Aim . To summarize the findings of studies investigating the clinical and prognostic significance of cardiac autonomic dysfunction (CAD) in patients with systemic sclerosis (SSc) in a systematic review. Material and methods. A literature search was performed in the eLIBRARY.ru and MEDLINE (PubMed) electronic bibliographic databases. The systematic review was reported in accordance with the PRISMA guidelines. No restrictions on the year of publication were applied during the literature search and study selection. A qualitative synthesis of the findings was performed. Results . The review included 29 studies reported in 32 publications. The number of patients with SSc ranged from 10 to 86. Two publications described prospective studies, whereas the remaining studies had a cross-sectional design. CAD was primarily assessed by heart rate variability (HRV) analysis; Ewing cardiovascular autonomic tests, questionnaires, and heart rate turbulence (HRT) analysis were used less frequently. Most studies demonstrated reduced time- and frequency-domain HRV indices, impaired parasympathetic regulation, and a relative predominance of sympathetic activity in patients with SSc. CAD parameters were associated with diffuse cutaneous disease, the severity of skin and microvascular involvement, pulmonary hypertension, structural and functional cardiac abnormalities, and ventricular arrhythmias. In several studies, reduced HRV and abnormal HRT parameters were associated with adverse outcomes. Conclusion . CAD in patients with SSc is characterised by impaired parasympathetic regulation, a relative predominance of sympathetic influences, reduced HRV, and abnormal HRT parameters. CAD indices were associated with clinical and laboratory characteristics of SSc reflecting disease severity and activity. The available evidence suggests that CAD may have adverse prognostic implications in patients with SSc, which requires further investigation in large prospective studies.
Aim . To identify independent clinical, laboratory, and instrumental factors associated with the occurrence of a composite endpoint (CEP) within two years in young patients (≤44 years) who have suffered an acute myocardial infarction (AMI). Material and methods . This single-center retrospective study included 331 patients (median age 41 years, 91.5% male) with AMI treated between 2015–2023. Inclusion criteria were: age ≤44 years, confirmed AMI diagnosis, and availability of coronary angiography (CAG). The CEP included recurrent AMI, emergency hospitalisations for cardiovascular reasons, and death during the two-year follow-up period. Patients were divided into a group that reached the CEP (Event, n=30) and a group that did not (Non-Event, n=301). Results . Over the two-year period, the CEP was recorded in 9% of patients. The groups differed significantly in the prevalence of diabetes mellitus/impaired glucose tolerance (46.7% vs. 16.3%; p<0.001), fasting glucose levels (6.8 [5.4; 8.7] vs. 5.7 [5.1; 6.7] mmol/L; p=0.008), systolic blood pressure upon admission (146.5 [130.0; 160.0] vs. 130.0 [120.0; 150.0] mmHg; p=0.034), and left atrial size (4.0 [3.9; 4.2] vs. 3.9 [3.6; 4.1] cm; p=0.007). The number of affected coronary arteries, revascularisation strategy, and traditional risk factors (smoking, dyslipidemia) showed no significant association with the outcome. Multivariate logistic regression analysis identified fasting glucose levels (odds ratio=1.177; 95% confidence interval 1.029-1.346; p=0.017) and left atrial size (odds ratio=4.270; 95% confidence interval 1.459-12.491; p=0.008) as independent factors associated with the risk of CEP. SBP at admission (p=0.082), age (p=0.086) and male sex (p=0.540) did not reach statistical significance in the multivariate model. Conclusion . In young postAMI patients, the risk of adverse twoyear outcomes is determined primarily by fasting glucose levels and left atrial size, rather than by the anatomical extent of atherosclerosis. These findings support a personalised approach to secondary prevention with a focus on glycemic control and assessment of structuralfunctional cardiac parameters.
Aim . To analyse the associations between instrumental and laboratory signs of subclinical target organ damage (TOD) and composite systemic inflammation indices in individuals with abdominal obesity (AO). Material and methods. A cross-sectional study included 122 non-smoking patients aged 40-60 years with low (<1%) or moderate (≥1% and <5%) CVR according to the SCORE scale. The main group consisted of 78 individuals with AO (waist circumference ≥94 cm for men and ≥80 cm for women), the comparison group — 44 individuals without AO. The study included questionnaire surveys, anthropometry, laboratory tests with calculation of inflammation indices (Systemic Inflammation Response Index, SIRI; Systemic Immune-Inflammation Index, SII; Aggregate Index of Systemic Inflammation, AISI; Neutrophil-to-Lymphocyte Ratio NLR; Platelet-to- Lymphocyte Ratio, PLR; Monocyte-to-Lymphocyte Ratio, MLR), echocardiography, ultrasound examination of brachiocephalic arteries (BCA) and abdominal organs. Results . Individuals with AO had a significantly higher prevalence of left ventricular hypertrophy (16.7% vs 2.3%; p=0.017), left ventricular diastolic dysfunction (34.6% vs 2.3%; p<0.001), BCA atherosclerotic plaque (43.6% vs 15.9%; p=0.003) and carotid intima-media thickening (68.0% vs 38.6%; p=0.002), hepatic steatosis (51.3% vs 11.4%; p<0.001), pancreatic steatosis (55.1% vs 4.6%; p<0.001), and hyperuricemia (32.1% vs 11.4%; p=0.015). Epicardial obesity (EO) was detected only in the AO group (29.5%). According to multivariate analysis, LV hypertrophy, diastolic dysfunction and BCA atherosclerosis were independently associated with hypertension, whereas hepatic steatosis, pancreatic steatosis and carotid intima-media thickening were associated with AO. Among the inflammatory indices, SIRI was independently associated with epicardial obesity (OR 3.83; p=0.048), and AISI with pancreatic steatosis (OR 1.003; p=0.017). Conclusion . Individuals with AO and low/moderate CVR have a high prevalence of subclinical TOD, indicating the limitations of traditional risk scales and the need for an individualized approach. In multivariate analysis, SIRI was independently associated with epicardial obesity, and AISI with pancreatic steatosis.
