A randomized controlled study included 44 patients with acute myocardial infarction. It was found that intracoronary injection of bone marrow mononuclear cells is safe, ensures fixation of the injected cells in the myocardium, reduces blood levels of IL-1beta and TNF-alpha, increases the content insulin-like growth factor, and does not provoke malignant arrhythmias.

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Autologous bone marrow mononuclear cells were transplanted by intracoronary infusion to patients with myocardial infarction after recovery of coronary perfusion. Controls received traditional therapy alone. Echocardiography was carried out before and 3 and 6 months after cell therapy. Cell transplantation did not appreciably improved left-ventricular contractility in comparison with the control group. In none patient cell therapy provoked malignant ventricular arrhythmias. Intracoronary infusion of bone marrow mononuclear cells in patients with myocardial infarction did not improve cardiac contractility and did not aggravate the course of the disease.

Попонина Татьяна Михайловна -д-р мед. наук, профессор, профессор кафедры кардиологии ФПК и ППС СибГМУ (г. Томск).Гундерина Ксения Ивановна () -аспирант кафедры кардиологии ФПК и ППС СибГМУ (г. Томск).Попонина Юлия Сергеевна -канд. мед.наук, доцент кафедры кардиологии ФПК и ППС СибГМУ, врач-кардиолог отделения неотложной кардиологии НИИ кардиологии СО РАМН (г. Томск).Марков Валентин Алексеевич -д-р мед. наук, профессор, зав. кафедрой кардиологии ФПК и ППС СибГМУ, руководитель отделения неотложной кардиологии НИИ кардиологии СО РАМН (г. Томск).

Here we present a clinical case of cardiac sarcoidosis. The article discusses the difficulties of differential diagnosis in patients emergently hospitalized in the cardiology department with recurrent chest pain, no changes in the electrocardiogram (ECG), and a presumptive diagnosis of acute coronary syndrome without ST segment elevation (NSTE-ACS). A careful history taking, invasive coronary angiography, and contrast-enhanced (gadolinium-based contrast media) cardiac magnetic resonance imaging (CMR) contributed to the correct diagnostic decision in search for and identification of cardiac sarcoidosis in the patient.

Funding Acknowledgements Type of funding sources: None. Background In clinical medicine, there is still a need for a highly sensitive laboratory marker that reflects brain damage. In some cases, myocardial infarction proceeds with aggravation of cerebral ischemia, stroke, psychosomatic disorders. One of the candidates for laboratory diagnosis of brain damage is the S 100B protein. Aim of the study to analyze the level of brain-specific protein S 100B in blood plasma in patients with acute coronary syndrome associated with anxiety-depressive disorders. Methods and Results All patients were diagnosed with clinically severe anxiety of 55.2 [40; 64] points and depression of an average degree of 24.5 [19; 28] points. In the hospital, blood samples were taken for S 100B protein. The intragroup analysis of the S 100B protein level revealed that in 3 patients (5%) the S 100B protein level was below the normal limit 42.56 [32.6; 52.6] ng/L, in 13 patients (24%) the S 100B was within the normal range of 84.1 [75.27; 86.57] ng/L. In 38 patients (70%), the concentration of S100B protein was increased to 129.65 [110; 144] ng/L. The analysis of the group with a high concentration of S 100B protein found that the highest indicators of the S 100B protein level were in patients suffering from carbohydrate metabolism disorders, with a long history of hypertension, high levels of anxiety and depression. When studying the mental status of patients, a positive correlation was found between the concentration of the S100B protein and the level of anxiety (p = 0.00065). In 5 patients (9%), the maximum increase in the level of protein S 100 B 184.6 [166.26; 209.34] ng/L was revealed. These patients aged 60 to 70 years, had stroke in the past, had a long history of ischemic heart disease, type 2 diabetes, the course of AMI proceeded with a decrease in left ventricular ejection fraction to 34-40%. Patients with a protein level of 84.1 [75.27; 86.57] ng/L were younger, age 50-60 years, without a history of diabetes, with preserved left ventricular ejection fraction. Conclusion An increase in the S 100B protein level was observed in polymorbid patients, with a history of possible impairment of the blood-brain barrier permeability, which could have formed due to the toxic effect of the S 100B protein. This group of patients has more pronounced anxiety-depressive symptoms. Thus, the S 100B protein can be considered as a potential therapeutic target.

The open randomized placebo-controlled prospective study was conducted; we documented improvement of global contractility and diastolic function of left ventricle, clinical and psychological status in 60 patients with chronic heart failure receiving a very low dose of antibodies to C-end fragment to AT1 receptors of angiotensin II for 6 months (Cardosten). The drug was well-tolerated.

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