Essential hypertension (EH) remains the leading modifiable risk factor for cardiovascular morbidity and mortality, yet even optimally treated patients carry residual cardiovascular risk. Emerging evidence suggests that chronic subclinical inflammation contributes to the pathogenesis of EH, leading to target organ damage. Neutrophil extracellular traps (NETs), which represent networks of decondensed chromatin carrying neutrophil proteins, have recently gained attention as potent drivers of a harmful thromboinflammatory milieu. While NETs are established contributors to atherosclerotic cardiovascular disease, including ischemic stroke, coronary artery disease and heart failure, their role in hypertension has only recently begun to be elucidated. Preclinical studies demonstrate that NETosis may promote endothelial dysfunction, vascular smooth muscle cell proliferation, and blood pressure elevation, while inhibition of NETs formation attenuates these processes. Clinical data, though limited, indicate that untreated hypertensives exhibit higher circulating NETs, linked to enhanced thrombogenicity, adverse vascular remodeling, and potentially to hypertension-mediated organ damage. Furthermore, therapeutic strategies targeting NETs, ranging from conventional immunomodulatory therapies to biologic agents, are under investigation. This review summarizes current knowledge on the role of NETs in the pathophysiology of EH and related cardiovascular diseases, while discussing potential anti-NETotic effects of currently available pharmacological agents. Hypertensive stimuli promote neutrophil extracellular traps (NETs) formation, leading to thromboinflammation, endothelial injury and vascular damage. These processes are involved in the occurrence of hypertension-mediated organ damage and cardiovascular disease, while sustaining elevated blood pressure. Targeting NET formation may interrupt this vicious cycle and reduce residual cardiovascular risk in hypertension. Ang II, angiotensin II; C5a, compliment component 5a; CVD, cardiovascular disease; HMOD, hypertension-mediated organ damage; IL, interleukin; IsoLGs, isolevuglandins; MPO, myeloperoxidase; NE, neutrophil elastase; NET, neutrophil extracellular traps; RAAS, renin-angiotensin-aldosterone system; ROS, reactive oxygen species; TF, tissue factor; TNFα, tumor necrosis factor α; VSMC, vascular smooth muscle cells.

Hypertension is a leading global cause of morbidity and mortality, increasingly prevalent among young adults with obesity. This epidemiologic shift is particularly concerning, as early‑onset hypertension confers an increased lifetime risk of cardiovascular disease. Obesity and hypertension share pathophysiological mechanisms, including sympathetic nervous system overactivation, leptin resistance, chronic low‑grade inflammation, renal fat deposition, endothelial dysfunction, and genetic predisposition. Dietary factors, sedentary lifestyle, poor sleep, psychosocial stress, and environmental exposures further exacerbate the risk. Hence, effective management requires an integrated approach targeting both obesity and blood pressure. Lifestyle interventions play a key role in therapy but are often hindered by poor adherence in younger populations. Pharmacological therapies have shown substantial efficacy in reducing weight and blood pressure, with emerging cardiovascular benefits. Bariatric surgery remains an alternative, achieving sustained weight loss and remission of hypertension in a significant proportion of patients. Early, multifaceted interventions tailored to this population can reduce premature cardiovascular disease, lower health care costs, and improve quality of life.

Rheumatoid arthritis (RA) is characterized by immune-mediated inflammation resulting in excess cardiovascular disease (CVD) risk. Increased sodium, decreased potassium intake and their ratio have been acknowledged as CVD risk modifiers, while pathophysiological studies suggest a role in autoimmunity and inflammation. We aimed to review in a systematic manner the literature regarding the effects of dietary sodium, potassium intake and their ratio, on cardiovascular and disease-related outcomes in patients with RA. We performed a systematic literature search in Medline and Cochrane. Our research concluded to 1,283 patients (8 studies). Although not all studies coincide, most agree that increased dietary sodium and reduced dietary potassium intake are adversely associated with disease related (rheumatic and immunologic) outcomes. The ratio between sodium and potassium emerges a potential indicator of autoimmunity state that needs to be further balanced. Only 4 studies reported associations with cardiovascular outcomes in RA, particularly hypertension, although not consistently and none with hard CVD endpoints. These findings support that interventions promoting a poor in sodium and rich in potassium diet in RA may have beneficial effects in terms of autoimmunity regulation, suppression of inflammation and improvement in cardiovascular health.

Obesity is a key contributor to heart failure, driving increased morbidity, mortality, and healthcare costs. This association is supported by multiple pathophysiological mechanisms and consistent epidemiological evidence, particularly not only in heart failure with preserved ejection fraction (HFpEF), but also in heart failure with reduced ejection fraction (HFrEF). Given the rising prevalence of both diseases, integrated management strategies are essential. This review outlines current management options in patients with heart failure and obesity, from lifestyle modification to pharmacological and surgical treatment, and explores emerging treatments aimed at mitigating this growing burden.

