6 research outputs found

    The effect of empagliflozin on the development of chronic heart failure after myocardial infarction according to a 12-month prospective study

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    BACKGROUND: Although the positive cardiovascular effect of empagliflozin has been established, its influence on the formation of heart failure (HF) in patients with type 2 diabetes mellitus (T2D) after myocardial infarction (MI) remains unknown. AIM: To study the effect of empagliflozin on the formation of chronic HF after MI in patients having diabetes mellitus of type 2 (DM 2), according to 12-month follow-up data. MATERIALS AND METHODS: 47 patients with MI and DM 2 were included; 21 received standard therapy for MI and diabetes (group 1); 26 patients, in addition, received empagliflozin (group 2). The patients were investigated in 3 and 12 months, to assess the dynamics of glycemic control, 6-minute walk test, echocardiography. RESULTS: During postinfarction period, the 6-minute walk distance was increasing in group 1 in a lesser degree (p = 0.18) than in group 2 (49.5%, p = 0.0004). The ejection fraction got better particularly in group 2 (p = 0.002). At baseline, the proportions of patients having HF with reduced and mid-range ejection fraction were 85.7% and 82.4% in groups 1 and 2 (p = 0.56) but in 12 months decreased to 71.4% and 29.4% (p = 0.012). In empagliflozin group diastolic function was improved in a third of the patients (p = 0.041). The pulmonary artery systolic pressure was increasing in group 1 (by 10,4%, p = 0.041) but decreasing in group 2 (by 24,0%, p = 0.019). Glycemic control was better in group 2 than in group 1. CONCLUSION: According to 12-month follow-up data, empagliflozin has a positive effect on HF formation and symptoms in patients having MI and DM 2. This effect may be based on the ability of empagliflozin to improve the state of the heart including the delay of postinfarction remodeling, the improvement of pulmonary artery hemodynamics, systolic and diastolic function, the reduction of risk of chronic HF with reduced and mid-range ejection fraction

    Design and baseline characteristics of the finerenone in reducing cardiovascular mortality and morbidity in diabetic kidney disease trial

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    Background: Among people with diabetes, those with kidney disease have exceptionally high rates of cardiovascular (CV) morbidity and mortality and progression of their underlying kidney disease. Finerenone is a novel, nonsteroidal, selective mineralocorticoid receptor antagonist that has shown to reduce albuminuria in type 2 diabetes (T2D) patients with chronic kidney disease (CKD) while revealing only a low risk of hyperkalemia. However, the effect of finerenone on CV and renal outcomes has not yet been investigated in long-term trials. Patients and Methods: The Finerenone in Reducing CV Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD) trial aims to assess the efficacy and safety of finerenone compared to placebo at reducing clinically important CV and renal outcomes in T2D patients with CKD. FIGARO-DKD is a randomized, double-blind, placebo-controlled, parallel-group, event-driven trial running in 47 countries with an expected duration of approximately 6 years. FIGARO-DKD randomized 7,437 patients with an estimated glomerular filtration rate >= 25 mL/min/1.73 m(2) and albuminuria (urinary albumin-to-creatinine ratio >= 30 to <= 5,000 mg/g). The study has at least 90% power to detect a 20% reduction in the risk of the primary outcome (overall two-sided significance level alpha = 0.05), the composite of time to first occurrence of CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. Conclusions: FIGARO-DKD will determine whether an optimally treated cohort of T2D patients with CKD at high risk of CV and renal events will experience cardiorenal benefits with the addition of finerenone to their treatment regimen. Trial Registration: EudraCT number: 2015-000950-39; ClinicalTrials.gov identifier: NCT02545049

    Clinical and pathogenetic features of lesions of the lower extremities in patients with type 2 diabetes mellitus and chronic venous insufficiency

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    Comorbid chronic venous insufficiency (CVI) and type 2 diabetes mellitus (T2DM) are common, particularly in older people. The severity of DM and its complications can worsen the course of CVI and affect its management.Aim. To assess the impact of T2DM on lesions of the lower extremities in patients with CVI.Materials and methods. Eighty patients with CVI of the lower limbs were examined. Forty patients had T2DM (main group) and 40 patients did not have T2DM (control group). Physical examination, clinical and biochemical tests, ultrasound scanning of veins and arteries of the lower extremities and electroneuromyography (ENMG) of the lower extremities were performed for all patients. The state of the microvasculature was studied by laser Doppler flowmetry (LDF) for 15 patients in the main group and 15 patients in the control group.Results. T2DM exacerbated the course of CVI, which was clinically characterized by a greater severity of trophic (p = 0.0001) and oedema (p = 0.03) syndromes. Morphological changes in the venous blood flow in patients with T2DM with CVI were characterized by bilateral lesions (p = 0.03), more frequent failure of sapheno-femoral anastomosis (p = 0.02) and perforating veins of the lower leg (p = 0.0004). The pathogenesis of such complications was associated with diabetic factors, including hyperglycaemia, НbА1с &gt; 10%, duration of DM &gt; 10 years and the presence diabetic microangiopathy of the lower limbs. Diabetic macroangiopathy and polyneuropathy were associated with disruption of the morphological and functional characteristics of the venous system and the disruption of the microcirculation in the lower extremities, contributing to increased oedema and trophic changes. At the same time, the presence of diabetic neuropathy masked the symptoms of CVI due to reductions in pain (p = 0.0004).Conclusion. Diabetes exacerbates the course of CVI due to poor glycaemic control (HbA1c &gt; 10%), long duration of diabetes (&gt;10 years) and the presence of macroangiopathy in the lower extremities. Diabetic neuropathy of the lower limbs and diabetic microangiopathy aggravates the venous disease through disruption of microcirculation and increases the expression of trophic changes in the lower extremities

