scholarly journals Hypoglycemic therapy in patients with type 2 diabetes and chronic heart failure

2014 ◽  
Vol 5 (1) ◽  
pp. 33-40
Author(s):  
S. V Kakorin ◽  
I. A Averkova ◽  
A. M Mkrtumyan

The article presents a literature review of prevalence, prognosis and treatment of overt tactics of chronic heart failure (CHF) in patients with type 2 diabetes mellitus (T2DM). Application of modern pharmacological preparations and instrumental treatment of cardiovascular disease (CVD) increases life expectancy and improves the quality of life of patients with CHF as with normal carbohydrate metabolism (UO), and with type 2 diabetes. However, the risk of cardiovascular mortality (CAS) in patients with type 2 diabetes, compared to having a normal carbohydrate metabolism remains unchanged.Insulin resistance (IR) and compensatory hyperinsulinemia (GI) play a key role in the pathogenesis of type 2 diabetes. Ongoing research in the twentieth century of coronary heart disease (CHD) and heart failure in patients with type 2 diabetes revealed adverse effects of sulfonylurea medications on the metabolic processes in the myocardium and increased risk of death in patients with severe coronary artery disease. In comparison with sulfonylurea drugs, metformin and insulin not only reduces the risk of cardiovascular disease, but also can prevent or delay the development of type 2 diabetes in individuals with impaired glucose tolerance (IGT) and impaired fasting glucose. Metformin acts on the key link of pathogenesis - insulin resistance, affecting the lower incidence of cardiovascular diseases, the development of chronic disease and mortality compared with insulin and sulfonylurea drugs. However, in patients with chronic heart failure is contraindicated the use of thiazolidinediones and metformin is limited tothe severity of CHF I-II FC NYNA. With effective treatment of chronic heart failure by cardiologists in patients with type 2 diabetes, affecting therapy with insulin resistance should be mandatory.

2015 ◽  
Vol 6 (1) ◽  
pp. 16-23
Author(s):  
S. V Kakorin ◽  
I. A Averkova ◽  
A. M Mkrtumyan

The article presents a literature review of prevalence, prognosis and treatment of overt tactics of chronic heart failure (CHF) in patients with type 2 diabetes mellitus (T2DM). Diabetes and heart failure acquire the status of the epidemic of the XXI century and require health care costs for prevention and treatment of these diseases. Application of modern pharmacological preparations and instrumental treatment of cardiovascular disease (CVD) increases life expectancy and improves the quality of life of patients with CHF as with normal carbohydrate metabolism (UO), and with type 2 diabetes. However, the risk of cardiovascular mortality (CAS) in patients with type 2 diabetes, compared to having a normal carbohydrate metabolism remains unchanged. The rapidly growing population of patients with type 2 diabetes will soon change this in recent years to improve representation treatment prognosis of cardiovascular disease. Violation of myocardial remodeling in type 2 diabetes is caused by a combination of factors associated with diabetic cardiomyopathy. Reduction of the metabolic activity of cardiomyocytes insufficient glucose transport into cells, endothelial dysfunction, diabetic macro and microangiopathy myocardial fibrosis leading to disruption of filling the left ventricle (LV) and the development of chronic heart failure.Insulin resistance (IR) and compensatory hyperinsulinemia (GI) play a key role in the pathogenesis of type 2 diabetes. With effective treatment of chronic heart failure by cardiologists in patients with type 2 diabetes, affecting therapy with insulin resistance should be mandatory.


2016 ◽  
Vol 94 (6) ◽  
pp. 439-444
Author(s):  
Mihail E. Statsenko ◽  
S. V. Turkina ◽  
N. N. Shilina ◽  
M. A. Kosivtsova

Patients with chronic heart failure and diabetes mellitus type 2 experience continuous progression of organ damage as a result of hemodynamic and metabolic disorders. An important role in pathogenesis of organ damage belongs to pathological types of microcirculation, endothelial dysfunction and insulin resistance. But the role of insulin resistance and its contribution to the formation of endothelial dysfunction and peculiarities of microcirculation in patients with chronic heart failure and type 2 diabetes mellitus is unknown. This study shows significant association between insulin resistance, disorders of carbohydrate and lipid metabolism, development of microcirculatory disturbances and endothelial dysfunction.


2018 ◽  
Vol 17 (4) ◽  
pp. 141-151
Author(s):  
A. T. Teplyakov ◽  
E. N. Berezikova ◽  
S. N. Shilov ◽  
A. A. Popova ◽  
I. V. Yakovleva ◽  
...  

