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.
Safarova M.S.,Russian Cardiology Research and Production Center |
Ezhov M.V.,Russian Cardiology Research and Production Center |
Afanasieva O.I.,Russian Cardiology Research and Production Center |
Pokrovsky S.N.,Russian Cardiology Research and Production Center
Journal of Clinical Apheresis | Year: 2015
Lipoprotein(a) [Lp(a)] is acknowledged to be an independent atherothrombotic risk factor. Although genetic studies have highlighted the causal relationship between coronary disease and Lp(a), it is uncertain which strategies maximize the therapeutic benefit of patients with high Lp(a) levels. We report the challenging case of a young coronary heart disease (CHD) patient who underwent 10 percutaneous coronary interventions due to repeated acute coronary syndromes (2006-2009) despite an optimally controlled, traditional risk-factor profile. For the first time, we performed specific Lp(a) immunoadsorption in the presence of very low levels of lowdensity lipoprotein cholesterol (LDL-C) while the patient was on a high-dose statin regimen. There have been no previous reports of patients with high Lp(a) levels who achieved LDL-C goals when treated with an isolated Lp(a)-lowering method. Despite the very high risk of cardiovascular death, targeting Lp(a) resulted in dramatic improvement of the patient's clinical condition. Thus, we suggest that specific Lp(a) apheresis should be considered an effective new treatment strategy for patients with progressive CHD who have reached LDL-C goals but harbor elevated Lp(a) levels. © 2014 Wiley Periodicals, Inc.
Connolly S.J.,Hamilton Health Sciences |
Eikelboom J.,Hamilton Health Sciences |
Joyner C.,University of Toronto |
Diener H.-C.,University of Duisburg - Essen |
And 27 more authors.
New England Journal of Medicine | Year: 2011
BACKGROUND: Vitamin K antagonists have been shown to prevent stroke in patients with atrial fibrillation. However, many patients are not suitable candidates for or are unwilling to receive vitamin K antagonist therapy, and these patients have a high risk of stroke. Apixaban, a novel factor Xa inhibitor, may be an alternative treatment for such patients. METHODS: In a double-blind study, we randomly assigned 5599 patients with atrial fibrillation who were at increased risk for stroke and for whom vitamin K antagonist therapy was unsuitable to receive apixaban (at a dose of 5 mg twice daily) or aspirin (81 to 324 mg per day), to determine whether apixaban was superior. The mean follow up period was 1.1 years. The primary outcome was the occurrence of stroke or systemic embolism. RESULTS: Before enrollment, 40% of the patients had used a vitamin K antagonist. The data and safety monitoring board recommended early termination of the study because of a clear benefit in favor of apixaban. There were 51 primary outcome events (1.6% per year) among patients assigned to apixaban and 113 (3.7% per year) among those assigned to aspirin (hazard ratio with apixaban, 0.45; 95% confidence interval [CI], 0.32 to 0.62; P<0.001). The rates of death were 3.5% per year in the apixaban group and 4.4% per year in the aspirin group (hazard ratio, 0.79; 95% CI, 0.62 to 1.02; P = 0.07). There were 44 cases of major bleeding (1.4% per year) in the apixaban group and 39 (1.2% per year) in the aspirin group (hazard ratio with apixaban, 1.13; 95% CI, 0.74 to 1.75; P = 0.57); there were 11 cases of intracranial bleeding with apixaban and 13 with aspirin. The risk of a first hospitalization for cardiovascular causes was reduced with apixaban as compared with aspirin (12.6% per year vs. 15.9% per year, P<0.001). The treatment effects were consistent among important subgroups. CONCLUSIONS: In patients with atrial fibrillation for whom vitamin K antagonist therapy was unsuitable, apixaban reduced the risk of stroke or systemic embolism without significantly increasing the risk of major bleeding or intracranial hemorrhage. Copyright © 2011 Massachusetts Medical Society.
Pooling and expanding registries of familial hypercholesterolaemia to assess gaps in care and improve disease management and outcomes: Rationale and design of the global EAS Familial Hypercholesterolaemia Studies Collaboration
PubMed | Hospital Militar Of Caracas, University of Witwatersrand, Victor Babes University of Medicine and Pharmacy Timisoara, University of the Philippines and 59 more.
