RESUMEN

Background: We conducted a study to determine the relationships between perirenal fat (PRF) thickness and urinary levels of monocyte chemoattractant protein-1 (MCP-1) and neutrophil gelatinase-associated lipocalin (NGAL) in patients with hypertension (HTN). Methods: In 338 HTN patients (aged 63.51±12.3 on average), MCP-1 and NGAL levels were studied using enzyme-linked immunosorbent assay (ELISA). To measure PRF thickness, all patients underwent CT scans. Results: We considered PRF thickness ≥1.91 cm as the diagnostic threshold for perirenal obesity. Patients with excessive PRF thickness exhibited significantly lower levels of MCP-1 and NGAL compared with those with PRF thickness ≥1.91 cm: 0.98 pg/mL (interquartile range, 0.21 to 2.05) vs. 2.35 pg/mL (0.37 to 5.22) for MCP-1 and 50.0 pg/mL (48.9 to 67.8) vs. 98.3 pg/mL (68.4 to 187.1) for NGAL. We found a relationship of PRF thickness with both MCP-1 (r=0.46, P<0.05) and NGAL (r=0.53, P<0.05), the levels of which were significantly different in patients with first- and third-stage chronic kidney disease: 0.33 pg/mL (0.21 to 1.35) vs. 4.47 pg/mL (0.23 to 10.81); 50.0 pg/mL (49.4 to 85.5) vs. 126.45 pg/mL (57.5 to 205.15), respectively (P=0.04). Patients with metabolically healthy obesity (MHO) had significantly lower MCP-1 levels than those with metabolically unhealthy obesity (MUHO): 0.65 pg/mL (0.21 to 2.15) vs. 3.28 pg/mL (2.05 to 5.22) (P=0.014). MHO patients showed significantly lower NGAL levels than MUHO patients: 50.0 pg/mL (49.4 to 62.2) vs. 98.3 pg/mL (50.0 to 174.8) (P=0.04). Multiple linear regression analysis revealed significant relationships of MCP-1 with PRF thickness (ß±standard error, 0.41±0.15; P<0.001) and smoking (0.26±0.13; P=0.01) and of NGAL with age (0.45±0.16; P<0.01) and PRF thickness (0.49±0.15; P<0.001). Conclusion: We identified higher concentrations of renal fibrosis markers in patients with perirenal and metabolically unhealthy obesity as well as a link between PRF thickness and MCP-1 and NGAL levels in urine.

RESUMEN

Background: Different variants of single nucleotide polymorphisms (SNPs) of angiotensinogen (AGT), angiotensin-converting enzyme type 1 (ACE1), and angiotensin II receptors type 1 (AGTR1) and 2 (AGTR2) genes determine different susceptibility to cardiovascular disease (CVD) and hypertension, which can be considered as risk factors for fatal outcomes among coronavirus disease 2019 (COVID-19) patients. The objective of our study was to assess the relation between the frequency of SNPs of the renin-angiotensin system (RAS) components, and the severity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Methods: The cross-sectional study included 100 patients with a laboratory-confirmed diagnosis of COVID-19 admitted to the hospital. Criteria for severe COVID-19 included respiratory rate (RR) > 30/min, blood oxygen saturation (SpO2) ≤ 93%, signs of unstable hemodynamics with systolic blood pressure (SBP) < 90 and/or diastolic blood pressure (DBP) < 60 mm Hg. All patients were identified with alleles and genotypes of the polymorphic markers rs4762 of the AGT gene, rs1799752 of the ACE1 gene, rs5186 of the AGTR1 gene and rs1403543 of the AGTR2 gene using the polymerase chain reaction method in human DNA preparations on real-time CFX96C1000 Touch, Bio-Rad equipment (Syntol, Russia). Statistical analysis was performed in R v.4.2. Results: Patients were divided into groups with severe (n = 44) and moderate COVID-19 (n = 56). For ACE1 rs1799752, a significant deviation from the population distribution was detected in both studied subgroups. A higher frequency of the C allele SNP rs5186 AGTR1 gene was detected in the group with severe disease. More frequent A/A genotype of SNP rs1403543 AGTR2 was detected among females with severe COVID-19. Haplotype analysis revealed more common DCG haplotype among patients with severe COVID-19. The odds ratio for severe COVID-19 in the presence of the DCG haplotype was 3.996 (95% confidential interval: 1.080 -14.791, P < 0.05). Conclusions: Our data suggest that the SNP genes of the RAS components, may allow to identify groups of patients predisposed to a more severe course of COVID-19.

