[Recommendations for the management of COVID 19 patients regarding proarrhythmic effects of some current treatments, specifically if these patients suffer from arrhythmias, and for those receiving antiarrhythmic therapy.]

Recommendation provides information to employees of medical departments at any level and primarily primary care about the possible proarrhythmic and adverse effects of drugs used for the treatment of COVID-19 patients and the features of therapy for COVID-19 patients with heart rhythm and conduction disorders receiving permanent antiarrhythmic therapy.

Cardiac Fibrosis in Patients With Atrial Fibrillation: Mechanisms and Clinical Implications.

Atrial fibrillation (AF) is associated with structural, electrical, and contractile remodeling of the atria. Development and progression of atrial fibrosis is the hallmark of structural remodeling in AF and is considered the substrate for AF perpetuation. In contrast, experimental and clinical data on the effect of ventricular fibrotic processes in the pathogenesis of AF and its complications are controversial. Ventricular fibrosis seems to contribute to abnormalities in cardiac relaxation and contractility and to the development of heart failure, a common finding in AF. Given that AF and heart failure frequently coexist and that both conditions affect patient prognosis, a better understanding of the mutual effect of fibrosis in AF and heart failure is of particular interest. In this review paper, we provide an overview of the general mechanisms of cardiac fibrosis in AF, differences between fibrotic processes in atria and ventricles, and the clinical and prognostic significance of cardiac fibrosis in AF.

Relationship between vascular endothelial function and vitamin D and parathyroid hormone levels in women with arterial hypertension.

INTRODUCTION: There are few studies indicating a relationship between vitamin D, parathyroid hormone (PTH), and parameters of endothelial function. OBJECTIVES: The aim of the study was to establish the relationship between vascular endothelial function and the level of vitamin D and PTH in women with arterial hypertension (AH). PATIENTS AND METHODS: It was a cross-sectional study of 141 women with AH stage II aged 50.8 ±6.0 years. We determined the serum levels of total 25-hydroxyvitamin D (25(OH)D), PTH, endothelin 1, as well as nitrites and nitrates. Endothelial function was measured by impedance rheography. Endothelium-dependent vasodilatation was measured by a reactive hyperemia test. Endothelium-dependent vasodilatation of less than 12% was considered as endothelial dysfunction (ED). RESULTS: Vitamin D deficiency was observed in 53 women (37.6%); insufficiency, in 42 (30.1%); and the optimal level, in 46 (32.3%). ED was determined in 49.6% of the patients. The serum PTH level was 36.6 ±20.1 pg/ml, and it was above the upper limit of the reference range only in 5.5% of the cases. We showed significant correlations between PTH and systolic blood pressure (R = 0.28; P = 0.003), PTH and 25(OH)D (R = -0.27; P = 0.025), and 25(OH)D and SBP (R = -0.23; P = 0.034). In the group with ED, the serum level of endothelin 1 was higher compared with the group without ED (0.57 ±0.18 vs. 0.49 ±0.21 pg/ml; P = 0.032) and that of nitrates and nitrites was lower compared with the group without ED (15.2 [11.1-29.9] vs. 22.8 [16.9-33.0] µmol/l; P = 0.0005). In the group without ED, PTH inversely correlated with endothelin 1 (R = -0.27; P = 0.043). In the group with ED, PTH inversely correlated with nitrates and nitrites (R = -0.48; P = 0.003). CONCLUSIONS: In women with AH and without ED, PTH affected the production of a vasoconstrictor, endothelin 1, while in those with ED, PTH was associated with a lower production of vasodilators, nitrates and nitrites, by the vascular endothelium.

The CD40-CD40L system in cardiovascular disease.

The CD40-CD40L system is a pathway which is associated with both prothrombotic and proinflammatory effects. CD40 and its ligand were first discovered on the surface of activated T cells, but its presence on B cells, antigen-presenting cells, mast cells, and finally platelets, is evident. The soluble form of CD40L (sCD40L) is derived mainly from activated platelets and contributes to the pathophysiology of atherosclerosis and atherothrombosis. Indeed, sCD40L has autocrine, paracrine, and endocrine activities, and it enhances platelet activation, aggregation, and platelet-leucocyte conjugation that may lead to atherothrombosis. It has even been suggested that sCD40L may play a pathogenic role in triggering acute coronary syndromes. Conversely, blockade of this pathway with anti-CD40L antibodies may prevent or delay the progression of atherosclerosis. Concentrations of sCD40L also predict risk of future cardiovascular disease in healthy women and clinical outcomes in patients with acute coronary syndromes. However, there are controversial and uncertain points over the application of this biomarker to clinical cardiology. In this review, we provide an overview of potential implications of CD40-CD40L signalling and sCD40L as a biomarker in patients with atherosclerotic vascular diseases.