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The present document developed by the Russian Association of Gerontologists and Geriatricians represents the Clinical guidelines on chronic pain in older and senile patients. The Clinical guidelines were endorsed by Scientific Council of the Ministry of Health of the Russian Federation in December 2020.Clinical guidelines are focused on geriatricians providing medical care in outpatient and hospital settings, general practitioners, and physiotherapists.The document sets out the pain syndrom screening and diagnosis principles in older patients, management and treatment approaches in patients with chronic pain, as well as the prevention, rehabilitation, medical care organization issues and quality control criteria for its provision in this category of persons.

Aim: to investigate clinical properties of course and outcomes of infective endocarditis (IE) depending on source of infection, to find predictors of mortality in a Moscow general hospital.Materials and methods. We included in this study 176 patients with definite and possible infective endocarditis (the Duke criteria), admitted in our hospital in 2010–2017. Patients were divided in three groups according to source of infection. All patients underwent standard clinical and laboratory assessment, echocardiography, blood culture test combined with blood PCR with sequencing. Inhospital and 1­year outcome were evaluated.Results. Among 176 patients with IE 65.3 % were men (median age 57 [35–72] years), most patients (n=149, 84.7 %) had native valve IE. Etiological factor was identified in 127 (72.2 %) cases. Gram­positive infective agents prevailed (54 %). Surgery in active phase of the disease was performed in 30 (17 %) patients. Among patients with healthcare­associated IE (n=76, 43.9 %) prevailed those older than 60 years, with high Charlson comorbidity index, with culture­negative IE, and complicated clinical course (mainly progressing heart failure). Patients with intravenous drug use associated IE (n=50, 28.4 %) had low Charlson index, association with hepatitis C viral infection, involvement of tricuspid valve with big vegetations, high frequency of embolic complications, and low inhospital mortality. Group of patients with community acquired IE (n=50, 28.4 %) more often had uncommon causative microorganisms, and had better long­term outcome. In­hospital mortality was 30.1 % (n=53) mostly due to sepsis with multi­organ failure, and heart failure. Risk factors of inhospital death were history of cardiovascular diseases, old age, kidney damage, methicillin­resistant Staphylococcus aureus (MRSA) infection, uncontrolled infection, and embolic events. Risk factors of 1­year mortality were history of stroke, and heart failure as IE complication. Independent predictors of in­hospital death were MRSA infection (odds ratio [OR] 50.32, 95 % confidence interval [CI] 1.66–213.92; p=0.002), persistent infection (OR 18.6, 95 %CI 5.37–64.40; p=0.001), duration of fever >7 days after initiation of antibacterial therapy (OR 13.41, 95 %CI 3.51–51.24; p=0.001); and of death during first year – history of cerebral infarction (OR 4.39, 95 %CI 1.32–14.70; p=0.016)), and heart failure as IE complication (OR 8.1, 95 %CI 1.97–67.09; p=0.016). Among patients subjected to surgery there were no fatal outcomes during 1 year after hospital discharge, while among conservatively treated patients were 21 (14.4 %) deaths (pConclusion. Main clinical features of IE course in patients urgently admitted to a general hospital was dominance of healthcare­associated IE among patients, who were older than 60 years with severe comorbidities. These patients had more complications and worse outcome. Modeling of prognosis identified uncontrolled infection as key factor of unfavorable outcome. Surgery significantly reduced long­term mortality.

Senile asthenia syndrome (SAS) is a geriatric syndrome characterized by age-associated decline of the physiological reserve and function in multiple systems, which results in higher vulnerability to effects of endo- and exogenous factors and a high risk of unfavorable outcomes, loss of self-sufficiency, and death. Generally, SAS is observed in elderly patients with comorbidities. In cardiovascular diseases, SAS is associated with a poor prognosis, including a higher incidence of exacerbation and death both during acute events and in chronic disease. However, SAS is often not taken into account in developing diagnostic and therapeutic programs for managing elderly patients with cardiovascular diseases (CVD). This article analyzes available scientific information about SAS, algorithms for SAS diagnosis, and the scales that may be useful in developing individual plans for management of elderly patients with CVD.