Aim . To evaluate the role of natriuresis as a marker of the effectiveness of diuretic therapy and a predictor of adverse outcome in patients with acute decompensated heart failure (ADHF). Material and methods . The single-center prospective study included 155 patients hospitalised with ADHF in the intensive care unit (mean age 71.9±11.9 years, men 56%). All patients underwent standard physical, laboratory, and instrumental examinations in the first 24 hours, including clinical assessment of congestion, N-terminal pro-brain natriuretic peptide, lung ultrasound, venous congestion assessment according to the Venous Excess Ultrasound (VExUS) protocol, and renal function assessment (creatinine, cystatin C, and urinary albumin/creatinine). An instrumental assessment of congestion (ultrasound of the lungs, venous congestion according to the VExUS protocol), as well as an assessment of renal function (creatinine, urinary albumin/creatinine ratio) was performed after 48, 72 hours and before discharge. The starting dose of furosemide was 20-40 mg IV if patients did not receive oral diuretics, if they did, the starting dose was equal to the oral dose. After 2 hours, a quantitative assessment of sodium in urine was performed. If natriuresis level was ≥70 mmol/L, furosemide was continued at the same dose every 12 hours; if <70 mmol/L, the furosemide dose was doubled. Urine sodium concentration was monitored every 12 hours. Long-term clinical outcomes were assessed via structured telephone interviews at 90, 180, and 365 days post-discharge. The primary endpoint was a composite of all-cause death and rehospitalisation for ADHF. Results . Patients with natriuresis <70 mmol/l, compared to those with ≥70 mmol/l, were characterised by more pronounced manifestations of congestion in both circulatory circles (B lines 35 versus 30, p<0.05; the frequency of venous congestion according to the VExUS protocol 69.4% versus 34.3%, p<0.001), significantly higher levels of N-terminal pro-brain natriuretic peptide (2504 pg/ml versus 1675 pg/ml, p<0.01), with a higher incidence of acute renal injury (71.1% versus 40.6%, p<0.001). Against the background of diuretic therapy in patients with natriuresis < 70 mmol/l, despite an increase in the dose of furosemide, there is a significantly worse response to diuretic therapy, lower values of daily diuresis, as well as a significantly less pronounced decrease in congestion, both according to lung ultrasound and according to the VExUS protocol. Conclusion . Natriuresis <70 mmol/L is a predictor of adverse outcomes in patients with ADHF during 1 year of follow-up and allows us to identify the most severe group of patients with a high risk of resistance to diuretic therapy.
Aim . To evaluate the diagnostic value of various non-invasive methods for assessing hepatic steatosis as potential markers of epicardial obesity (EO) in individuals without cardiovascular disease. Material and methods . This cross-sectional study included 303 patients without cardiovascular diseases with a median age of 55 [40;65] years. Epicardial adipose tissue (EAT) thickness was assessed by echocardiography, and EO was determined according to age-specific threshold values. Hepatic steatosis was verified using liver transient elastography with measurement of the controlled attenuation coefficient (AC) and hepatorenal index (HRI). AC >0.67 dB/cm/MHz was used as the criterion for hepatic steatosis. The cutoff value for HRI was >1.49. In addition, validated non-invasive indices, including the Fatty Liver Index (FLI) and Hepatic Steatosis Index (HSI), were calculated. FLI >60 and HSI >36 was considered diagnostic criteria for hepatic steatosis according to the original formulas. Results . Sex distribution in the study cohort was balanced (49.8% men and 50.2% women). The prevalence of arterial hypertension was 66.3%, dyslipidemia 46.8%, and abdominal obesity 50.4%. EO was detected in 68% of patients. The prevalence of hepatic steatosis assessed by ultrasonography with AC measurement was 41.3%, while HRI-based steatosis was detected in 45% of patients. According to calculated indices, hepatic steatosis was identified in 50.1% of patients using HSI and in 32.3% using FLI. Statistically significant correlations were observed between EAT thickness and hepatic steatosis markers (HSI, FLI, HRI, and AC) (ρ =0.401, ρ =0.507, ρ =0.545, and ρ =0.622, respectively). AC demonstrated the highest diagnostic performance for EO detection (AUC=0.715; 95% CI: 0.575-0.855; p=0.002). Similar results were obtained for FLI (AUC=0.722; 95% CI: 0.598-0.847; p=0.003). Pairwise comparisons revealed statistically significant differences between AC and HSI (p=0.044), as well as between HSI and FLI (p=0.007). Statistically significant differences between the ROC curves (p=0.0417) were confirmed. ROC analysis was additionally performed to determine cutoff values of AC and FLI for EO detection. The optimal AC cutoff value was 0.65 dB/cm/MHz (specificity 70.91%, sensitivity 88%), whereas the optimal FLI cutoff value was 29 (specificity 68.97%, sensitivity 75.44%). Conclusion . The identified associations between hepatic steatosis markers (FLI, HSI, HRI, and AC) and EO are consistent with the concept of a “metabolic dysfunction cluster”, according to which hepatic steatosis may reflect the severity of metabolic disturbances and serve as a marker of cardiovascular risk.
