Patients with metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) have high risk of microcirculation complications and microangiopathies. An increase in thrombogenic risk is associated with platelet hyperaggregation, hypercoagulation, and hyperfibrinolysis. Factors leading to platelet activation in MetS and T2DM comprise insulin resistance, hyperglycemia, non-enzymatic glycosylation, oxidative stress, and inflammation. This review discusses the role of nitric oxide (NO) in the regulation of platelet adhesion and aggregation processes. NO is synthesized both in endotheliocytes, smooth muscle cells, macrophages, and platelets. Modification of platelet NO-synthase (NOS) activity in MetS patients can play a central role in the manifestation of platelet hyperactivation. Metabolic changes, accompanying T2DM, can lead to an abnormal NOS expression and activity in platelets. Hyperhomocysteinemia, often accompanying T2DM, is a risk factor for cardiovascular accidents. Homocysteine can reduce NO production by platelets. This review provides data on the insulin effects in platelets. Decrease in a number and sensitivity of the insulin receptors on platelets in T2DM can cause platelet hyperactivation. Various intracellular mechanisms of anti-aggregating insulin effects are discussed. Anti-aggregating effects of insulin are mediated by a NO-induced elevation of cGMP and upregulation of cAMP- and cGMP-dependent pathways. The review presents data suggesting an ability of platelets to synthesize humoral factors stimulating thrombogenesis and inflammation. Proinflammatory cytokines are considered as markers of T2DM and cardiovascular complications and are involved in the development of dyslipidemia and insulin resistance. The article provides an evaluation of NO-mediated signaling pathway in the effects of cytokines on platelet aggregation. The effects of the proinflammatory cytokines on functional activity of platelets are demonstrated.

Aim. To study the relationship between the epicardial fat thickness (EFT), biomarkers of inflammation and metabolic dysfunction in patients with coronary artery disease (CAD) and various severity of coronary atherosclerosis.Material and methods. The study consisted of 89 patients (47 men and 42 women) with stable CAD at the age of 62,2±6,5 years, who assessed the presence and severity of coronary atherosclerosis according to angiography with the calculation of the Gensini Score (GS). We conducted an ultrasonic evaluation of the EFT. We determined the content of glucose, lipid fractions, apoproteins, pro-inflammatory cytokines and adipokines, C-reactive protein by a highly sensitive method (hsCRP).Results. In the total sample of patients, the median GS index was 13,5 (3,5; 43) points, the median EFT was 4,93 (3,95; 6,0) mm, the median hsCRP was 2,1 (1,02; 3,65) mg/l. There were no correlation relationships between the GS index and the body mass index, waist circumference, EFT, hsCRP, lipid and carbohydrate metabolism in the general group of patients. In the course of linear regression analysis, an independent contribution of hsCRP >2,1 mg/l to the formation of the first two tertiles of a sample of GS values was established (0≤ GS ≤28, paired linear regression hsCRP at GS β=0,55, p=0,0221), whereas in patients with GS values from the third tertile (GS >28 points), the growth of this parameter had an independent association with an increase in the EFT (estimation of the coefficient of paired linear regression of the EFT on GS β=0,56, p=0,0015). The range of hsCRP changes did not affect the value of the β coefficient in paired linear regression models in patients with GS >28 points (n=29) and in the subgroup of patients with GS >28 and hsCRP >2,1 mg/l (n=18).Conclusion. The absence of an independent association between EFT and minor or moderate severity of atherosclerotic lesions of the coronary arteries (for GS ≤28 points) in patients with CAD, while an independent marker of GS index increase is higher than 2,1 mg/l. An independent contribution to the formation of a severe coronary atherosclerosis (with a GS value of >28 points) is equally made by thickening of EFT, and a moderately elevated level of hsCRP.

Aim. To develop a progressive multifaceted approach to the management of geriatric patients with cardiac arrhythmias.Material and methods. The study was carried out in 2 stages. The study sample consisted of 262 elderly and senile people (mean age, 69,5±1,1 years). There 145 elderly (mean age, 68,4±1,2 years) and 117 senile patients (mean age 74,4±1,3 years). We analyzed medications used for six months in geriatric patients with arrhytmias and senile asthenia (SA) and without it. The combined strategy of management of geriatric patients with arrhytmias and SA was tested.Results. SA is most common in geriatric patients who are taking drugs such as class I a, b, c antiarrhythmics, class V antiarrhythmics (cardiac glycosides), diuretics (torasemide, furosemide), and statins. This indicates the need to avoid polypharmacy and to adjust the treatment of geriatric patients with cardiac arrhythmias in accordance with Beers criteria. Presented study revealed that in patients with SA, the total antioxidant activity is reduced, which indicates the need to restore antioxidant defence to such patients. A combined strategy has been developed for the management of geriatric patients with cardiac arrhytmias and SA.Conclusion. The combined strategy of managing older patients with arrhytmias and SA helped to improve the geriatric status, prevent SA, and increase antioxidant defence. A significant improvement in the quality of life was noted, in particular, in relation to the mental and psychological well-being.

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