Diabetes mellitus (DM) and heart failure (HF) are frequent comorbidities with a bidirectional relationship. Patients with HF have increased risk of developing DM, and those with DM are at greater risk of developing HF. HF does not fit clearly into the microangiopathy and macroangiopathy groups. It is known that coronary artery disease and arterial hypertension are the major causes of HF; however, it has been shown that DM can trigger functional and structural abnormalities in the myocardium via diabetic cardiomyopathy, a condition with either restrictive or dilated phenotype. While HF treatment is equally effective and safe in patients with and without DM, this statement is not applicable for antidiabetic treatment. Several antidiabetic drugs, such as rosiglitazone, pioglitazone and saxagliptin increase the risk of hospitalisation for HF, therefore these antidiabetic drugs are contraindicated in patients with DM and HF or patients at risk of developing HF. Despite a large number of clinical evidence, uncertainty about the safety of antidiabetic drugs in patients with HF always exists. In this review, the issues of DM treatment in patients with HF are addressed in detail.
AL cardiac amyloidosis is a relatively rare disorder that belongs to the group of infiltrative cardiomyopathies. Diagnosis of primary amyloidosis is challenging due to many unspecific symptoms and sings, which often leads to late diagnosis when treatment options are limited. Primary amyloidosis particularly needs to be excluded in patients with heart failure with preserved ejection fraction. Therapy in cardiac amyloidosis has to main vectors: 1) chemotherapy to eliminate amyloidogenic plasmatic cells 2) heart failure treatment. The main challenge for cardiologists is to support hemodynamics until response to chemotherapy occurs. In the article the issue of diagnostics, risk stratification and treatment of primary cardiac amyloidosis is addressed.
Objective: A considerable proportion of the population due to both economic reasons and traditions appear to be experiencing chronic deficit in micronutrients, which may be deteriorated on the background of drug therapy being performed. The purpose of our study was to optimize pharmacotherapy of patients with first-ever prescribed diuretic-containing combined therapy for arterial hypertension (AH) by means of adding a vitamin-mineral complex. Method: To determine B-group vitamins (thiamine, riboflavin, pyridoxine) in blood plasma by means of high-performance liquid chromatography (HPLC) and, on achieving the target values of arterial pressure (AP), to analyse the patients' quality of life by means of such neuropsychological tests as the General Health Questionnaire -36 (GHQ-36) and WAM (wellbeing, activity, mood) questionnaire. Results: The group of patients receiving antihypertensive therapy alone demonstrated a decrease in blood plasma thiamine, riboflavin and pyridoxine from 34.5±4.2 to 25.4±3.2 ng/ml (p<0.05), from 11.3±1.5 to 7.8±1.1 ng/ml (p<0.05) and from 13.4±1.5 to 9.1±1.3 ng ng/ml, respectively. In patients receiving the vitamin-mineral complex additionally to drug therapy of AH, no significant alterations in the content of micronutrients in blood plasma were revealed. We noted more pronounced dynamics in the scores by the GHQ-36 and a more pronounced increase in the patients' activity by the WAM test, amounting to 28,9 Δ % and 15.51 Δ %, respectively (p<0.05). Conclusion: Supplementing antihypertensive pharmacotherapy with a vitamin-mineral complex makes it possible not only to maintain the level of micronutrients at the level of the physiological requirements but to improve the patients' quality of life as assessed by neuropsychological scales. Shikh et al. / Effect of vitamin-mineral complexes on quality of life of patients with arterial hypertension 2 / 6
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