There is cumulative evidence that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) can offer cardiovascular protection extending beyond glucose-lowering and weight reduction, but the underlying mechanisms contributing to these effects remain incompletely understood. Modulation of platelet function might contribute to the aforementioned benefits. In the current literature review article, we synthesized available preclinical and clinical data evaluating the effects of GLP-1 RAs on platelet activation and function. Preclinical data indicate that GLP-1 RAs might decrease platelet activation via both GLP-1 receptor-dependent and -independent mechanisms with the involvement of cyclic adenosine monophosphate signaling, increase in nitric oxide bioavailability, and suppression of thromboxane-mediated pathways, particularly under inflammatory or shear-stress conditions. Additionally, clinical studies, despite being limited and heterogeneous, support a reduction in platelet activation markers, even independently of glycemic control or weight loss. However, most of them are characterized by small sample sizes and significant heterogeneity among them. In summary, existing evidence suggests that GLP-1 RAs exhibit potential antiplatelet effects that could contribute to their cardioprotective profile. Larger, well-designed clinical studies are crucial to better understand the clinical importance of platelet modulation by GLP-1 RAs and their potential implications for cardiovascular risk reduction.

BACKGROUND:Early vascular aging (EVA) reflects accelerated arterial stiffening and is closely linked to cardiovascular and renal target organ damage. The Early Vascular Aging Ambulatory score (EVAAs) estimates EVA using ambulatory blood pressure monitoring (ABPM) and routinely available clinical parameters. We aim to investigate the association between EVAAs-defined early vascular aging and markers of kidney involvement-particularly albumin-to-creatinine ratio (ACR)-in a hypertensive population. METHODS:Fifty treated hypertensive adults undergoing 24 h ABPM were enrolled. All participants underwent laboratory evaluation, including serum electrolytes and 24 h urine collection for albumin, creatinine, sodium, and potassium. EVAAs was calculated using ABPM-derived parameters and established cardiovascular risk factors. RESULTS:EVAAs was positively correlated with ACR (r = 0.276, p = 0.049). In addition, inverse correlations were observed between EVAAs and serum potassium (r = -0.290, p = 0.038) and serum sodium (r = -0.284, p = 0.046). Participants with moderately increased albuminuria tended to exhibit higher EVAAs values, although this difference did not reach statistical significance. CONCLUSIONS:EVAAs is associated with early markers of renal involvement in hypertensive patients, supporting its potential role as a non-invasive indicator of subclinical target organ damage. Larger studies are warranted to confirm these findings and to further validate EVAAs as a clinically useful marker of EVA.

Background Statins remain to date the primary therapeutic option for dyslipidemia. However, a significant portion of patients with dyslipidemia fail to achieve optimal low-density lipoprotein targets for reasons often related to treating physicians. The aim of STAtin Treatment in Routine clinical Practice (STATRIP) survey was to report and quantify perceptions and common beliefs regarding treatment with statins, among physicians implicated in the primary and secondary care of patients with dyslipidemia. Methods and results This observational cross-sectional study was conducted using an online-distributed questionnaire, which was designed to cover a wide range of physicians’ knowledge and perceptions on treatment with statins. A total of 261 health care providers filled out the survey, mostly general practitioners and internists (93.5%). Study participants clearly expressed their concerns regarding statin-related side effects, including fears on interactions with other medication, muscle aches and pain, increase in liver enzymes, and gastrointestinal disorders. Myalgias were observed by physicians in as many as 29.2% of patients receiving rosuvastatin, and in as many as 26.5% receiving atorvastatin. Combination lipid-lowering therapy with ezetimibe was reported by only 53.6% of participants as a prevalent strategy for uncontrolled individuals. Only 58.6% apply non-HDL cholesterol measurements in their clinical practice. Conclusions Our study provides a clear perspective of treating physicians regarding statin prescription patterns. Several misconceptions, especially regarding statin-related adverse effects, hold well among treating physicians. Insufficient implementation of dyslipidemia guidelines calls for more targeted educational interventions to achieve optimal management of patients with dyslipidemia.

INTRODUCTION:PCSK9 inhibitors (PCSK9i) are at the center of research for their pleiotropic effects. The aim of this study is to systematically review the literature for their effect on vascular endothelial dysfunction. METHODS:We systematically researched Embase, Ovid MEDLINE and CENTRAL for this purpose. Eligible studies were those assessing endothelial function by available noninvasive vascular methods. Meta-analysis was performed to compare differences on endothelial dysfunction between PCSK9i and placebo. Qualitative analysis was used for observational studies evaluating the outcome before and after PCSK9i. RESULTS:We found 8 articles eligible, with the main outcome, among others, to be changes on flow-mediated dilation (FMD). Observational studies report an increase on FMD after PCSK9i treatment. Only 5 studies (415 participants) were eligible for the meta-analysis. Compared to placebo, PCSK9i increased FMD but not statistically significant (MD:0.84, 95%CI:-0.07,1.74). Alirocumab was associated with no difference in two studies (MD:-0.20, 95%CI:-0.73,0.34), whereas evolocumab with a statistically significant increase in FMD in four studies (MD:1.31, 95%CI:0.22,2.4). CONCLUSION:This is the first effort to summarize evidence on the effect of PCSK9i on endothelial function. PCSK9i may improve FMD, suggesting additional therapeutic roles beyond the traditional ones. Further, high-quality, large population studies are needed to confirm these findings. PROTOCOL REGISTRATION:The protocol utilized for this research is available in the Open Science Framework (OSF) database (https://osf.io/hz4d2/).