RESUMEN

Background: Epidemiological studies have demonstrated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-positive patients often develop atrial fibrillation, premature ventricular contractions (PVCs), and conduction disorders. The manifestation of ventricular cardiac arrhythmias accentuates the risk of sudden cardiac death. Methods: A retrospective study was conducted on the cohort of 1,614 patients admitted for coronavirus disease 2019 (COVID-19). Patients were categorized into two groups based on the occurrence of PVCs. Group I comprised 172 patients diagnosed with PVCs of Lown-Wolf class II - IV upon hospital admission; group II (control group) consisted of 1,442 patients without this arrhythmia. Each patient underwent comprehensive clinical, laboratory, and instrumental evaluations. Results: The emergence of PVCs in individuals afflicted with COVID-19 was associated with a 5.879-fold heightened risk of lethal outcome, a 2.904-fold elevated risk of acute myocardial infarction, and a 2.437-fold increased risk of pulmonary embolism. Upon application of diagnostic criteria to evaluate the "cytokine storm", it was discovered that the occurrence of the "cytokine storm" was notably more frequent in the group with PVCs, manifesting in six patients (3.5%), compared to 16 patients (1.1%) in the control group (P < 0.05). The mean extent of lung tissue damage in group I was significantly greater than that of patients in group II (P < 0.05). Notably, the average oxygen saturation level, as measured by pulse oximetry upon hospital admission was 92.63±3.84% in group I and 94.20±3.50% in group II (P < 0.05). Conclusions: The presence of PVCs in COVID-19 patients was found to elevate the risk of cardiovascular complications. Significant independent predictors for the development of PVCs in patients with SARS-CoV-2 infection include: age over 60 years (risk ratio (RR): 4.6; confidence interval (CI): 3.2 - 6.5), a history of myocardial infarction (RR: 3.5; CI: 2.6 - 4.6), congestive heart failure (CHF) with reduced left ventricular ejection fraction (RR: 5.5; CI: 3.9 - 7.6), respiratory failure (RR: 2.3; CI: 1.7 - 3.1), and the presence of a "cytokine storm" (RR: 4.5; CI: 2.9 - 6.0).

RESUMEN

Background: The course of coronavirus disease 2019 (COVID-19) is associated with the progression of a wide range of complications, among which thrombosis and thromboembolism are of particular importance. The significance of hypoalbuminemia in the development of thromboembolic complications (TECs) in patients with a severe course of COVID-19 is currently under active discussion. The objective of our study was to evaluate the significance of hypoalbuminemia in the development of TECs in patients with severe SARS-CoV-2 coronavirus infection. Methods: In a single-center observational retrospective study, case histories of 1,634 patients with a verified diagnosis of SARS-CoV-2 coronavirus infection were analyzed. Patients were divided into two groups according to the presence of TECs: 127 patients with venous TECs constituted the main group and 1,507 patients, in whom the course of COVID-19 was not complicated by the development of TECs, constituted the comparison group. Results: The patients with TECs were older, and the prevalence of arterial hypertension, coronary heart disease, chronic heart failure, chronic kidney disease, and diabetes mellitus was higher than that in the comparison group. A single-factor regression analysis showed that a decrease in albumin levels of less than 35 g/L is associated with an eightfold increase in the risk of developing TECs in patients with severe SARS-CoV-2 coronavirus infection (area under the curve (AUC): 0.815, odds ratio (OR): 8.5389, 95% confidence interval (CI): 4.5637 - 15.977, P < 0.001). The sensitivity of the method was 76.34%, and the specificity was 72.58%. Conclusion: The study revealed that hypoalbuminemia is a predictor of development of TECs in severe cases of SARS-CoV-2 coronavirus infection.

