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

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

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

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

Drug-Induced Liver Injuries (Clinical Guidelines for Physicians)

Aim. Clinical guidelines for the management of adult patients suffering from drug-induced liver injuries (DILI) are intended for all medical specialists, who treat such patients in their clinical practice.Key findings. The presented recommendations contain information about the epidemiological data, terminology, diagnostic principles, classification, prognosis and management of patients with DILI. The recommendations list pharmacological agents that most commonly cause DILI, including its fatal cases. Dose-dependent and predictable (hepatotoxic), as well as dose-independent and unpredictable (idiosyncratic) DILI forms are described in detail, which information has a particular practical significance. The criteria and types of DILI are described in detail, with the most reliable diagnostic and prognostic scales and indices being provided. The pathogenesis and risk factors for the development of DILI are considered. The clinical and morphological forms (phenotypes) of DILI are described. The diseases that are included into the differential diagnosis of DILI, as well as the principles of its implementation, are given. The role and significance of various diagnostic methods for examining a patient with suspected DILI is described, with the liver biopsy role being discussed. Clinical situations, in which DILI can acquire a chronic course, are described. A section on the assessment of causal relationships in the diagnosis of DILI is presented; the practical value of using the CIOMS-RUCAM scale is shown. All possible therapeutic measures and pharmacological approaches to the treatment of patients with various DILI phenotypes are investigated in detail. A particular attention is paid to the use of glucocorticosteroids in the treatment of DILI.Conclusion. The presented clinical recommendations are important for improving the quality of medical care in the field of hepatology

Drug-Induced Liver Injuries (Clinical Guidelines for Physicians)

Aim. Clinical guidelines for the management of adult patients suffering from drug-induced liver injuries (DILI) are intended for all medical specialists, who treat such patients in their clinical practice.Key findings. The presented recommendations contain information about the epidemiological data, terminology, diagnostic principles, classification, prognosis and management of patients with DILI. The recommendations list pharmacological agents that most commonly cause DILI, including its fatal cases. Dose-dependent and predictable (hepatotoxic), as well as dose-independent and unpredictable (idiosyncratic) DILI forms are described in detail, which information has a particular practical significance. The criteria and types of DILI are described in detail, with the most reliable diagnostic and prognostic scales and indices being provided. The pathogenesis and risk factors for the development of DILI are considered. The clinical and morphological forms (phenotypes) of DILI are described. The diseases that are included into the differential diagnosis of DILI, as well as the principles of its implementation, are given. The role and significance of various diagnostic methods for examining a patient with suspected DILI is described, with the liver biopsy role being discussed. Clinical situations, in which DILI can acquire a chronic course, are described. A section on the assessment of causal relationships in the diagnosis of DILI is presented; the practical value of using the CIOMS-RUCAM scale is shown. All possible therapeutic measures and pharmacological approaches to the treatment of patients with various DILI phenotypes are investigated in detail. A particular attention is paid to the use of glucocorticosteroids in the treatment of DILI.Conclusion. The presented clinical recommendations are important for improving the quality of medical care in the field of hepatology