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Despite considerable advances in pharmacological treatments, hypertension remains a major cause of premature morbidity and mortality worldwide since elevated blood pressure (BP) adversely influences cardiovascular and renal outcomes. Accordingly, the current hypertension guidelines recommend the adoption of dietary modifications in all subjects with suboptimal BP levels. These modifications include salt intake reduction and a healthy diet, such as the Dietary Approaches to Stop Hypertension (DASH) diet or the Mediterranean diet (MedDiet), independently of the underlying antihypertensive drug treatment. However, dietary modifications for BP reduction in adults with prehypertension or hypertension are usually examined as stand-alone interventions and, to a lesser extent, in combination with other dietary changes. The purpose of the present review was to summarize the evidence regarding the BP effect of salt restriction in the context of the DASH diet and the MedDiet. We also summarize the literature regarding the effects of these dietary modifications when they are applied as the only intervention for BP reduction in adults with and without hypertension and the potent physiological mechanisms underlying their beneficial effects on BP levels. Available data of randomized controlled trials (RCTs) provided evidence about the significant BP-lowering effect of each one of these dietary strategies, especially among subjects with hypertension since they modulate various physiological mechanisms controlling BP. Salt reduction by 2.3 g per day in the DASH diet produces less than half of the effect on systolic blood pressure (SBP)/diastolic blood pressure (DBP) (–3.0/–1.6 mmHg) as it does without the DASH diet (–6.7/–3.5 mmHg). Although their combined effect is not fully additive, low sodium intake and the DASH diet produce higher SBP/DBP reduction (–8.9/–4.5 mmHg) than each of these dietary regimens alone. It is yet unsettled whether this finding is also true for salt reduction in the MedDiet.

Obesity and hypertension have become an international health issue, with detrimental consequences on patients. Obesity and hypertension share common pathophysiological mechanisms, such as overactivity of the renin–angiotensin–aldosterone and the sympathetic nervous systems, insulin resistance, and disruption of the leptin pathway. Approved therapies for obesity and overweight include phentermine/topiramate, orlistat, naltrexone/bupropion, the glucagon-like peptide-1 receptor agonists liraglutide and semaglutide, tirzepatide, and bariatric surgery. This review gives the clinical data in a thorough manner and explains in detail how each of the previously mentioned therapies affects blood pressure levels.

Abstract Aims The beneficial cardiovascular effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors irrespective of the presence of diabetes mellitus are nowadays well established and they already constitute a significant pillar for the management of heart failure, irrespective of the ejection fraction. The exact underlying mechanisms accountable for these effects, however, remain largely unknown. The direct effect on endothelial function and microcirculation is one of the most well studied. The broad range of studies presented in this review aims to link all available data from the bench to bedside and highlight the existing gaps as well as the future directions in the investigations concerning the effects of SGLT2 inhibitors on the endothelium and the microcirculation. Methods and results An extensive search has been conducted using the MEDLINE/PubMed database in order to identify the relevant studies. Preclinical data suggest that SGLT2 inhibitors directly affect endothelial function independently of glucose and specifically via several interplaying molecular pathways, resulting in improved vasodilation, increased NO production, enhanced mitochondrial homeostasis, endothelial cell viability, and angiogenesis as well as attenuation of oxidative stress and inflammation. Clinical data systematically confirm this beneficial effect on the endothelium, whereas the evidence concerning the effect on the microcirculation is conflicting. Conclusion Preclinical and clinical studies indicate that SGLT2 inhibitors attenuate endothelial and microvascular dysfunction via a combination of mechanisms, which play a role in their beneficial cardiovascular effect. Graphical Abstract Graphical Abstract