Aim.To study the link of increased serum concentrations of osteoprotegerin (OPG) in patients with chronic heart failure (CHF) associated with type 2 diabetes mellitus (DM 2), osteoporosis or osteopenia with the development of cardiovascular events (primarily, decompensation of CHF, including those requiring hospitalization, death from cardiovascular disease, acute coronary syndrome or acute ischemic stroke) to determine the possibility of using this biomarker as a predictor of a severe course of cardiovascular disease in these patients.Materials and methods.In a 12-month cohort observational study included 75 patients (mean age 57.4 ± 5.4 years) with CHF associated with DM 2, osteoporosis or osteopenia. Cardiovascular events were analyzed in three groups of patients formed based terteling ranges of concentration of the OPG level in serum: in the 1st group (n= 25) included patients with serum OPG concentration is less than 5.0 pmol/l; in the 2nd group (n= 25) OPG level of 5.0–7.2 pmol/l; in the 3rd group (n= 25) - with the content of OPG more than 7.2 pmol/L. The serum OPG, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) serum levels were determined by ELISA. Assessment of bone mineral density (BMD) was performed by a densitometric method using dual-energy X-ray absorptiometry.Results.Highly reliable increased expression of OPG in 2 and 3th tertiles was found in patients with CHF associated with type 2 diabetes in comparison with the control group. The frequency of adverse events gradually increased from the 1st tertile to the 3rd tertile OPG. With the median for OPG more than 5.2 pmol/L and BMD less than -2.5 standard deviations, the highest frequency (60.9%) of adverse cardiovascular events was identified. A close correlation of OPG with the values of pro-inflammatory cytokines-TNF-α (r= 0.46;p= 0.019) and IL-1β (r= 0.4;p= 0.01), glycated hemoglobin (r= 0.55;p= 0.009) and the severity of CHF (r= 0.49;p= 0.013).Conclusions.Osteoprotegerin is an independent risk factor for the development of comorbid cardiovascular pathology: CHF associated with DM 2 and osteoporosis. It seems clinically justified to use OPG to stratify the risk of progression of cardiovascular pathology.


2020 ◽  
Vol 15 ◽  
Author(s):  
Raveendran Arkiath Veettil ◽  
Cornelius James Fernandez ◽  
Koshy Jacob

: Type 2 diabetes mellitus (T2DM) is characterized by a progressive beta cell dysfunction in the setting of peripheral insulin resistance. Insulin resistance in subjects with type 2 diabetes and metabolic syndrome is primarily caused by an ectopic fat accumulation in liver and skeletal muscle. Insulin sensitizers are particularly important in the management of T2DM. Though, thiazolidinediones (TZDs) are principally insulin sensitizers, they possess an ability to preserve pancreatic β-cell function and thereby exhibit durable glycemic control. Cardiovascular outcome trials (CVOTs) have shown that Glucagon-like-peptide 1 receptor agonists (GLP-1 RAs) and sodium glucose transporter-2 inhibitors (SGLT2i) have proven cardiovascular safety. In this era of CVOTs, drugs with proven cardiovascular (CV) safety are often preferred in patients with preexisting cardiovascular disease or at risk of cardiovascular disease. In this review, we will describe the three available drugs belonging to the TZD family, with special emphasis on their efficacy and CV safety.


2021 ◽  
Vol 22 (15) ◽  
pp. 7797
Author(s):  
Joseph A. M. J. L. Janssen

For many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin secretion, decrease insulin pulses and/or reduce hepatic insulin clearance, thereby causing hyperinsulinemia. Hyperinsulinemia disturbs the balance of the insulin–GH–IGF axis and shifts the insulin : GH ratio towards insulin and away from GH. This insulin–GH shift promotes energy storage and lipid synthesis and hinders lipid breakdown, resulting in obesity due to higher fat accumulation and lower energy expenditure. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, cancer and premature mortality. It has been further hypothesized that nutritionally driven insulin exposure controls the rate of mammalian aging. Interventions that normalize/reduce plasma insulin concentrations might play a key role in the prevention and treatment of age-related decline, obesity, type 2 diabetes, cardiovascular disease and cancer. Caloric restriction, increasing hepatic insulin clearance and maximizing insulin sensitivity are at present the three main strategies available for managing hyperinsulinemia. This may slow down age-related physiological decline and prevent age-related diseases. Drugs that reduce insulin (hyper) secretion, normalize pulsatile insulin secretion and/or increase hepatic insulin clearance may also have the potential to prevent or delay the progression of hyperinsulinemia-mediated diseases. Future research should focus on new strategies to minimize hyperinsulinemia at an early stage, aiming at successfully preventing and treating hyperinsulinemia-mediated diseases.


