[Case of a Сombination of Lupus Erythematosus, Antiphospholipid Syndrome and Myocardial Infarction].

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of unknown etiology characterized by a wide range of clinical manifestations with damage to various organs and systems of the body. There are bad prognostic factors for SLE: damage to the heart, kidney, central nervous system, the development of hematological crises and secondary antiphospholipid syndrome. A number of authors consider systemic lupus erythematosus a "new" risk factor for atherosclerosis. The overall risk of myocardial infarction (MI) in patients with SLE is 10 times higher than in the general population. The article presents clinical case report of the development of myocardial infarction in a woman with SLE, receiving therapy for secondary antiphospholipid syndrome.

[Prognostic markers for the development of adverse outcomes in patients with chronic obstructive pulmonary disease and chronic heart failure].

AIM: To identify markers of adverse outcomes in patients with a combination of chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF). MATERIALS AND METHODS: 35 patients with COPD (without an anamnesis of coronary heart disease), 68 patients with COPD and CHF, 28 patients with CHF of ischemic genesis who were on treatment at the State Regional Clinical Hospital of Saratov were examined. The levels of the N-terminal fragment of the natriuretic peptide, galectin-3, the highly sensitive C-reactive protein, the proteins that bind fatty acids, the stiffness parameters of the arterial wall were determined; echocardiography was performed, calculated the index of comorbidity of Charlson. A year after entering the study, patients or their relatives were interviewed for their adverse outcomes. RESULTS: The combination of COPD and CHF is accompanied by an increase in the likelihood of the development of heart failure decompensation compared with the isolated course of COPD. The main causes of death of patients with combined pathology were respiratory failure and cardiovascular complications. Decompensation of CHF was 3,6 times more likely in patients with COPD and CHF of ischemic origin than in patients without previous myocardial infarction. The risk group the development of acute decompensation of heart failure within the next year is composed of patients with COPD and CHF having 3-4 functional classes of CHF, signs of decompensation in the small circulation, angina pectoris, past myocardial infarction. The most significant prognostic echocardiographic parameters were marked dilatation of the left auricles, reduction of the left ventricular ejection fraction less than 45%. The development of cardiovascular complications in patients with COPD and CHF is interrelated with an increase in arterial rigidity. The increase in total mortality is associated with the severity of heart failure and increased 24-hour arterial rigidity. CONCLUSION: The obtained results will allow to form high-risk groups and optimize the treatment-diagnostic process.

[Vascular remodeling indicators and their impact on prognosis in patients with chronic heart failure].

AIM: To estimate vascular remodeling indicators and their impact on prognosis in patients with chronic heart failure (CHF). SUBJECTS AND METHODS: The study enrolled 128 patients with prior myocardial infarction and CHF and 40 individuals as a comparison group. Endothelium-dependent and -independent vasodilation (EDV and EIDV) was studied in the reactive hyperemia (RH) test and nitroglycerin (NTG) test. Carotid artery (CA) intima-media thickness (IMT) and great arterial rigidity were studied. RESULTS: As compared to the control subjects, the patients with CHF were found to have EDV and EIVD reductions that were more pronounced in those with Functional Class IV CHF, more CA IMT, and abnormal arterial rigidity. There were relationships of EDV and EIDV to CA IMT (r = -0.30; p = 0.02) and aortic pulse wave velocity (APWV) (r = -0.30; p = 0.05). Multivariate analysis showed that the risk for cardiovascular events (CVE) in the CHF patients with an APWV of > 12 m/sec during a year was 2.02 times higher than in those with an APWV of < or = 12 m/sec (relative risk 2.02, 95 confidence interval, 1.01-4.03). CONCLUSION: APWV is an independent risk factor of CVE in patients with CHF.

[Prognostic significance of cardiac rhythm variability in patients with chronic heart failure].

Prognosis of chronic heart failure (CCF) is a challenging clinical problem. The role of heart rhythm variability (HRV) in CCF pathogensis is poorly known. This study was aimed at estimating the possibility of using HRV for prognosis of CCF. It included 110 patients (mean age 55.1 +/- 6.4 yr) with CCF symptoms after myocardial infarction. HRV analysis was based on 5 minute records. During the first year; 44 patients developed cardiovascular complications, 20 aggravation of CCF 5 unstable angina, 7 repeated infarction, 9 died. The low-frequency component (LF) of the spectrum was inversely related to age, HR, NT-proBNP, CRP and left ventricular election fraction. Based on the low-frequency component median, the patients were allocated to 2 groups (less than 5.2 ln ms2 and 5.2 ln ms2 or more). Comparison of survival curves by the Kaplan-Meier method showed that at LF < 5.2 ln ms2 the probability of CCF decompensation (p = 0.03), secondary infarction (p = 0.007), lethal outcome (p = 0.03) is significantly higher than at LF of 5.2 ln ms2 or more. It means that LF < 5.2 ln ms is an independent risk factor of CCF decompensation, repeated myocardial infarction, amd lethal outcome.