RESUMEN

BACKGROUND: COVID-19 is characterized by an acute inflammatory response with the formation of endothelial dysfunction and may affect arterial stiffness. Studies of cardio-ankle vascular index in COVID-19 patients with considered cardiovascular risk factors have not been conducted. OBJECTIVE: The purpose of our study was to assess the association between cardio-ankle vascular index and COVID-19 in hospitalized patients adjusted for known cardiovascular risk factors. METHODS: A cross-sectional study included 174 people hospitalized with a diagnosis of moderate COVID-19 and 94 people without COVID-19. Significant differences in the cardio-ankle vascular index values measured by VaSera VS - 1500N between the two groups were analyzed using parametric (Student's t-criterion) and nonparametric (Mann-Whitney) criteria. Independent association between COVID-19 and an increased cardio-ankle vascular index ≥ 9.0 adjusted for known cardiovascular risk factors was assessed by multivariate logistic regression. RESULTS: There were significantly higher values of the right cardio-ankle vascular index 8.10 [7.00;9.40] and the left cardio-ankle vascular index 8.10 [6.95;9.65] in patients undergoing inpatient treatment for COVID-19 than in the control group - 7.55 [6.60;8.60] and 7.60 [6.60;8.70], respectively. A multivariate logistic regression model adjusted for age, hypertension, plasma glucose level, glomerular filtration rate and diabetes mellitus showed a significant association between increased cardio-ankle vascular index and COVID-19 (OR 2.41 [CI 1.09;5.30]). CONCLUSION: Hospitalized patients with COVID-19 had significantly higher cardio-ankle vascular index values compared to the control group. An association between an increased cardio-ankle vascular index and COVID-19 was revealed, independent of age, hypertension, plasma glucose level, glomerular filtration rate and diabetes mellitus.

Asunto(s)

RESUMEN

BACKGROUND: Cardio-ankle vascular index (CAVI) and its modified version (CAVI0) are promising non-invasive markers of arterial stiffness, extensively evaluated primarily in the Japanese population. In this work, we performed a model-based analysis of the association between different population characteristics and CAVI or CAVI0 values in healthy Russian subjects and propose a tool for calculating the range of reference values for both types of indices. METHODS: The analysis was based on the data from 742 healthy volunteers (mean age 30.4 years; 73.45% men) collected from a multicenter observational study. Basic statistical analysis [analysis of variance, Pearson's correlation (r), significance tests] and multivariable linear regression were performed in R software (version 4.0.2). Tested covariates included age, sex, BMI, blood pressure, and heart rate (HR). RESULTS: No statistically significant difference between healthy men and women were observed for CAVI and CAVI0. In contrast, both indices were positively associated with age (r = 0.49 and r = 0.43, P < 0.001), however, with no clear distinction between subjects of 20-30 and 30-40 years old. Heart rate and blood pressure were also identified as statistically significant predictors following multiple linear regression modeling, but with marginal clinical significance. Finally, the algorithm for the calculation of the expected ranges of CAVI in healthy population was proposed, for a given age category, HR and pulse pressure (PP) values. CONCLUSIONS: We have evaluated the quantitative association between various population characteristics, CAVI, and CAVI0 values and established a method for estimating the subject-level reference CAVI and CAVI0 measurements.

Asunto(s)

RESUMEN

We conducted a systematic review and meta-analysis aimed at estimating the association between perivascular adipose tissue (PVAT) and some of the cardiovascular risk factors. A systematic search was conducted from January 1980 up to and including 2022 to identify studies that examined the relationship between PVAT and cardiovascular risk factors as obesity and its indices, hypertension, lipids, and glucose intolerance/diabetes. The Medline and Embase databases were searched using the PubMed and Scopus. Data were extracted from 23 studies that fit the criteria. To conduct meta-analysis, we used an approximation of equating the method of correlating assessment because different authors used either Pearson or Spearman correlation. Interrelations of PVAT and body mass index were analyzed in eight studies. Most studies revealed reliable direct correlation; the results of the meta-analysis also showed a significant (P = 0.37, P < 0.01, n = 12,346) correlation. PVAT and waist circumference were analyzed in six studies. Meta-analysis on the selected sample (n = 10,947) showed a significant (r = 0.45, P < 0.01) correlation. Relationship between PVAT and hypertension was revealed in three studies. Direct correlations were found in all studies. Meta-analysis showed the reliability of the correlation dependence (r = 0.21, P < 0.01, n = 3996). PVAT and blood glucose was evaluated in three studies (n = 3689). In each study a reliable (P < 0.05) direct correlation was obtained. Meta-analysis showed a significant correlation of weak strength (r = 0.24, P < 0.01). We demonstrated significant positive correlations of PVAT with the levels of total cholesterol (r = 0.05, P < 0.01), low-density lipoprotein cholesterol (r = 0.13, P < 0.01), and triglycerides (r = 0.29, P < 0.01), and a negative relationship with high-density lipoprotein cholesterol (r = -0.18, P < 0.01) in this meta-analysis. Despite some limitations, the findings of this systematic review and meta-analysis confirmed that PVAT significantly correlates with studied cardiovascular risk factors. Because PVAT presents a great interest in terms of cardiovascular remodeling and cardiovascular disease, its assessment in patients with and without cardiovascular pathology needs further research.