A novel coronavirus infection SARS-CoV-2 (COVID19) is especially dangerous for elderly and senile patients. Preventive measures for elderly people should cover three areas: 1) direct prevention of the viral infection, 2) preservation of the functional status and prevention of geriatric syndromes, including the use of social support measures, 3) control of comorbidities. The clinical pattern of COVID-19 in older patients may be atypical, while the mildness of symptoms (no fever, cough, shortness of breath) may not correspond to the severity of the prognosis. Delirium may be the first manifestation of COVID-19, which requires special care in its screening. Management of elderly and senile patients with COVID19 should include measures for delirium prevention, the detection and improvement of nutrition. The risk of malnutrition with sarcopenia increases with hospitalization of a patient, especially when using artificial ventilation, is associated with an unfavorable prognosis during hospitalization, accelerates the progression of senile asthenia and reduces the quality of life. Geriatric assessment is the cornerstone of determining the management of an elderly patient.

Aim . Expert assessment of real clinical practice compliance with national guidelines on management of patients with chronic heart failure (HF) before the opening of the Expert Center of HF treatment. Material and methods . All patients admitted to 2 city clinical hospitals of Moscow with HF were included into the register. Clinical, demographic, laboratory and instrumental characteristics and medical treatment before and during hospitalization were evaluated, as well as recommendations contained in the discharge summary. Results . 300 patients with HF were included into the register. The mean age was 75 years (39, 95); the proportion of men – 44%. 95% of patients had HF IIIV (NYHA), among them 24% HF II, 61% HF III, 15% HF IV (NYHA). HF with reduced ejection fraction (HFrEF) was found in 45% of patients. 22% of the patients did not receive medical treatment before admission. 34% of patients with HFrEF received ACE inhibitors/angiotensin receptor blockers (ARBs), of which only 23% in effective dose. β-blockers were prescribed in 41% of HFeEF patients, of which 22% in the target dose. A third of patients needed in mineralocorticoid receptor antagonists (MRA) received spironolactone. During hospitalization 81% of HFrEF patients received ACEI therapy, 12% – ARBs, 91% – β-blockers, 90% – MRA, 81% – loop diuretics and 13% – thiazide diuretics. According to the discharge summary 5% of patients did not receive post-discharge blocker of the renin-angiotensin-aldosterone system without explanation in the medical documentation. β-blocker with proven efficacy was prescribed to 70% of HFrEF patients. Spironolactone was recommended after discharge in 89% of HFrEF patients. Conclusion . Implementation of register of hospitalized patients with HF gives an opportunity to identify shortcomings in the provision of medical care both in outpatient and inpatient stages.

The article is devoted to the study of a one-center experience of routine application of transradial access (TRD) by default in the treatment of patients with ACS in a short-term clinic, which has neither a vascular or cardiovascular surgery department. The experience of treatment of 3436 patients with acute coronary syndrome was analyzed, of which 72.64% were patients with acute myocardial infarc-tion. The use of TRD was considered successful in the case of completion of the procedure of stenting through the arm without the need for conversion of arterial access to the thigh. By default, right transradial access was used, except for cases of known anamnesis of mammarocoronary shunting. Time for puncture of the radial artery, installation of the introducer and catheterization of the arch of the aorta was 2.8 - 1.1 min. The average duration of fluoroscopy was 13.36 ± 8.86 minutes. The immediate success of the intervention, performed by transradial access, was 98%, of which the need for conversion to contralateral access was in 6.5% of patients. In total, two patients developed access point hematomas, which required the transfusion of blood components, managed to stop bleeding conservatively, in no case did vascular surgeons need help.

