Aim. To assess arterial wall stiffness, plasma levels of of N-terminal prohormone of brain natriuretic peptide (NT-proBNP), as well as functional state and structure of the myocardium in patients with type 2 diabetes mellitus (T2DM) and cardiac autonomic neuropathy (CAN). Materials and Methods. The study involved a total of 65 patients with T2DM. 12 had no evidence of cardiovascular disease (CVD) or CAN, 14 were diagnosed with subclinical stage of CAN, 18 ? with functional stage, and 21 ? with organic stage. We measured aortic pulse wave velocity (PWV), aortic augmentation index (AIx), brachial artery AIx, ambulatory arterial stiffness index (AASI) and plasma levels of NT-proBNP. Clinical examination included ECG, Holter monitoring, ambulatory BP measurement and echocardiography. Results.  Patients with isolated T2DM showed a trend for increased vascular wall stiffness. PWV was increased in patients with subclinical stage of CAN. Aortic and brachial AIx, PWV and AASI were elevated in patients with functional stage of CAN, PWV being significantly higher vs. subclinical CAN subgroup. Organic stage was characterized by pathologically increased values of all primary parameters; PWV and AASI were significantly higher compared with other groups. Development and progression of CAN was accompanied by an increase in NT-proBNP plasma levels. Concentration of NT-proBNP was in direct correlation with left ventricular mass (LVM) and PWV. PWV and LVM values also directly correlated between themselves. Conclusion. Development and progression of CAN in patients with T2DM is accompanied by an increase in vascular wall stiffness. The elevation of plasma NT-proBNP in patients with T2DM correlates with the development of CAN and is significantly and independently associated with an increase in LVM and PWV. Our data suggests the pathophysiological interconnection between metabolic, functional and structural myocardial abnormalities in patients with T2DM and CAN.

OBJECTIVE Finerenone significantly improved cardiorenal outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) in the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease trial. We explored whether baseline HbA1c level and insulin treatment influenced outcomes. RESEARCH DESIGN AND METHODS Patients with T2D, urine albumin-to-creatinine ratio (UACR) of 30–5,000 mg/g, estimated glomerular filtration rate (eGFR) of 25 to <75 mL/min/1.73 m2, and treated with optimized renin–angiotensin system blockade were randomly assigned to receive finerenone or placebo. Efficacy outcomes included kidney (kidney failure, sustained decrease ≥40% in eGFR from baseline, or renal death) and cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) composite endpoints. Patients were analyzed by baseline insulin use and by baseline HbA1c <7.5% (58 mmol/mol) or ≥7.5%. RESULTS Of 5,674 patients, 3,637 (64.1%) received insulin at baseline. Overall, 5,663 patients were included in the analysis for HbA1c; 2,794 (49.3%) had baseline HbA1c <7.5% (58 mmol/mol). Finerenone significantly reduced risk of the kidney composite outcome independent of baseline HbA1c level and insulin use (Pinteraction = 0.41 and 0.56, respectively). Cardiovascular composite outcome incidence was reduced with finerenone irrespective of baseline HbA1c level and insulin use (Pinteraction = 0.70 and 0.33, respectively). Although baseline HbA1c level did not affect kidney event risk, cardiovascular risk increased with higher HbA1c level. UACR reduction was consistent across subgroups. Adverse events were similar between groups regardless of baseline HbA1c level and insulin use; few finerenone-treated patients discontinued treatment because of hyperkalemia. CONCLUSIONS Finerenone reduces kidney and cardiovascular outcome risk in patients with CKD and T2D, and risks appear consistent irrespective of HbA1c levels or insulin use.

This review article summarizes the existing literature on the current state of the problem of diabetes mellitus and arterial hypertension. According to the World Health Organization, hypertension and type 2 diabetes mellitus, after obesity, are among the leading cardiovascular risk factors that are most common among the world’s population. Over the past 30 years, the prevalence of hypertension has decreased to a quarter of the world’s population, but the incidence of diabetes mellitus has increased from 4.7 to 8.5 %, and the forecast for the future indicates a further dramatic increase. Improving awareness, treatment and control of these diseases is a major goal of the global health system. The prevalence of hypertension in patients with type 2 diabetes mellitus is up to three times higher than in patients without diabetes mellitus, and the combination of hypertension and diabetes mellitus significantly increases the likelihood of developing cardiovascular disease. The unfavorable relationship between these two conditions, accelerating the processes of atherosclerosis, can cause negative pathophysiological changes in the cardiovascular system. Also, it is known that cardiovascular autonomic neuropathy, resulting from damage to the autonomic nerve fibers that innervate the heart and blood vessels, is a significant complication of type 2 diabetes mellitus, especially in the presence of systemic hypertension. In particular, the issues related to common pathophysiological mechanisms, main systemic and metabolic factors that may contribute to the development of diabetes mellitus and hypertension comorbidity are analyzed. Classification, features of diagnosis of arterial hypertension, assessment of the disorders of the organs mediated by arterial hypertension are presented. Issues related to the main approaches of arterial hypertension treatment in diabetes mellitus are analyzed, namely prescription of the inhibitors of the renin-angiotensin system, calcium channel blockers, thiazide, and thiazide-like diuretics, beta-adrenergic receptor antagonists, alpha-blockers, mineralocorticoid-receptor antagonists as well as the features of combined therapy and treatment of resistant arterial hypertension.

Огляд літератури /Literature Review/ Визначення «діабетична кардіоміопатія» є одним з найбільш дискусійних і невирішених питань. Зв'язок між цукровим діабетом (ЦД) і серцево-судинними захворюваннями (ССЗ) відомий вже багато років, але вперше описаний у 1881 р. Leyden et al., який вважав, що серцева недостатність (СН) є «частим і вираженим ускладненням цукрового діабету». Термін «діабетична кардіоміопатія» для диференціації з іншими видами кардіоміопатії запропонований S. Rubler et al. в 1972 р. після аналізу патологоанатомічних досліджень хворих на ЦД із хронічною серцевою недостатністю (ХСН), в яких ішемічна хвороба серця (ІХС) та інші захворюван-ня, що супроводжувались структурними змінами серця, а також артеріальна гіпертензія (АГ) і зловживання алкоголем були виключені як можливі причини [1]. На сьогодні до мінімальних критеріїв діагностики діабетичної кардіоміопатії (КМП) відносять діастолічну дисфункцію (ДД) лівого шлуночка (ЛШ) та/або зменшену фракцію викиду ЛШ, патологічну гіпертрофію ЛШ та інтерстиціальний фіброз. Отже, діабетична КМП -це шлуночкова дисфункція, що спостерігається у хворих на ЦД, яка приєднується та/або прогресує незалежно від ІХС, захворювань клапанного апарату міокарда або артеріальної гіпертензії. Діабетична КМП

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