    Prediktory vyzhivaemosti bol'nykh khronicheskoy serdechnoy nedostatochnost'yu, stradayushchikh sakharnym diabetom 2 tipa

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    Цель. Оценить выживаемость больных ХСН, страдающих СД 2; выявить параметры диабета, влияющие на течение и прогноз пациентов с недостаточностью кровообращения. Материалы и методы. Проведено исследование когорты дожития, которую составили 72 больных ХСН, страдающих СД 2. Судьба больных прослежена в течение 12 мес. У всех больных был собран анамнез и проведено физикальное обследование. Производилась оценка ФК ХСН. Выполнено Эхо-КГ. Исследовали уровень предсердного натрийуретического пептида (ПНУП). Результаты. Всего за 12 мес. наблюдения скончались 17 больных. Достоверно с выживаемостью связаны показатели тяжести ХСН, отражающие переносимость нагрузки (функциональный класс), клиническую характеристику (ШОКС) и нейрогуморальную активацию (ПНУП). Уровень ПНУП, более чем в 4 раза превышающий норму (т.е. более 8000 фмоль/мл), явился мощным предиктором неблагоприятного исхода в течение одного года. В группе выживших больные со ?стажем? СД более 10 лет составили 43% против 76% в группе скончавшихся. В группе больных с уровнем НвА1с менее 6,5% в половине случаев отмечались признаки хронической почечной недостаточности. При ХПН снижается активность почечной инсулиназы. достоверно на выживаемость оказывали влияние тяжесть ХСН и наличие уремической стадии диабетической нефропатии. На каждый балл увеличения ШОКС риск смерти в течение года возрастает на 25%. Наличие ХПН увеличивает риск смерти в 3 раза. Выводы. Почти 1/4 часть больных ХСН, страдающих СД 2, погибает в течение года. Существенное влияние на выживаемость оказывает исходная тяжесть ХСН. Наибольшее значение для прогноза среди характеристик СД 2 имеет диабетическая нефропатия. Ухудшение выживаемости отмечено уже на стадии микроальбуминурии. При наличии уремии риск смерти возрастает в 3 раза. Для быстрой оценки риска смерти в течение года можно ориентироваться на ШОКС и на наличие признаков ХПН. Для улучшения прогноза больных ХСН, страдающих СД 2, необходимо особое внимание уделять профилактике, ранней диагностике и лечению диабетического поражения почек

    Side effects of statins in patient with compensated hypothyroidism and SLCO1B1 *5 (c.521T>C) polymorphism

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    Aim: to assess the influence of compensated hypothyroidism and SLCO1B1 *5 (c.521TC) gene polymorphism on the clinical and laboratory signs of the muscle damage during statin therapy. Methods: assessment of symptoms and markers of the muscle damage and SLCO1B1 *5 (c.521TC) genotyping were performed in 33 patients with primary hypothyroidism taking statins, in 31 patients taking statins without hypothyroidism and in 33 patients with primary hypothyroidism without statins taking. Results: muscle pain was observed more often in the group of the patients with compensated hypothyroidism on the background of statins taking compared with other groups (45,5, 16,1 and 30,3 %, respectively, p=0,048). Only in this group the pain was associated with increased levels of creatine- kinase (171,0108,12 and 110,043,81U/L, in the presence and absence of the pain, p=0,049), LDH (369,566,22 and 305,641,98 U/L, р=0,007), myoglobin titer (90,7109,89 and 41,128,56, р=0,005), and more frequent occurrence of TC and CC genotypes of SLCO1B1*5 (c.521TC) (68,4 и 28,6%, р=0,0027). Conclusions: the patients with compensated hypothyroidism have a higher risk of statin-induced myopathy increasing if the TC heterozygotes or CC homozygotes of SLCO1B1 *5 (c.521TC) gene are present, which requires thorough monitoring of clinical and biochemical muscle damage signs in case of its detection

    Russian national clinical recommendations for morbid obesity treatment in adults. 3rd revision (Morbid obesity treatment in adults)

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    The presented paper is a third revision of the clinical recommendations for the treatment of morbid obesity in adults. Morbid obesity is a condition with body mass index (BMI) &ge;40 kg / m2 or a BMI &ge;35 kg / m2 in the presence of serious complications associated with obesity. The recommendations provide data on the prevalence of obesity, its etiology and pathogenesis, as well as on associated complications. The necessary methods for laboratory and instrumental diagnosis of obesity are described in detail. In this revision of the recommendations, the staging of prescribing conservative and surgical methods for the treatment of obesity are determined. For the first time, a group of patients with obesity and type 2 diabetes mellitus is selected, in whom metabolic surgery allows a long-term improvement in the control of glycemia or remission of diabetes mellitus
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