Background Kidney involvement in IE has a huge contribution in failure of the treatment. Frequency of kidney lesions is still high. There are several risk calculators for prognosing embolic events, perioperational mortality, 6-month mortality, but there is none for prognosing kidney events in IE. Materials/Methods 209 patients with verified IE (DUKE 2009, 2015), hospitalized from 2010 to 2018, were included in the study. Kidney function was assessed using CKD-EPI formula. AKI was diagnosed according to current guidelines (KDIGO 2012). Clinical, hematological and echocardiographic features were analysed to look for predictors of AKI. To create a simple risk calculator independent predictors obtained from log-regression analysis were used. The risk formula was derived using the coefficients: Pr(Y) = 1/[1 + exp(−XB)] where Pr(Y) = prognosed risk of AKI, XB = coef1*predictor1 + ... + logit-regression constant. Results AKI was presented in 66% cases and mainly was I (41%) and III (37%) stages. Predictors for AKI were established: MRSA OR 8.0 (95% CI 1.01–68.48; p=0.054), emergence or worsening of the HF sympthoms OR 2.83 (95% CI 1.27–6.32; p=0.011), gentamycin OR 2.71 (95% CI 1.33–5.53, p=0.006), history of CAD OR 2.35 (95% CI 1.05–5.27) p=0.038, WBC at admission >11.5x109/l OR 1.07 (95% CI 1.01–1.13), duration of hospitalization >20.7 days OR 1.03 (95% CI 1.01–1.05) p=0.005, C-reactive protein >90 mg/l OR 1.01 (95% CI 1.01–1.02) p=0.001. Simple risk calculator Coef OR Indicator MRSA 2.0755 8 0 Emergence or worsening of the heart failure sympthoms 1.04041 2.83 0 Gentamycin 0.3640833 2.71 1 History of coronary artery disease 0.8542633 2.35 1 White blood count at admission 0.0691979 1.07 13 Duration of hospitalization 0.0308953 1.03 2 C-reactive protein 0.0075288 1.01 180 Constant −3.275098 0.0378132 Logit 0.259795900 P 0.564586119 Scaling parameter 100 Points 56 Result 56 Conclusions A simple risk calculator for AKI is developed for patients with IE.

Background Infective endocarditis (IE) is frequently complicated by kidney damage of various pathogenesis. The essential differences in pathophysiological mechanisms of kidney lesions (glomerular and tubular damage, mixed mechanisms) create different therapeutical targets. Nowadays these mechanisms are only possible to differentiate with the use of nephrobiopsy or autopsy. Non-invasive methods to assess the genesis of kidney damage are eagerly wanted. It is possible that kidney biomarkers may be such method. Materials and methods 209 patients with verified IE (DUKE 2009, 2015), hospitalized and treated in city clinical hospital named after V.V. Vinogradov in Moscow from January 2010 to June 2018, were included in the study. Kidney function was assessed using CKD-EPI formula. Acute kidney injury (AKI) and acute kidney disease (AKD) were diagnosed according to current guidelines (KDIGO 2012) and the work group consensus (ADQI 16 Workgroup 2017). Serum creatinine decrease on ≥26,5 mcmol/L in 48 hours after the hospitalization was counted as early-onset AKI. Patients with serum creatinine elevation on ≥26,5 mcmol/L in 48 hours during the hospitalization were diagnosed with late-onset AKI. Biomarkers were assessed at the admission. Cystatin C level was assessed in serum; neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), albumin levels were assessed in urine. Results Kidney damage biomarkers' levels were analyzed in 65 patients with IE. Patients with kidney dysfunction (n=45) comparing to ones without AKI (n=20) had higher mean value of all kidney biomarkers, however, the significant difference was established only for cystatin C. (1.9 vs 1.3 mg/l respectively; p Conclusions The results of a study allow to consider serum cystatin C as AKI marker, AKI predictor and in-hospital mortality predictor in patients with IE, and urinal NGAL and serum cystatin C may be considered as AKD markers.

