Introduction. Recent publications indicate that the most common comorbidities in hospitalized patients with coronavirus infection were arterial hypertension (AH), diabetes mellitus (DM), and coronary heart disease. However, the peculiarities of AH course in post-COVID-19 patients, especially with concomitant DM, are insufficiently covered in the relevant literature. The aim of the study. Тo investigate the peculiarities of hypertension course in patients with concomitant diabetes mellitus previously affected with COVID-19 infection. Materials and methods. We examined 48 patients with essential hypertension of stage II-III of 1-3 degrees, and concomitant DM, previously affected with Covid-19, 52-72 years of age. Results. It has been estimated that more than 1/3 of patients with hypertension who relapsed to COVID-19 complained of frequent headaches, palpitations, coughs, muscle and joint pain, fatigue and sleep disturbances. However, patients with concomitant DM were significantly more likely to complain of general weakness and indigestion. In many patients, regardless of the presence of concomitant pathology, in the postcocious period there was indicated an increase in C-reactive protein more than 3 mg/l and enhanced fibrinogen levels, indicating an increased risk of cardiovascular complications in this group patients. Most patients experienced worsening of blood pressure control during COVID-19 treatment. Uncontrolled hypertension was significantly more common in patients hospitalized for the treatment of acute COVID-19, regardless of DM presence. Conclusions. In patients with AH and concomitant DM significantly more often (76.0 % of cases (p is equal to 0.01)) – compared to patients with AH without DM (60.9 %) was detected uncontrolled hypertension in the post-COVID period. Worsening of blood pressure control in patients with concomitant DM is significantly more common (p value less than 0.001) in those patients who took three or more antihypertensive drugs, this notion require additional correction of antihypertensive therapy.

The aim. To analyze current evidence about etiology, pathogenesis, clinical manifestation, diagnosis, and treatment of patients with COVID-19 associated myocarditis. Multisystem inflammatory syndrome is possible in COVID-19 including inflammatory damage to the myocardium, which may last over several months and worsen the disease outcome. Mechanisms of inflammatory cardiac damage include direct damage by SARS-CoV-2, massive release of cytokines, dysregulation of the renin-angiotensin system. All these factors can aggravate pre-existing overload of the right heart chambers in patients with multifocal pneumonia, thrombosis of coronary arteries and myocardial ischemia. Inflammation of the myocardium manifests with typical symptoms of myocarditis and pericarditis. It can be accompanied by heart failure with rapid decompensation, arrhythmia, acute coronary syndrome or even sudden death. Laboratory findings in COVID-19 associated myocarditis include high levels of CRP, BNP, NT-proBNP, and D-dimer. Transthoracic echocardiography allows for an assessment of the left ventricular dysfunction and diagnosis of a pericardial effusion. Heart MRI according to the Lake Louise Diagnostic Criteria is the most sensitive diagnostic method in acute myocarditis. Medical imaging is indicated only in cases when results obtained can potentially influence the patient management tactics and should be performed according to the shortest protocol due to high risks of virus transmission. Conclusions. ESC experts (2020) do not provide unanimous recommendations for the treatment of SARS-CoV-2 associated myocarditis, considering a lack of the evidence base. Patient management is limited to adequate treatment of heart failure, arrhythmia, acute coronary syndrome, and prevention of thrombotic complications. Ongoing studies are aiming to evaluate potential place of glucocorticoids, intravenous immunoglobulins, antibodies against IL-6 receptor, colchicine in the treatment of COVID-19.

The aim of this review is to analyze and summarize the existing evidence regarding the possibilities of using acetylsalicylic acid (ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) to reduce cancer risk. Conclusions. Chronic inflammation facilitates the onset and progress of tumour growth. Anti-cancer properties of acetylsalicylic acid and other non-steroidal anti-inflammatory drugs are mediated via cyclooxygenase COX-dependent mechanisms, as well as other tumorigenic pathways. Current systematic review addresses potential role of ASA and other NSAIDs in reduction of cancer risk for the following localizations: head and neck, lungs, gastrointestinal tract, breast, ovaries, prostate, and skin. The role of ASA in primary prevention of colorectal cancer in specific populations is presented in 2016 U. S. Preventive Services Task Force guidelines. Studies indicate heterogeneous protective potential of ASA against different cancer types, depending on studied population, duration of intake and dose. Influence of non-aspirin NSAIDs on cancer morbidity and mortality is more controversial.