Background and Aims There is little information on the incremental prognostic importance of frailty beyond conventional prognostic variables in heart failure (HF) populations from different country income levels. Methods A total of 3429 adults with HF (age 61 ± 14 years, 33% women) from 27 high-, middle- and low-income countries were prospectively studied. Baseline frailty was evaluated by the Fried index, incorporating handgrip strength, gait speed, physical activity, unintended weight loss, and self-reported exhaustion. Mean left ventricular ejection fraction was 39 ± 14% and 26% had New York Heart Association Class III/IV symptoms. Participants were followed for a median (25th to 75th percentile) of 3.1 (2.0–4.3) years. Cox proportional hazard models for death and HF hospitalization adjusted for country income level; age; sex; education; HF aetiology; left ventricular ejection fraction; diabetes; tobacco and alcohol use; New York Heart Association functional class; HF medication use; blood pressure; and haemoglobin, sodium, and creatinine concentrations were performed. The incremental discriminatory value of frailty over and above the MAGGIC risk score was evaluated by the area under the receiver-operating characteristic curve. Results At baseline, 18% of participants were robust, 61% pre-frail, and 21% frail. During follow-up, 565 (16%) participants died and 471 (14%) were hospitalized for HF. Respective adjusted hazard ratios (95% confidence interval) for death among the pre-frail and frail were 1.59 (1.12–2.26) and 2.92 (1.99–4.27). Respective adjusted hazard ratios (95% confidence interval) for HF hospitalization were 1.32 (0.93–1.87) and 1.97 (1.33–2.91). Findings were consistent among different country income levels and by most subgroups. Adding frailty to the MAGGIC risk score improved the discrimination of future death and HF hospitalization. Conclusions Frailty confers substantial incremental prognostic information to prognostic variables for predicting death and HF hospitalization. The relationship between frailty and these outcomes is consistent across countries at all income levels.
As a rule, heart damage in patients with sarcoidosis of respiratory organs (SOD) is not diagnosed in time, so a very important and urgent task is to identify common heart rhythm and conduction disorders.The aim of the study was to investigate the main clinical manifestations of sarcoidosis in SOD, depending on the peculiarities of the disease course and to compare the frequency and severity of pulmonary and extrapulmonary manifestations of sarcoidosis, including myocardial lesions and electrocardiographic (ECG) signs of heart rhythm disorders.Methods. In the period 2006– 2016, the pilot open prospective uncontrolled study conducted at the Pulmonology Department of the Regional State Autonomous Healthcare Institution "Tomsk Regional Clinical Hospital" included patients (n = 84) aged 20–67 years with the diagnosis of SOD. Patients were divided into 2 clinical groups: the 1st comprised 45 (53.5%) patients with a favorable course of sarcoidosis, the second one included 39 (46.4%) patients with an unfavorable course of the disease. A full range of studies was carried out, including the analysis of medical history and clinical and epidemiological data, instrumental methods (including ECG and Holter ECG monitoring (HM), pathomorphological study of lung biopsy samples.Results. According to the data of frequency analysis of occurrence of pulmonary and extrapulmonary clinical manifestations in ODS, it was shown that the leading clinical manifestations, most frequently occurring in patients of both groups, included asthenia syndrome (72.6%), bronchial syndrome (66.7%) and fever syndrome (33%). In 33% of cases, clinical manifestations of myocardial damage were detected. In 41 (51.2%) patients in both groups, changes on ECG were recorded at rest. Regardless of the course of the disease, in 23.5% of patients of both clinical groups, according to the results of the HM ECG, rhythm and conduction disturbances were found – a combination of ventricular arrhythmias and conduction disorders (ventricular extrasystole and right His bundle branch block of various degrees) and a combination of supraventricular arrhythmias and conduction disturbances (supraventricular extrasystole and right His bundle branch block of various degrees).Conclusion. Thus, regardless of the severity of the disease course, SOD patients are concerned about complaints from both respiratory system and extrapulmonary manifestations, including cardiac complaints, as well as heart rhythm and conduction disorders (according to the results of ECG and HM ECG), the frequency of which, according to the comparative analysis, has not significantly changed in both clinical groups, which indicates the non-specific character of clinical manifestations.
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.
Aim: to study the changes in heart rate variability (HRV) in patients with anxiety and depressive disorders who suffered acute coronary syndrome (ACS) and to determine the effects of antidepressant agomelatine on HRV and sleep quality during six-month follow up.Material and Methods. The study included 54 people with ACS, anxiety, and depressive disorders. Patients were randomly assigned to two groups. Antidepressant agomelatine 25 mg/day was administered to patients of group 1 in addition to standard therapy for ACS; group 2 received placebo. Twenty four-hour Holter ECG monitoring, HRV study, mental status monitoring, and sleep quality assessment were performed during hospitalization and at six-month follow up.Results. Patients of both groups had clinically significant anxiety, subclinical depression, and insomnia of varying severity. According to Holter monitoring data, all patients had decline in HRV parameters. After six months, anxiety and depression significantly improved in patients administered with agomelatine; these patients had sleep normalization and improved HRV. The comparison group did not have similar changes.Conclusion. Additional administration of agomelatine 25 mg/day to patients with anxiety and depressive disorders after ACS resulted in improvement of mental status, heart rate variability, and sleep quality. Due to the absence of pro-arrhythmogenic effects, administration of agomelatine allows to correct anxiety-depressive disorders in patients with ACS.
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.
9903 subjects aged ¼>20 years, randomly selected from state resident register were invited to first visit where BP was measured and questionnaire was filled in. Office BP was calculated as the mean of 2 measurements using a validated automatic BP device (Omron 705IT). Subjects with systolic BP ¼>140 and/or diastolic BP ¼>90 mmHg were invited to repeated BP measurement in the next 3 to 6 weeks. Data about history and treatment of hypertension were acquired by questionnaire.
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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