Background Kidney involvement in infective endocarditis (IE) has a huge contribution in failure of the antimicrobal therapy and in rejection of the surgical treatment. Frequency of kidney lesions is still high and is diagnosed in 50–80% cases intravitaly, and in 91,6% post-mortem. Materials/Methods 28 patients with verified IE (DUKE 2009, 2015), hospitalized and treated in clinical hospital from 2010 to 2018, were included in the study. Kidney function was assessed using CKD-EPI formula. Acute kidney injury (AKI) was diagnosed according to current guidelines (KDIGO 2012). Intravital nephrobiopsy was performed in 2 (7,1%) patients, in 26 patients (92,9%) morphological assessment was made on the autopsy tissue specimens. Autopsy material was assessed grossly and microscopically with H&E staining. Morphological changes in kidney were estimated based on standart histological criteria. Results Majority of patients with IE (92.9%) had structural changes in kidney tissue: 3 (12%), 16 (64%) and 6 (24%) patients had respectively isolated glomerular, tubular and mixed lesions. Significantly higher is rate of tubular lesion than glomerular (p=0.014). Main pattern in glomerular damage was mesangial proliferation, we didn't found any cases of crescentic GN. Herewith, proliferation was mainly diffuse (87.5%) rather than focal (12.5%). Glomerular damage in subacute IE (>56 days) appears more often than in acute IE ( Morphological diagnosis n (%) Morphological diagnosis n (%) Glomerulonephritis 8 (28.6) Tubulointerstitial nephritis 3 (10.7) Membranoproliferative glomerulonephritis 3 (10.7) Allegrgic tubulointerstitial nephritis 2 (7.2) Mesangioproliferative glomerulonephritis 5 (17.9) Infective tubulointerstitial nephritis 1 (3.6) Extracapillar crescentic glomerulonephritis 0 (0) Kidney abscess 3 (10.7) Acute tubular necrosis 22 (78.6) Kidney infarction 1 (3.6) Acute tubular necrosis (ischaemic) 11 (39.3) Renal artery embolism 1 (3.6) Acute tubular necrosis (toxic) 11 (39.3) Shock kidney 4 (14.3) Conclusions A morphological study of patients with IE revealed a wide range of kidney damage, however, the frequency of tubular lesions, mediated by nephrotoxic drugs and hemodynamic disorders significantly exceeds the frequency of immune complex glomerular lesions, as previously thought.

