No abstract

In this review we cover key issues, concerned with the effects of cytokines in cardiac tissue and cardiac cells. We discuss the effects of proinflammatory cytokines under non-pathological conditions and their mechanisms dependent and independent of nitric oxide. The role of proinflammatory cytokines is considered in acute myocardial infarction and in heart failure. We also describe proinflammatory cytokines as inductors of arrhythmia. We discuss ionic current alternation as possible mechanisms of cytokines action in heart. We consider TNF-α as a possible player in this signaling cascade. It was shown that TNF-α induced alternation of transmembrane action potentials. Influence of TNF-α on transient outward current (I to ), I Kur , I Kr , I Ks , I K1 is also reported. We discuss the interplay between TNF-α and Ca 2+ current, influence of TNF-α on SERCA. Then we consider influence of IL-1 on action potentials, I Na , I Ca , I K . We also address the role of IL-2, IL-6, and IL-11. Finally using TNF-α and IL-6 as an example we discuss the effects of cytokines on mechanoelectrical feedback. Perfusion of cardiac tissue with TNF-α containing solution leads to abnormalities in cardiac electrical activity, majorly to prolongation of APD90 and appearance of hump-like depolarization at APD90 level. After reaching E c hump-like depolarization transforms into extra-AP, leading to sustained arrhythmias. TNF-α activates NO cardiomyocyte synthases and the rise of intracellular NO levels opens MGCs, which leads to sodium entry into the cell, which depolarizes cellular membrane, shifting resting potential towards E C . We proposed and proved that TNF-α triggered arrhythmias can be mediated through activation of MGCs. Stretching of preparations removed TNF-α. Perfusion of preparation with IL-6 containing solution leads to fibrillation in response to low levels of stretch. IL-6 mechanisms of action are mediated by NO synthases A. Kamkin (B)

The role of specific approaches to the management of patients with heart failure (HF) increases steeply with increasing age, as the patients of this age need attention to geriatric problems: reduced mobility, multiple diseases and cognitive impairment. Senile asthenia is a syndrome that reflects a decline in physiological reserve and increased vulnerability to various stressors. Senile asthenia is detected in 15–74% of patients with heart failure, the prevalence depends on the method of diagnosis and the studied population. This review discusses the effects of senile asthenia, comorbidity and geriatric syndromes on diagnosis, treatment, and outcomes in elderly patients with heart failure. The detection of senile asthenia in patients with HF is important from a clinical point of view, since this condition has an adverse effect on the course of heart failure and is associated with a higher incidence of emergency hospitalization and mortality. Bodily exercises can improve mobility, and the introduction of nursing observation can enhance treatment adherence among patients.