IMPACT OF ANXIETY AND DEPRESSIVE DISORDERS ON THE NEUROPEPTIDE-CYTOKINE STATUS OF IMMUNE SYSTEM IN VARIOUS VARIANTS OF THE CLINICAL COURSE OF CHRONIC ISCHEMIC HEART DISEASE

Occurrence of coronary artery disease in combination with anxiety-depressive disorders is common in clinical practice. In such patients, affective disorders significantly may cause progression of atherosclerotic processes, thus complicating the course of cardiac pathology and prognosis. Distinct markers of immune inflammation, first of all, cytokines are of particular importance for the pro-atherogenic effects in atherosclerotic foci. Endogenous opiate peptides are considered the main regulators of these processes at the neuroimmune level. Their role for stabilization of cytokine levels in evolving inflammation in atherosclerotic plaque, and during adaptation of heart muscle to stressful effects was previously shown. Despite reliable data on the role of immune inflammatory markers in atherogenesis, the validity of the regulatory role of opiate peptides in this process, questions still exist about the effects of affective disorders upon neuropeptide-cytokine status of the immune system in the patients with chronic ischemic heart disease (IHD). Another issue concerns the ranges of these changes in painful and painless forms of myocardial ischemia.Therefore, the purpose of our study was to assess the impact of severity of anxiety-depressive disorders upon the neuropeptide-cytokine status of immune system in patients with various clinical variants of chronic IHD, as well as comparisons of these changes expressed in painlul and painless myocardial ischemia.Appropriate groups were formed, then being divided into subgroups, according to the percentage of painful and painless episodes of angina pectoris: Group 1 (n = 36) included patients with chronic coronary artery disease occurring and moderate-grade anxiety/depression; Group 2 (n = 34) consisted of patients with chronic coronary artery disease and mild anxiety-depressive disorders; Group 3 (n = 20) included patients with chronic coronary artery disease without anxiety and depressive disorders; Group 4 (n = 22) represented controls (healthy persons). As based on presence of painful and painless episodes of stenocardia, the following subgroups were specified: in the 1 st group of patients, painful form of IHD was detected in 44% of cases (n = 17); painless form of IHD was detected in 56% of patients (n = 19); in the 2 nd group of patients, painful form of IHD is in 52% of the examined persons (n = 18), painless form of IHD was revealed in 48% of cases (n = 16); in the 3 rd group, the painful form of IHD was confirmed in 37% of patients (n = 8), painless form of IHD was observed in 63% of patients (n = 12). In all these groups, the following parameters were evaluated: the state of psychophysiological status determined by psychological testing, the levels of vegetative regulation (β-endorphin), the function of cardiovascular system (SMECG), and the levels of peripheral blood TNFα, IL-1β, IL-6 and IL-4, IL-10 were also measured.As based on the data of clinical and laboratory examination, we have suggested that, in the patients with chronic IHD, anxiety and depressive disorders exert a direct pathological effect on the neuropeptide-cytokine status of immune system expressed as suppression of β-endorphin, increased level of pro-inflammatory cytokines and a decrease in anti-inflammatory factors. Meanwhile, these changes are especially pronounced in the patients with painless myocardial ischemia.