Current Issue : July-September Volume : 2026 Issue Number : 3 Articles : 5 Articles
Background/Objectives: Oxidative stress and extracellular redox alterations are involved in the pathophysiology of essential hypertension, but their clinical assessment is limited by the invasiveness and preanalytical complexity of blood-based measurements. Urine represents an attractive non-invasive biological matrix; however, the relationship between urinary and plasma DTNB-reactive reduced thiols in hypertensive patients remains insufficiently characterized. This study aimed to evaluate the association between plasma and urinary reduced thiols in essential hypertension. Methods: In this paired observational study, plasma and urine samples were obtained from 40 patients with treated essential hypertension. Reduced thiols were quantified using a DTNB-based colorimetric assay under identical analytical conditions. Plasma thiols were normalized to total plasma protein concentration, and urinary thiols were normalized to creatinine. Associations between plasma and urinary thiols were assessed using non-parametric correlation analyses. Results: Protein-normalized plasma thiols and creatinine-normalized urinary thiols showed a significant positive correlation (Spearman’s ρ ≈ 0.7, p < 0.001). Conclusions: In patients with essential hypertension, creatinine-normalized urinary reduced thiols are strongly associated with protein-normalized plasma reduced thiols, as measured by the DTNB reaction method. These findings provide hypothesis-generating evidence that urinary thiols may reflect extracellular thiol-related redox alterations, warranting further validation in independent and more diverse cohorts....
Background: Cardiovascular comorbidities are major determinants of poor outcomes among patients admitted with COVID-19. However, the prognostic role of arterial hypertension alone remains uncertain. Little is known about the cumulative impact of concomitant hypertension and heart failure. This study assessed whether the combined burden of arterial hypertension and pre-existing heart failure identifies a high-risk phenotype for adverse in-hospital outcomes among COVID-19 patients. Methods: In this retrospective, real-world cohort study, 395 consecutive adults hospitalized with confirmed COVID-19 at a single infectious diseases center between March 2020 and December 2024 were included. We categorized patients into three cardiovascular phenotype groups: no hypertension or heart failure (n = 23), hypertension without heart failure (n = 193), and concomitant hypertension and heart failure (n = 178). The primary outcome was in-hospital all-cause mortality, while ICU admission served as a secondary outcome, invasive mechanical ventilation, and length of hospital stay. Multivariable logistic regression included age, sex, BMI, diabetes mellitus, and vaccination status to evaluate independent associations between the cardiovascular risk group and outcomes. Results: Overall in-hospital mortality was 7.3% (29/395). Mortality increased stepwise across the cardiovascular risk groups: 8.7% in patients without hypertension or heart failure, 3.1% in those with hypertension only, and 11.8% in patients with concomitant hypertension and heart failure (p = 0.004). In adjusted analyses, concomitant hypertension and heart failure were linked to higher adjusted odds of in-hospital death than no cardiovascular disease (odds ratio, 3.49; 95% confidence interval, 1.46–8.35). Isolated hypertension was not significantly associated with mortality. ICU admission and length of hospital stay also increased with cumulative cardiovascular burden. Patients with combined hypertension and heart failure showed more pronounced inflammatory and renal abnormalities at admission. Conclusions: Among hospitalized COVID-19 patients, the coexistence of arterial hypertension and heart failure identifies a vulnerable cardiovascular phenotype associated with higher in-hospital mortality and resource use than either no cardiovascular disease or hypertension alone. These findings support evaluating cardiovascular comorbidities cumulatively rather than in isolation. These findings are exploratory and require external validation in independent, larger multicentre cohorts. Findings may support careful use for short-term risk stratification and closer monitoring strategies during COVID-19 hospitalization....