Anabolic–androgenic steroids (AASs) are synthetic derivatives of testosterone and are increasingly misused to enhance muscle growth and physical performance, particularly among athletes and recreational bodybuilders. Although AASs affect multiple organ systems, their severe and potentially life-threatening complications involve the cardiovascular system. This review summarizes current knowledge on the pathophysiological mechanisms and clinical manifestations of AAS-induced cardiomyopathy. Chronic supraphysiologic AAS use promotes cardiac injury and adverse cardiac remodeling via oxidative stress, androgen receptor overactivation, RAAS dysregulation, and pro-apoptotic signaling. These changes could lead to hypertension, dyslipidemia and atherosclerosis, myocardial fibrosis and hypertrophy, arrhythmias, heart failure, and kidney injury. Vascular dysfunction, increased arterial stiffness, and a prothrombotic state further compound the cardiovascular risks. Diagnostic approaches involve biomarker evaluation, echocardiography, and cardiac magnetic resonance imaging, revealing structural and functional cardiac abnormalities such as reduced ejection fraction, concentric hypertrophy, myocardial fibrosis, and impaired diastolic function. Although cessation of AAS use may lead to partial or complete reversal of cardiac dysfunction in some individuals, others may experience irreversible myocardial damage. The reversibility appears to depend on dosage, duration of exposure, and early intervention. This review explores the cardiovascular consequences of AAS use, with a focus on the mechanisms, diagnosis, and management of AAS-induced cardiomyopathy, and underlines the importance of education and early detection.

The prevalence of nonalcoholic fatty liver disease (NAFLD) has been increasing rapidly worldwide, affecting 25-30% of the population. Fatty liver index (FLI) is a validated marker of NAFLD and can be used as a screening tool for hepatic steatosis. The purpose of the study was to evaluate the relationship between FLI and the risk of major cardiovascular events in never treated hypertensive patients. We included 903 hypertensive patients without a history of cardiovascular disease (mean age 52.7 ± 11.4 years; men 55%; baseline clinic BP 149.8 ± 15.2/95.5 ± 10.1 mmHg). Participants were prospectively evaluated for a mean follow-up period of 5.2 ± 3.2 years with at least one annual visit. Patients were also categorized into two groups using an FLI of 60 units. The incidence of cardiovascular events during follow-up was 8.5% (n = 77). Patients with FLI < 60 (n = 625) had a better BP control compared to their counterparts with FLI ≥ 60 (n = 278) during follow up (43% vs 33%, p = 0.02). Cox-regression analysis indicated that FLI (Hazard Ratio [HR], 1.05; 95% Confidence Interval [CI], 1.03-1.07, p < 0.001), FLI z-scores (HR, 3.66; 95% CI, 2.22-6.04) and high-risk FLI (HR, 7.5; 95% CI, 3.12-18.04) were independent determinants of the outcome after adjustment for baseline and follow-up variables. Stratification by diabetes mellitus indicated that FLI predicted the outcome to a greater extent in those with than those without diabetes (P-interaction < 0.001). In conclusion, FLI has an independent prognostic value for the incidence of cardiovascular events in newly diagnosed, never-treated hypertensive patients. Therefore, FLI might identify higher-risk patients in the primary prevention of hypertension.

This study explores the use of advanced 3D imaging and printing technologies to digitally document and physically replicate cultural artifacts from the Archaeological Museum of Alexandroupolis. By employing structured light scanning and additive manufacturing techniques, detailed digital models and precise physical replicas of two significant artifacts were created—a humanoid ceramic vessel and a glass cup. A handheld 3D scanner was utilized for capturing intricate surface details, with post-processing methods to refine and colorize the digital models. Regarding 3D printing, both Fused Deposition Modeling (FDM) and Stereolithography (SLA) were employed, tailored to the artifacts’ unique requirements for resolution and material properties. This dual approach supports heritage preservation by generating tangible educational resources and providing alternative exhibits to safeguard original artifacts. Our results demonstrate that integrating 3D scanning and printing effectively enhances the accessibility, durability, and educational utility of cultural heritage assets, offering a sustainable model for artifact preservation and study.

