypoglycemia, HRV parameters decrease, QT elongates and episodes of arrhythmia occur more frequently. History of autonomic and peripheral neuropathy contributes to the development of arrhythmias. Source


Penkov D.N.,Russian Cardiology Research and Production Center | Egorov A.D.,Moscow State University | Mozgovaya M.N.,Moscow State University | Tkachuk V.A.,Moscow State University
Biochemistry (Moscow) | Year: 2013

Insulin stimulates carbohydrate uptake by cells and induces their conversion into lipids as a more efficient form of energy storage. Insulin resistance is associated with a decrease in glucose uptake by muscle and adipose cells and also with a decrease in glycogen synthesis on retention of glucose synthesis by liver cells. Disorders in the insulin signaling cascade on development of insulin resistance can be caused by both changes in functioning of transcriptional factors and in the secretion profile of hormone-like substances. Diacylglycerols and ceramides responsible for activation of some kinases and phosphatases can directly trigger these changes in muscle and liver cells. In adipose tissue, insulin mainly stimulates adipogenesis (adipocyte differentiation) and lipogenesis (lipid accumulation in the cells). Thus, studies on the action mechanisms of factors influencing adipogenesis can be of help for understanding the molecular mechanisms of insulin resistance. © 2013 Pleiades Publishing, Ltd. Source


Titov V.N.,Russian Cardiology Research and Production Center
Voprosy Pitaniia | Year: 2012

Fatty acids (FA), keep in food and organisms divide on FA as saturated which have no double bonds (DB), monoenic (1 DB), unsaturated (2 or 3 DB) and polyenic (4,5, or 6 DB). Saturated and monoenic FA are used predominantly as oxidation and energy substrate, unsaturated as plasma membrane constituents, polyenic as precursors in eicosanoid and aminophospholipid production. Bearing in mind specific features of metabolism and transport in vivo, FA can be regarded as short-chain (C4-C8) and middle-chain (C10-C14), their etherification with glycerol yielding short triglycerides (TG) which are not associated with apoproteins, while long-chain FA form long TG which in enterocytes are structured into chylomicrons by apoB-48. There are grounds to believe that a) outflow of middle-chain FA as short TG from enterocytes into the portal vein bed that includes the omentum veins and b) outflow of long-chain FA as chylomicron TG via d. thoracicus into major veins of systemic circulation are associated with pathogenesis of isolated omental obesity syndrome and metabolic syndrome, which wet by obesity. Source


Titov V.N.,Russian Cardiology Research and Production Center
Vestnik Rossiiskoi Akademii Meditsinskikh Nauk | Year: 2012

We believe that etiological factor of insulin resistance is phylogenetically late formation of insulin and its specific functionality, i.e., providing energy substrates for the biological function of locomotion. According to biological subordination, insulin cannot change regulation formed at the early stages of phylogenesis in all cells, including those that become insulin-dependent at the late stages of phylogenesis. This involves a) ß-oxidation of fatty acids in the mitochondria, b) synthesis of C 16:0 palmitic saturated fatty acid, c) glucose metabolism in pro- and eukaryotes, d) regulation of biochemical reactions in insulin-independent cells, e) humoral effects of mediators at the level of paracrine cell communities which are structural and functional units of all internal organs, andf) hormonal regulation at the entire organism level. Pathogenetic factors of insulin resistance are biochemical and functional disorders occurring in vivo upon activation of biological functions and reactions that formed phylogenetically earlier than insulin. During phylogenesis the insulin system has intrinsically built up over the regulatory mechanisms of mitochondria, early unicellular organisms and paracrine cell communities. Insulin functionally interacts with them all, but it cannot abolish the effects of any phylogenetically earlier humoral mediator. Insulin resistance is a pathophysiological disparity between humoral regulation of metabolism at the level of phylogenetically earlier paracrine cell communities and at the level of phylogenetically late total organism, on the one hand, and successive phylogenetic formation of passive cellular uptake of fatty acids as unesterified fatty acids and later triglycerides, on the other. If insulin resistance results from changes in the primary structure of transport proteins, in glucose storage and cellular insulin reception, it can be referred to as type II diabetes mellitus. Source


Connolly S.J.,Hamilton Health Sciences | Camm A.J.,St Georges, University of London | Halperin J.L.,Mount Sinai Medical Center | Joyner C.,Sunnybrook Health science Center | And 49 more authors.
New England Journal of Medicine | Year: 2011

BACKGROUND: Dronedarone restores sinus rhythm and reduces hospitalization or death in intermittent atrial fibrillation. It also lowers heart rate and blood pressure and has antiadrenergic and potential ventricular antiarrhythmic effects. We hypothesized that dronedarone would reduce major vascular events in high-risk permanent atrial fibrillation. METHODS: We assigned patients who were at least 65 years of age with at least a 6-month history of permanent atrial fibrillation and risk factors for major vascular events to receive dronedarone or placebo. The first coprimary outcome was stroke, myocardial infarction, systemic embolism, or death from cardiovascular causes. The second coprimary outcome was unplanned hospitalization for a cardiovascular cause or death. RESULTS: After the enrollment of 3236 patients, the study was stopped for safety reasons. The first coprimary outcome occurred in 43 patients receiving dronedarone and 19 receiving placebo (hazard ratio, 2.29; 95% confidence interval [CI], 1.34 to 3.94; P = 0.002). There were 21 deaths from cardiovascular causes in the dronedarone group and 10 in the placebo group (hazard ratio, 2.11; 95% CI, 1.00 to 4.49; P = 0.046), including death from arrhythmia in 13 patients and 4 patients, respectively (hazard ratio, 3.26; 95% CI, 1.06 to 10.00; P = 0.03). Stroke occurred in 23 patients in the dronedarone group and 10 in the placebo group (hazard ratio, 2.32; 95% CI, 1.11 to 4.88; P = 0.02). Hospitalization for heart failure occurred in 43 patients in the dronedarone group and 24 in the placebo group (hazard ratio, 1.81; 95% CI, 1.10 to 2.99; P = 0.02). CONCLUSIONS: Dronedarone increased rates of heart failure, stroke, and death from cardiovascular causes in patients with permanent atrial fibrillation who were at risk for major vascular events. Our data show that this drug should not be used in such patients. (Funded by Sanofi-Aventis; PALLAS ClinicalTrials.gov number, NCT01151137.) Copyright © 2011 Massachusetts Medical Society. All rights reserved. Source

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