Background: Eating habits influence cardiometabolic health alongside traditional dietary measures. However, the links between dietary patterns, body composition, and hearthealthy food preferences remain under-explored in large cohorts. Methods: In this crosssectional study, 2461 adults (aged 18 to 75 years) completed an online survey on eating behaviors, food preferences, and lifestyle. Principal component analysis (PCA) of seven behaviors identified dietary profiles. A heart-healthy diet score (range −2 to 10; higher = greater preference for fruit, vegetables, legumes, fish, and less meat/processed meat) was derived from these food preferences. ANOVA and adjusted regressions linked the profiles to BMI, fat mass, waist circumference, and diet score. Results: Four profiles emerged: structured, social, irregular, and disordered eaters. Structured eaters had the lowest BMI (26.8 ± 5.1 kg/m2), lowest fat mass (28.9 ± 9.4%), and highest dietary score (4.73 ± 2.0). Disorganized eaters had the highest BMI (29.0 ± 5.5 kg/m2), the highest fat mass (31.2 ± 8.8%) and the lowest score (3.93 ± 2.0); all p < 0.05. Dose–response analyses confirmed that greater disordered eating (PCA1) was associated with worse outcomes. Conclusions: Dietary profiles are associated with body composition and cardioprotective preferences. Behavioral assessment could refine the identification of cardiometabolic risk and personalize nutrition....
Background: Sex-related differences in outcomes after implantable cardioverter-defibrillator (ICD) implantation remain incompletely understood. Although women receive ICDs less frequently, whether their long-term survival differs from that of men in real-world clinical practice is not well established. We aimed to evaluate sex-specific mortality and relative survival in a large consecutive cohort of ICD recipients from a tertiary hospital. Methods: We conducted a retrospective cohort study including all consecutive patients who underwent ICD implantation at a tertiary hospital between 2015 and 2025. Demographic features, device indication, and mortality were obtained through clinical records. Relative survival (observed vs. expected) was estimated using the Ederer II method with national life tables. A Cox proportional hazards model assessed the effect of sex on mortality. Results: A total of 1091 patients (82.1% men; mean age 63.1 ± 13.1 years) were included. During a mean follow-up of 4.33 ± 3.22 years, 230 patients died (21.1%). Women showed lower unadjusted all-cause mortality than men: 24 deaths (18.0%) vs. 206 (20.6%). Women had significantly higher left ventricular ejection fraction (41.5 ± 23.6% vs. 37.2 ± 18.1%, p = 0.0046), less ischemic cardiomyopathy, and lower prevalence of cardiovascular risk factors. Although univariable analysis suggested lower mortality in women (HR 0.58, 95% CI 0.38–0.90; p = 0.014), multivariable analysis indicated that sex was not an independent predictor of mortality (HR 0.81, 95% CI 0.53–1.26). Relative survival revealed a substantial long-term mortality burden in ICD carriers, especially in men: men: 4-year survival 82.3% (expected 93.2%); 8-year 66.7% (85.6%); 12-year 56.0% (76.8%); women: 4-year survival 89.1% (expected 96.7%); 8-year 77.1% (92.8%); 12-year 77.1% (89.2%). Conclusions: In this large real-world cohort of ICD recipients, women showed lower unadjusted mortality and a smaller excess mortality compared with the general population. However, sex was not an independent predictor of survival after multivariable adjustment. These findings may indicate that observed survival differences are largely explained by differences in clinical profile and comorbidity burden rather than by sex itself....
Oxidative stress and sarcopenia are increasingly perceived as interdependent processes that significantly affect the course of cardiovascular diseases. Excessive production of reactive oxygen species leads to muscle cell damage, mitochondrial disorders, and chronic inflammation, which promote progressive loss of muscle mass and function. Methods: The aim of the study was to analyze the mechanisms linking oxidative stress and sarcopenia in the course of cardiovascular diseases. Our scoping review initially identified 854 articles, of which 3 were ultimately included in the review (after removing duplicates (n = 118), 736 articles remained; after re-screening the articles according to the inclusion and exclusion criteria (n = 302), 434 articles remained; 196 publications lacked full text and were excluded, leaving 238 articles). Results: An examination of the available literature indicates a potential association between increased oxidative stress and the possible development of sarcopenia in individuals with cardiovascular diseases. The studies identified in this review suggest that elevated levels of reactive oxygen species, together with reduced antioxidant capacity, may contribute to muscle fiber damage, mitochondrial disturbances, and the activation of chronic inflammatory processes, which could in turn be involved in the accelerated decline of muscle mass and strength. Conclusions: These results confirm that oxidative stress is a key pathophysiological element linking both disease entities and may be an important target of therapeutic interventions....
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