Type: | Journal: Atherosclerosis. Supplements | Year: 2016
The potential for global collaborations to better inform public health policy regarding major non-communicable diseases has been successfully demonstrated by several large-scale international consortia. However, the true public health impact of familial hypercholesterolaemia (FH), a common genetic disorder associated with premature cardiovascular disease, is yet to be reliably ascertained using similar approaches. The European Atherosclerosis Society FH Studies Collaboration (EAS FHSC) is a new initiative of international stakeholders which will help establish a global FH registry to generate large-scale, robust data on the burden of FH worldwide.The EAS FHSC will maximise the potential exploitation of currently available and future FH data (retrospective and prospective) by bringing together regional/national/international data sources with access to individuals with a clinical and/or genetic diagnosis of heterozygous or homozygous FH. A novel bespoke electronic platform and FH Data Warehouse will be developed to allow secure data sharing, validation, cleaning, pooling, harmonisation and analysis irrespective of the source or format. Standard statistical procedures will allow us to investigate cross-sectional associations, patterns of real-world practice, trends over time, and analyse risk and outcomes (e.g. cardiovascular outcomes, all-cause death), accounting for potential confounders and subgroup effects.The EAS FHSC represents an excellent opportunity to integrate individual efforts across the world to tackle the global burden of FH. The information garnered from the registry will help reduce gaps in knowledge, inform best practices, assist in clinical trials design, support clinical guidelines and policies development, and ultimately improve the care of FH patients.
Korotaeva A.,Russian Cardiology Research and Production Center |
Samoilova E.,Russian Cardiology Research and Production Center |
Pavlunina T.,Russian Cardiology Research and Production Center |
Panasenko O.M.,Karpov Institute of Physical Chemistry
Chemistry and Physics of Lipids | Year: 2013
Secretory phospholipase A2 group IIA (sPLA2-IIA) is an active participant of inflammation. The enzyme destroys bacterial cell wall and induces production of biologically active lipid mediators. It is involved in various pathological processes and high serum content and activity of sPLA2-IIA are associated with adverse cardiovascular events. Study of sPLA2-IIA regulation is of great physiological and clinical importance and is necessary for better understanding of mechanisms underlying inflammation. Another major participant of inflammatory response is the enzyme myeloperoxidase (MPO) which is secreted by neutrophils in the focus of inflammation and catalyzes formation of HOCl and HOBr. Both halogenated (chloro- and bromohydrins) and oxidized lipids are formed due to interaction between HOCl and HOBr with unsaturated bonds of phospholipid acyl chains. Previously we showed that oxidized phospholipids stimulate sPLA2-IIA activity. In this study we examined the effects of chloro- and bromohydrins of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) on sPLA2-IIA activity. In contrast to POPC, chloro- and bromohydrins of POPC (POPC-Cl and POPC-Br, respectively) were not hydrolyzed by sPLA2-IIA. In addition, phospholipids which are sPLA2-IIA substrates, were not cleaved by the enzyme in the presence of POPC-Cl and POPC-Br. Halogenohydrins of POPC prevented the activity of both purified and serum sPLA2-IIA. Blocking effects of POPC-Cl and POPC-Br were abolished by increased concentrations of phospholipid-substrate. These results suggest that halogenated phospholipids formed in MPO-dependent reactions can be considered as a new class of biologically active compounds potentially capable of regulating sPLA2-IIA activity in the areas of inflammation and producing the effects opposite to those of oxidized phospholipids. Control over sPLA2-IIA can be useful in the therapy of diseases involving systemic inflammation. © 2013 Elsevier Ireland Ltd.
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.
Starostin I.V.,Russian Cardiology Research and Production Center |
Talitskiy K.A.,Russian Cardiology Research and Production Center |
Bulkina O.S.,Russian Cardiology Research and Production Center |
Karpov Y.A.,Russian Cardiology Research and Production Center
Diabetes Mellitus | Year: 2013
Although collateral circulation is the essential means of perfusion for ischemized myocardium, its efficiency varies substantially within and between the species. There is both experimental and clinical evidence for association of glycemic disorders with inadequate collateral circulation. Current article reviews general mechanisms of collateral circulation failure due to such metabolic disturbances with regard for stages of arteriogenesis. We also highlight horizons of further studies in this field.
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.
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.
PubMed | Russian Cardiology Research and Production Center and Russian Academy of Sciences
Type: Journal Article | Journal: Doklady. Biochemistry and biophysics | Year: 2017
It is shown that endothelial cells from human umbilical vein have a reduced activity and gene expression of the classic antioxidant enzymes (Cu,Zn-superoxide dismutase, catalase, and Se-containing glutathione peroxidase). At the same time, a high expression level of peroxiredoxin genes was identified in the same endothelial cells, which obviously indicates the predominant involvement of these enzymes in protecting the endothelium from the damaging effect of free radical peroxidation.