Asunto(s)

RESUMEN

Background: Obesity and related cardiovascular diseases (CVDs) are important public health problems. The role of visceral ectopic fat remains contested. We studied the relationship between pericardial fat tissue (PFT) volume and CVD risk factors. Methods: We examined 320 patients (average age 63.8 ± 19.9 years) without manifested CVD. Anthropometric indicators were measured, and body mass index (BMI) was calculated. The total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), and triglycerides were assessed. Cardiovascular (CV) risk was calculated using the SCORE system. All patients underwent chest computed tomography with detection of PFT volume using specialized semiautomatic software. Results: Among study participants with normal body mass, the PFT volume was 1.95 cm3 [2.1; 3.9], while it was 3.0 cm3 [2.0; 3.7] in overweight patients and 3.6 cm3 [2.7; 4.7] in obese patients (P < 0.001). Patients with hypertension (HTN) also had significantly higher PFT volumes compared with individuals without HTN: 3.1 cm3 [2.3; 4.15] versus 1.8 cm3 [1.0; 2.5] (P < 0.001). Patients with higher CV risk had significantly higher PFT volume, categorized as follows: 1.6 cm3 [1.0; 2.4], low risk; 2.24 cm3 [2.0; 3.1], moderate risk; 3.1 cm3 [2.4; 3.7], high risk; and 3.9 cm3 [3.0; 5.1], very high risk, respectively (P < 0.001). Results of multiple regression demonstrated that waist circumference and HDL-C were significantly associated with PFT volume. Another model revealed a significant association of BMI and PFT volume with the level of CV risk. Conclusions: This study demonstrates the association of PFT volume with the major diagnostic criteria of obesity, HTN, lipid disorders, and CV risk measured by the SCORE system.

Asunto(s)

RESUMEN

INTRODUCTION/OBJECTIVE: Tobacco smoking is a well-known risk factor for cardiovascular and renal diseases. In recent years, alternative types of smoking, including vaping, have been becoming popular. The contribution of vape to vascular and renal injury is not known. We studied the relation between smoking of traditional/electronic cigarettes and arterial stiffness and albuminuria, which is also a vascular dysfunction marker. METHODS: We examined 270 young volunteers without significant clinical cardiovascular diseases (mean age: 21.2 ± 2.3 years). Twenty-seven percent of the subjects in the study group were smokers; 69.9% of them smoked traditional cigarettes and 30.1% smoked electronic cigarettes. The urine albumin level was assessed by a dipstick test, and the augmentation index was determined by photoplethysmography. A linear correlation test and multiple regression analysis were applied. RESULTS: The study groups did not differ in basic characteristics. The smokers demonstrated generally higher blood pressure levels and were overweight. Most of the smokers were male. In the groups of smokers, albuminuria was more frequent, especially among vapers (94 vs. 79% in tobacco smokers and 29% in nonsmokers). AU values (median [quartile 25; quartile 75]) were significantly higher in vapers (160 mg/L [150; 207.5]) vs. tobacco smokers (115 mg/L [60; 200]) and vs. nonsmokers (20 mg/L [10; 50]) (р < 0.05). Photoplethysmographic results showed relevant higher augmentation indices among tobacco smokers (-4, [-6.6; -1.9]) and vapers (-5.05 [-13.4; -3.3]) compared to nonsmokers (-16.2 [-23.9; -7]) (р < 0.05). Results of multiple regression analysis demonstrate that smoking of both traditional and electronic cigarettes is related to an increase in the albuminuria level and the augmentation index. CONCLUSIONS: Smoking of both traditional and electronic cigarettes is related to albuminuria and an increase in the augmentation index, which is a noninvasive marker for arterial stiffness.

Asunto(s)