To investigate the specific features of conventional bacteriological methods and current molecular biological techniques for the etiological diagnosis of infective endocarditis (IE).Examinations were made in 53 patients treated at City Clinical Hospital Sixty-Four, Moscow Healthcare Department, in 2012-2015 who underwent simultaneous bacteriological and molecular biological (polymerase chain reaction (PCR) or PCR with further sequencing) examinations of blood or resected cardiac valve tissues.The investigation included 53 patients (31 men; median age, 62 years) with IE (Duke 2009); its primary form was observed in 32 (60.4%) patients. Blood bacteriological tests and PCR assays were positive in 28 (52.8%) and 34 (64.2%) patients, respectively. There were concordant results in 21 of the 28 positive blood culture cases and discordant results in 7 (25%); at the same time 3 cases showed a compete discordance in the detected causative agents (the growth of Enterococcus spp. was revealed by bacteriological examination and that of Staphylococcus spp., Streptococcus spp., and Escherichia coli by DNA PCR) and a pathogen could not be identified by DNA PCR in 4 patients who had positive blood bacteriological results. The positive PCR results for cocci and fungi were obtained in 10 of the 25 (47.2%) examinees with culture-negative IE. Rare causative agents were not revealed. The tissues obtained from 8 resected damaged heart valves displayed a wider spectrum of pathogens than did blood samples, which was associated with the formation of bacterial films.The etiological agent of IE was revealed in venous blood by bacteriological examination in 52.8% of the examinees, by PCR in 64.2%, and by either in 71.7%. There were concordant and discordant results in 67.9 and 32.1% of the patients, respectively; among whom 18.9% were found to have pathogen DNA revealed by PCR in culture-negative IE.Цель исследования. Изучить особенности традиционных бактериологических и современных молекулярно-биологических методов этиологической диагностики инфекционного эндокардита (ИЭ). Материалы и методы. Обследовали 53 больных, госпитализированных в 2012-2015 гг. в ГБУЗ ГКБ #64 ДЗМ, которым проводилось одновременное бактериологическое и молекулярно-биологическое (полимеразная цепная реакция - ПЦР или ПЦР с последующим секвенированием) исследования крови или тканей резецированного сердечного клапана. Результаты. В исследование включены 53 пациента с ИЭ (Duke 2009), медиана возраста 62 года (31 мужчина), первичная форма ИЭ у 32 (60,4%). Положительные результаты бактериологического исследования крови получены у 28 (52,8%) пациентов, ПЦР - у 34 (64,2%). Конкордантные результаты имелись в 21 из 28 случаев положительной культуры крови, дискордантные - у 7 (25%), при этом у 3 выявлено полное несоответствие по выявленным возбудителям (при бактериологическом исследовании рост Enterococcus spp., методом ПЦР - ДНК Staphylococcus spp., Streptococcus spp., Escherichia coli), а у 4 пациентов при положительном результате бактериологического исследования крови идентифицировать ДНК возбудителя не удалось. Среди 25 (47,2%) обследованных с культуронегативным ИЭ положительные результаты, представленные кокковой и грибковой флорой ПЦР, получены у 10. Редких возбудителей не выявлено. В тканях 8 резецированных пораженных сердечных клапанов выявлен более широкий спектр возбудителей, чем в образцах крови, что связано с образованием бактериальных пленок. Заключение. Бактериологическим методом этиологический агент ИЭ в венозной крови выявлен у 52,8% обследованных, методом ПЦР - у 64,2%, а при сочетанном применении обоих методов - у 71,7%. Конкордантные результаты имеются у 67,9%, дискордантные - у 32,1%, среди которых ДНК возбудителя методом ПЦР при культуронегативном ИЭ получены у 18,9% пациентов.Резюме Цель исследования. Изучить особенности традиционных бактериологических и современных молекулярно-биологических методов этиологической диагностики инфекционного эндокардита (ИЭ). Материалы и методы. Обследовали 53 больных, госпитализированных в 2012—2015 гг. в ГБУЗ ГКБ №64 ДЗМ, которым проводилось одновременное бактериологическое и молекулярно-биологическое (полимеразная цепная реакция — ПЦР или ПЦР с последующим секвенированием) исследования крови или тканей резецированного сердечного клапана. Результаты. В исследование включены 53 пациента с ИЭ (Duke 2009), медиана возраста 62 года (31 мужчина), первичная форма ИЭ у 32 (60,4%). Положительные результаты бактериологического исследования крови получены у 28 (52,8%) пациентов, ПЦР — у 34 (64,2%). Конкордантные результаты имелись в 21 из 28 случаев положительной культуры крови, дискордантные — у 7 (25%), при этом у 3 выявлено полное несоответствие по выявленным возбудителям (при бактериологическом исследовании рост Enterococcus spp., методом ПЦР — ДНК Staphylococcus spp., Streptococcus spp., Escherichia coli), а у 4 пациентов при положительном результате бактериологического исследования крови идентифицировать ДНК возбудителя не удалось. Среди 25 (47,2%) обследованных с культуронегативным ИЭ положительные результаты, представленные кокковой и грибковой флорой ПЦР, получены у 10. Редких возбудителей не выявлено. В тканях 8 резецированных пораженных сердечных клапанов выявлен более широкий спектр возбудителей, чем в образцах крови, что связано с образованием бактериальных пленок. Заключение. Бактериологическим методом этиологический агент ИЭ в венозной крови выявлен у 52,8% обследованных, методом ПЦР — у 64,2%, а при сочетанном применении обоих методов — у 71,7%. Конкордантные результаты имеются у 67,9%, дискордантные — у 32,1%, среди которых ДНК возбудителя методом ПЦР при культуронегативном ИЭ получены у 18,9% пациентов.