2021 ◽  
pp. 43-47
Author(s):  
Liliia Mogylnytska

Cardiovascular disease is the leading cause of death in diabetes mellitus. Endothelial dysfunction is the first step in the development of atherosclerotic vascular lesions, which underlies cardiovascular pathology, and adhesion molecules secreted by the endothelium during inflammatory changes are involved in the progression of this lesion. The objective: the serum level of adhesive molecules (ІCAM-1, VCAM-1, Е-selectin) in hypertensive and non-hypertensive type 2 diabetes patients as a marker of endothelial dysfunction and its relationship with other risk factors for cardiovascular disease was studied. Materials and methods. We examined 64 patients with type 2 diabetes, which were divided into two subgroups: the first subgroup – 41 hypertensive type 2 diabetes patients (age – 53,56±7,14 years, BMI – 32,2±87,4; HbA1c – 9,97±2,02%), the second subgroup – 23 nonhypertensive type 2 diabetes patients (age – 50,5±4,92 years, BMI – 25,4±5,22; HbA1c – 9,09±1,95%). The control group included 18 people without diabetes with normal blood pressure (age – 50,72±6,98 years, BMI – 24,71±4,88; HbA1c – 5,26±0,42%). The serum level was determined by immunoenzyme assay. The significance of the difference between the mean values was determined by the t-Student test. Multifactor regression analysis was used to assess the relationships between the studied factors. Results. We revealed an increase of serum levels of ІCAM-1, VCAM-1, Е-selectin in hypertensive (+71,62%, +68,42%, +66,95%, respectively) and non-hypertensive type 2 diabetes patients (+46,17%, +62,79%, +42,85%, respectively) compared with the control group (p<0,01). The serum concentration of ІCAM-1, Е-selectin was higher in hypertensive type 2 diabetes patients compared to non-hypertensive type 2 diabetes patients (+17,27%, +16,86%, respectively, p<0,01). There was a significant effect of Hb1Ac, lipids, insulin resistance on the serum level of ІCAM-1, VCAM-1, Е-selectin (p<0,01). The corresponding regression equations are derived. Conclusion. There is an increase of serum level of ІCAM-1, VCAM-1, Е-selectin in hypertensive and non-hypertensive type 2 diabetes patients, which indicates the development of endothelial dysfunction. Hypertension, hyperglycemia, dyslipidemia and insulin resistance contribute to the development of these changes.


2020 ◽  
Vol 66 (4) ◽  
pp. 35-44
Author(s):  
Ekaterina N. Dudinskaya ◽  
Olga N. Tkacheva ◽  
Natalia V. Brailova ◽  
Irina D. Strazhesko ◽  
Marina V. Shestakova

BACKGROUND: Insulin resistance accelerates the aging process, but its speed depends on the individual characteristics of the metabolism. One of the reasons for the different aging rates in individuals with insulin resistance is the initially different “genetic protection” of cells, which many scientists associate with replicative cellular aging.AIMS: to study the relationship between the state of carbohydrate metabolism and markers of replicative cell aging in individuals with different sensitivity to insulin.MATERIALS AND METHODS: The observation study included 305 patients. The parameters of glucose metabolism and telomere biology were studied.RESULTS: The mean age of the patients was 51.5±13.3 years. Patients were divided into three groups depending on presence of insulin resistance: healthy, with insulin resistance and with type 2 diabetes. The mean age of healthy patients was 48.82±13.87 years, in insulin resistance group — 53.04±12.8, in 2 diabetes mellitus — 58.4±7.90. The median telomere length was 9.76. The median telomerase activity was 0.48. Both telomere length and telomerase activity progressively decrease as insulin resistance increases. In patients with diabetes, short telomere lengths and low telomerase activity predominated. The insulin resistance index has the greatest impact on the risk of detecting “short” telomeres. In patients with insulin resistance, an increase in glycated hemoglobin increases the likelihood of detecting short telomeres by 2.4 times, and in diabetes mellitus by 4.26 times, an increase in fasting plasma glucose by 90%, and an increase in HOMA-IR by 35%. An increase in insulin resistance increases the risk of detecting «low» telomerase activity by 53% and the risk of detecting «very low» telomerase activity by 92%. A decrease in synsulin resistance increases the chance of increasing telomerase activity to «very high» by 51%.CONCLUSION: Shorter telomeres are associated with more pronounced disorders of carbohydrate metabolism and a higher degree of insulin resistance. Further studies of metabolic status are necessary to personalize their lifestyle and treatment goals.


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