Although the effect of face masks on preventing airborne transmission of SARS-CoV-2 is well studied, no study has evaluated their effect on blood pressure (BP). Therefore, we investigated the effect of surgical masks on BP in 265 treated hypertensive patients. Following the routine mask-on office BP measurement, patients were left alone and randomized to automated office BP measurement, with measurements taken after first wearing a mask for 10 min, then without wearing the mask for 10 min, and vice versa. Among the participants, 115 were women (43.4%), the mean age was 62 ± 12 years, and the mean office BP was 134 ± 15/81 ± 12 mmHg. There was no significant difference between mask-on unattended systolic BP (133 ± 15 mmHg) and mask-off unattended systolic BP (132 ± 15 mmHg) ( P  = 0.13) or between mask-on unattended diastolic BP (77 ± 13 mmHg) and mask-off unattended diastolic BP (76 ± 13 mmHg) ( P  = 0.32). Surgical masks had no effect on BP in treated hypertensive patients. Design of the study.

Current evidence on the prognosis of patients with a hypertensive crisis and predisposing factors is limited. We registered the clinical phenotype of patients with HC admitted to the emergency department, while those with a hypertensive emergency (HE) were hospitalized. One-year outcomes, i.e., composite of death or cardiovascular hospitalizations, were determined in patients with HE after hospital discharge. Out of 38,589 patients assessed in the emergency department, 256 hypertensive urgencies and 97 HE was registered. After stratification of the HE by sex, 48 men and 46 women completed the one-year follow-up. Men had more events than women (27 vs. 13, Ηazard Ratio 2.2, 95% Confidence Interval 1.03-4.7, p = 0.042) after adjustment for age, cardiovascular or chronic kidney disease, and diabetes mellitus. Our study raises the hypothesis that the male sex is an independent risk factor for cardiovascular outcomes in HE patients. CV Cardiovascular, BP blood pressure. The diagram presents the groups of comparison, men versus women in hypertensive emergencies that completed the 1-year follow-up for outcomes, in terms of hospitalizations or deaths.

Introduction: Chronic kidney disease (CKD) affects roughly 10% of the global population and significantly increases cardiovascular risk. While renin–angiotensin system inhibitors (RASi) remain a therapeutic mainstay, recent evidence supports the renoprotective value of sodium–glucose cotransporter-2 inhibitors (SGLT2i) and finerenone. This study evaluated the real-world use of guideline-directed medical therapy (GDMT) among patients with cardiorenal disease in Greece and explored factors influencing prescribing patterns. Methods: The Hellenic Cardiorenal Morbidity Snapshots (HECMOS 1 and 2) enrolled all cardiology inpatients across Greece on 3 March, 2022, and 5 June, 2024. Comorbidities and medication data were based on self-report and chart review. CKD patients eligible for SGLT2i and finerenone were identified per guideline criteria. Multivariable logistic regression was used to identify predictors of SGLT2i use. Results: From a total of 923 and 1222 patients enrolled in HECMOS 1 and 2, CKD was present in 26% and 27%, respectively. SGLT2i use prior to hospitalization rose from 15% in HECMOS 1 to 30.4% in HECMOS 2. In HECMOS 1, diabetes mellitus was the strongest predictor of SGLT2i use (OR 12.01, 95% CI 3.31–45.56, p < 0.001), while heart failure predicted use in HECMOS 2 (OR 4.10, 95% CI 1.70–9.88, p = 0.002). Finerenone was prescribed in only 1.7% of eligible patients in HECMOS 2. RASi usage among CKD patients remained stable across both cohorts (42.1% vs. 41.7%), with renal dysfunction showing no impact on prescribing patterns. Conclusions: SGLT2i use in patients with CKD and cardiovascular disease doubled over 2 years, indicating progress in implementing GDMT. However, overall use of disease-modifying therapies remains suboptimal, underscoring the need for further improvement in real-world care.

Obesity can cause the onset of heart failure and exacerbate the status of the pre-existing disease. Through intricate pathways, obesity activates hormonal factors that encourage the development of inflammation and lead to increased congestion. Consequently, this complex parallel pathophysiological cascade contributes to the echocardiographic and clinical signs of heart failure. In these patients, obesity frequently coexists with nutritional and muscular profile abnormalities that manifest as cachexia or sarcopenia. Patients with heart failure have a higher chance of surviving when obesity is treated. Interventional, pharmaceutical, and dietary strategies are used as forms of therapy. This review delves into the evaluation of the relationship between obesity and heart failure, and it targets to highlight the therapeutical impact of weight-loss programs on cardiac function in individuals with heart failure and obesity.