Objective: to study the evolution of ECG left ventricular hypertrophy (LVH) in patients with high risk arterial hypertension (AH) with during long-term antihypertensive treatment. Design and methods. 102 patients (48% males, average age 67,1+0,6) with AH of high risk were randomized to antihypertensive therapy based on AT1 angiotensine II receptors anatagonists (ARA) or dihydropiridine calcium channel blockers (CCB). To achieve target blood pressure (BP) 35 mV, Cornell voltage criteria>20 mV in females and > 28 mV in males and Cornell product >2442 msec*mV). Results: In 1 year of treatment regress of LVH was observed in 8 from 31 (25,85%) patients with initially ECG- LVH. Patients with regress of ECG - LVH were younger and had lower BMI versus patients with of ECG-LVH persistence (65,5±2,4 vs 66,7±5,9 years and 28,6±5,6 vs 29,2±4,3 kg/m 2 respectively, n.s.); and significantly lower systolic BP (SBP) after 1 year treatment (137,8±7,6 mmHg vs 142,3±6,2 mmHg respectively). Step logistic regression analysis revealed that SBP was the only independent factor related with regress of ECG-LVH. baseline. Those patients were non significantly older (69,4±6,4 vs 66,0±6,2 years) and had higher blood glucose and total cholesterol levels both at baseline and after 1-year treatment and higher SBP after 1 treatment. Independent correlation with ECG-LVH development was found only for SBP, glucose and total cholesterol vlaues after 1-year treatment. There was no correlation between evolution of LVH and the type of treatmen. Conclusion. Persistence and development of ECG-LVH in patients with high risk AH during long-term antihypertensive treatment is mainly associated with insufficient SBP control. Data on value of glucose and total cholesterol levels suggests potential benefit of treatment regimens with complex correction of risk factors for prevention of ECG-LVH development.

The structural and functional features of the microcirculatory heel (MCB) were studied in patients with arterial hypertension (AH) in relation to the presence or absence of type 1 diabetes mellitus (DM). Two hundred and twelve patients were examined. These included 110 patients with grades 1 and 2 arterial hypertension (AH) and type 2 DM, 82 patients with AH without type 2 DM, and 20 apparently healthy individuals. Laser Doppler flowmetry (LDF) was used to estimate basal blood flow, the loading test parameters characterizing the structural and functional status of MCB, and the incidence of hemodynamic types of microcirculation. Patients with AH concurrent with type 1 DM were found to have the following microcirculatory features: an increase in perfusion blood flow (microcirculation index, 8,8±1,8 perf. units versus 4,9±0,8 perf, units in patients with AH without DM and 6,7±0,9 perf. units in the control group), a drastic reduction in myogenic activity to 13,2±5,7 % versus 16,7±6,8 and 25,2±6,4 %, respectively, a decrease in vascular resistance, impairment of autoregulation, and low reserve capacities (reserve capillary blood flow was 197,8±31,6 % versus 429,9±82,01 % in the group of AH without DM and 302,8±50,1 % in the control group), a predominance of the hyperemic hemodynamic type (58,8 % in patients with AH and DM, 20,9 % in those with AH without DM, and 20,0 % in the controls). The specific features of the altered microcirculatory bed in patients with AH concurrent with type 2 DM were ascertained. These included the predominance of hyperemic microcirculation, impaired autoregulation. diminished microvascular resistance, and the low reserve capacities of the microcirculatory bed.