Интегральная модель диагностики и наблюдения больных саркоидозом в современных условия

The aim of the work performed was to develop a modern model of diagnosis and observation of sacroidosis patients. We examined 144 patients, and sarcoidosis was diagnosed in 109 of them. Each the third case of sarcoidosis was histologically verified. The phthysiatric facilities played the leading role in detecting sarcoidosis-like diseases and definition of the patients' contagiosity. The diagnosis of sarcoidosis and topic detection of injured organs require a complex examination in a modern diagnostic centre including various specialists' consultations. Such approach allows to assess a real spread of the disease, a rate of extrapuimonary lesions and efficacy of different therapeutic methods. The authors propose to create a national consensus on sarcoidosis.Задачей работы была отработка современной модели диагностики и наблюдения за больными саркоидозом. Были обследованы 144 пациента, у которых в 109 был подтвержден саркоидоз. В каждом третьем случае была проведена гистологическая верификация диагноза. В раннем выявлении состояний, сходных с саркоидозом, и исключения контагиозности пациентов при дальнейшем обследовании ведущая роль была отведена фтизиатрической службе. Верификация диагноза и топическая диагностика поражения органов и систем при саркоидозе требует комплексного обследования в условиях современного диагностического центра с привлечением специалистов различного профиля. Это позволит оценить реальную распространенность саркоидоза, частоту внелегочных поражений и эффективность различных методов лечения. Авторы предлагают приступить к выработке национального соглашения по данному заболеванию

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

EARLY DIAGNOSTICS OF HEART FAILURE IN PATIENTS WITH CORONARY HEART DISEASE

A screening of chronic heart failure (CHF) in patients with Coronary Heart Disease (CHD) has been done. An echocardiography study (echo) was used to reveal possible variants of left ventricle myocardium dysfunction. A group of patients with left ventricle diastolic dysfunction (LVDD) was selected. After a meticulous clinical examination including stress tests the diagnosis of CHF has been made in 85.9 % patients. An attempt has been made to determine most diagnostically valuable echo parameters characterizing left ventricle relaxation function in various CHF functional classes in coronary patients. Therefore the presence of normal contractile function of left ventricle myocardium probably does not rule out the presence of CHF in patients with long term CHD. Patient assessments must include evaluation of LV diastolic function with subsequent physical stress tests for final decision on the presence of CHF

POSSIBILITIES OF NON-DRUG CORRECTION OF IMPAIRED BLOOD REOLOGY IN CORONARY HEART DISEASE

The work has studied the therapeutic action of ozone-oxygenated crystalloids as a factor of compensation of hemoreology disorders in coronary patients. 109 coronary patients with II-III unctional class angina at effort, aged 40 to 79, have been followed up. All patients received traditional anti-anginal treatment. Patients in principal groups received ozone therapy in conjunction with traditional treatment. Apparent blood viscosity, fluidity threshold and shift tension were measured before and after the treatment. Study parameters have been found to decrease in all studied groups; with no dynamics inpatients receiving traditional therapy. A conclusion has been made that parenteral introduction of ozone-oxygenated crystalloids in therapeutic dosage promotes improvement of blood reology properties

Antiinflammatory therapy with canakinumab for atherosclerotic disease

BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society