[Dynamics of structural functional parameters of cardiovascular system in patients with Stable Angina and Congestive Heart Failure treated with Ivabradine for six months].

UNLABELLED: URGENCY: Frequency of warm reductions (FWR) is the independent risk factor increasing frequency of the general death rate, sudden death rate and death rate from cardiovascular diseases. Aim of the work was to study dynamics of parameters of cardiovascular system in Patients with Stable Angina (SA) and Congestive Heart Failure (CHF) treated with Ivabradin within six months were investigated. MATERIALS AND METHODS: 78 patients having symptoms of SA and CHF and also FWR more than 70 per 1 minute treated the maximum dose blokatorov, are divided into 2 groups. The patient of the first group (40 people) to standard therapy was added ivabradin. Patients of the second group (38 people) received the standard treatment of a SA and CHF. Before and after six months of the treatment the following findings were evaluated: the 6 minute walk test results, echocardiographic parameters, of heart rate variability (HRV), von Willebrand factor, endothelium dependent and independent vasodilation, main arteries rigidity. RESULTS: The complex therapy including ivabradin, at examined patients promotes heart rate fall, to reduction of quantity of attacks of a stable angina and number of the accepted tablets of nitroglycerine, increase of CHF functional class, increase in shock volume left ventricular (LV) and certainly diastolichesky volume LV, to decrease in activity of the factor of Willebrand, quality of life. Indicators of HRV, endothelium dependent and independent vasodilation, main arteries rigidity during against 6 monthly therapies improve, but do not reach reliability degree.

Cold acclimation-associated changes in brown adipose tissue do not necessarily indicate an increase of nonshivering thermogenesis in C57BL/6J mice.

We have reported previously that a cold acclimation procedure (3-hr partial restraint at 6 degrees C, repeated 3 times at 2-week intervals) usually improves the cold tolerance of adult C57BL/6J mice. Those mice that did not improve their cold tolerance had lower cold-induced sympathetic nervous outflow to the interscapular brown adipose tissue (IBAT), suggesting a failure in the mechanisms of nonshivering thermogenesis. To understand the origin of this failure, this study was intended to measure nonshivering thermogenesis in mice that did not improve their cold tolerance after the cold acclimation procedure. After being subjected 3 times to a partial restraint at 6 degrees C, mice were anesthetized with urethane, immobilized with vecuronium bromide, and placed on artificial ventilation. The VO2 and VCO2 in expired air were measured and metabolic heat production (MHP) was calculated while body temperature was artificially lowered to 7.5 degrees C below control level. In a separate group of mice, the total amount and concentration of mitochondrial uncoupling protein, thermogenin (UCP), in IBAT was measured immediately after completion of the cold-acclimation procedure. The concentration and the amount of UCP in the mitochondria of IBAT was significantly higher in all mice that had been presented to the cold acclimation procedure, regardless of its outcome, than in mice that had never been exposed to an environment below room temperature (NAIVE). MHP increased significantly during body cooling in all mice. However, MHP before and during cold stimulation in mice that did not improve their cold tolerance as a result of the cold-acclimation procedure was significantly lower than the MHP of animals in which cold tolerance was improved, and was not different from MHP of the NAIVE group. Therefore, in mice in which cold tolerance did not improve after repeated cold exposure, the anatomical and biochemical changes in brown adipose tissue typical of cold acclimation were not associated with a cold-induced increase in MHP. We infer that the expression of UCP in brown adipose tissue is a necessary, but not sufficient, attribute of cold acclimation. Cold acclimation, measured as increased cold tolerance, occurs only if synthesis of UCP in BAT is associated with an increased cold-induced response of the sympathetic nervous system.

Nonshivering thermogenesis in adult and aged C57BL/6J mice housed at 22 degrees C and at 29 degrees C.

Twelve- and 28-month-old C57BL/6J male mice were housed either at room temperature of 22 degrees C or at thermoneutrality (29 degrees C) during the two months prior to experiments. Acute experiments were conducted under anesthesia, myorelaxation, and artificial ventilation. We recorded efferent electrical impulse activity in one of the sympathetic nerves innervating the interscapular brown adipose tissue in response to acute cold stimulation, when body temperature was lowered 7.5 degrees C below control level. In separate experiments we measured O2 consumption and CO2 production and calculated the nonshivering thermogenesis. We also measured the concentration of uncoupling protein in interscapular brown adipose tissue before and after three-hour cold stress. In aged mice, both sympathetic nervous activity and nonshivering thermogenesis were lower in animals housed at thermoneutrality (29 degrees C) than in mice housed at 22 degrees. Among mice maintained at 22 degrees C, but not at thermoneutrality, aged animals had greater nonshivering thermogenesis and greater cold induced concentration of uncoupling protein in the brown adipose tissue than adults. Sympathetic nervous outflow to brown adipose tissue was always greater in aged mice, regardless of the temperature of acclimation. We concluded that aged mice, housed at 22 degrees C, showed the changes in nonshivering thermogenesis associated with cold acclimation. However, an increased sympathetic outflow to brown adipose tissue in aged animals reflects an age-related elevation of the tone and responsiveness of the sympathetic nervous system.

Immunosorbent for IgG apheresis: an in vitro study.

We obtained anti-IgG Sepharose-an immunosorbent with sheep monospecific polyclonal antibodies against human IgG-for extracorporeal removal of human IgG. Appropriate conditions for effective usage of the immunosorbent were chosen. Binding capacity and selectivity of anti-IgG Sepharose were determined and compared with the corresponding properties of other sorbents for IgG apheresis; these properties appeared to be acceptable for immunoapheresis procedures. Methods for therapeutic application of anti-IgG Sepharose is expected to be effective when used in immunoapheresis procedures for treatment of autoimmune diseases and for preparation of patients for organ transplantation.

Nonshivering thermogenesis during acute cold exposure in adult and aged C57BL/6J mice.

In C57BL/6J adult and aged mice, housed at room temperature (22.5 +/- 1 degrees C), we measured O2 consumption and CO2 production and calculated metabolic heat production under conditions of anesthesia and myorelaxation during acute cold stimulation when body temperature was lowered 7.5 degrees C below control level. An independent group of mice was subjected to a three hour partial physical restraint at 6 degrees C and concentration of uncoupling protein (thermogenin) was measured in interscapular brown adipose tissue mitochondria at different times after cold exposure. Heat production under anesthesia and myorelaxation was about 57-66% lower than in nonanesthetized conditions, but increased significantly during cold stimulation in both age groups. Under anesthesia and myorelaxation before and during cold stimulation aged mice produced about 20% more heat than adult mice. Because in these experiments all sources of facultative thermogenesis, except nonshivering, were suppressed by anesthesia and myorelaxation, and because brown adipose tissue is the major source of nonshivering thermoproduction, we concluded that aged mice housed at room temperature have an increased thermogenesis in brown adipose tissue. This conclusion was also supported by the finding that the concentration of uncoupling protein measured in the mitochondria of brown adipose tissue after single cold exposure was significantly higher in aged than in adult mice. Therefore, we propose that the lower, cold-induced, heat production typically observed in nonanesthetized aged mice may reflect reduced thermogenic capacity of skeletal muscles. While aged mice have less brown adipose tissue than adult animals, the remaining brown adipose tissue may compensate by increasing the concentration of uncoupling protein.

[Clinical and experimental studies of the combined use of dibasol and furosemide]. / Kliniko-éksperimental'noe izuchenie sochetannogo ispol'zovaniia dibazola i furosemida.

A combined use of dibasol and furosemide was demonstrated to be followed by a decrease of furosemide toxic effect on the rat liver, an increase of its diuretic effect in patients and changes of furosemide metabolism kinetics in individuals.

[Effects of dibasol and levamisole on the microsomal enzyme system]. / Izuchenie vliianie lekarstvennykh preparatov dibazola i levamizola na sistemu mikrosomal'nykh fermentov.

It was shown that single doses of levamisole (10 mg/kg) and dibasole (50 and 100 mg/kg) suppressed the activity of cytochrome P-450 that was indicated by an increase of hexenal-induced sleep in mice. Administration of dibasole (100 mg/kg) three times was not followed by a significant change in the sleep duration. It was also established that dibasole administered at the concentration of 5 10(-4) M suppressed approximately by 50% the activity of aminopyrindemethylase and benzopyrenmonooxygenase and exerted no influence on methylcholantrene-induced activity of benzpyrenmonooxygenase.