Background/Objectives: Several studies in the literature support that endovascular aortic repair (EVAR) could exert a harmful effect on heart function, causing myocardial injury. The aim of this study is to investigate the correlation of high-sensitivity cardiac troponin I (hs-cTnI) levels during the immediate postoperative period after EVAR with various factors. Methods: A total of 104 patients were enrolled from February to December 2024 prospectively and consecutively. Patient demographics, cardiovascular comorbidities, laboratory tests, including hemoglobin and hs-cTnI levels, EVAR procedure duration and type of anesthesia were recorded. A generalized linear mixed model with a Gamma distribution and log link was fitted to analyze postoperative hs-cTnI concentrations across three time points (6 h, 24 h, and 48 h). Results: The mean age of patients was 71.6 ± 7.3 years, the mean transverse AAA diameter was 5.7 ± 1.1 cm and the mean preoperative hemoglobin was 14.2 ± 1.64 g/dL. In total, 72 patients received general anesthesia and 32 patients regional anesthesia. A total of 18 patients presented myocardial injury. Patients under general anesthesia had significantly higher mean hs-cTnI than those under regional anesthesia (p < 0.01). Older age, longer operations, and higher baseline hs-cTnI all predict higher follow-up hs-cTnI. Meanwhile higher preoperative hemoglobin predicts lower hs-cTnI. Conclusions: General anesthesia compared to regional anesthesia, older age, longer surgery, and higher baseline hs-cTnI are associated with higher postoperative hs-cTnI levels, while higher preoperative hemoglobin predicts lower hs-cTnI levels. Understanding the factors that are related to myocardial injury during EVAR could contribute to the improvement in procedures in order to minimize the harmful effect of EVAR on heart function.

Hypertension in obesity represents a major global health challenge, closely linked to the global epidemics of obesity, type 2 diabetes and metabolic dysfunction. Excess adiposity contributes to elevated blood pressure through multiple, interrelated mechanisms, including activation of the renin-angiotensin-aldosterone system, sympathetic nervous system overactivity, insulin resistance, inflammation and adipokine dysregulation. Importantly, emerging evidence indicates that body composition plays a critical role in modulating hypertension risk, treatment response and cardiovascular outcomes. This article highlights the need for a more individualized pharmacotherapeutic approach to hypertension in people with obesity. While lifestyle modification and weight reduction remain essential, pharmacological treatment should be tailored to underlying pathophysiological drivers, such as volume expansion, neurohormonal activation and metabolic abnormalities. The potential different antihypertensive drug classes in hypertension related with obesity are also discussed. A precision medicine approach that incorporates body composition and metabolic risk factors may improve blood pressure control and decrease residual cardiovascular risk in this high-risk population.

BACKGROUND:Estimated pulse wave velocity (ePWV), an easy to calculate proxy of carotid to femoral PWV (cfPWV), can be derived from 24-hour blood pressure monitoring (24h-BPM). Its role in acute ischemic stroke (AIS) has not previously been investigated in large multinational datasets. METHODS:A pooled individual patient data analysis from 13 cohorts across seven countries was conducted, including 2933 AIS patients who underwent 24h-BPM during the hyperacute to subacute phase. ePWV was calculated using a validated equation. Associations with clinical characteristics, stroke severity, etiologic subtypes, and outcomes were assessed with logistic regression. The primary outcome was poor functional outcome at 90 days, defined as a modified Rankin Scale (mRS) >2. RESULTS:Patients with higher ePWV presented with more severe strokes (median NIHSS 7 vs. 3, P < .001) and had poorer outcomes both at 90 days (63.7% vs. 23.7%, P < .001) and discharge (61.9% vs 29.1%, P < .001). ePWV was associated with poor outcome at 90 days (aOR: 1.24, 95% CI: 1.05-1.45) and discharge (aOR: 1.26, 95% CI: 1.12-1.42), per 1 m/s increase in ePWV, after adjustment for conventional risk factors and stroke severity. In patients ≤50 years, ePWV was highest in those with small vessel disease (SVD), who also had more cardiovascular risk factors than other stroke subtypes. CONCLUSIONS:ePWV derived from 24h-BPM is a simple, widely applicable measure of vascular aging that is associated with functional outcome after AIS. The higher ePWV observed in young patients with SVD underscores a potential early arteriosclerotic burden in this subgroup.

Super Normal Vascular Aging (SUPERNOVA) describes individuals whose vascular system remains protected, despite exposure to cardiovascular risk factors. Understanding the determinants of arterial stiffness in this population may provide valuable insights into protection mechanisms. This study aims to investigate the key features of SUPERNOVA individuals and examine factors associated with carotid-femoral pulse wave velocity (cf-PWV) across different age subgroups. This cross-sectional study included individuals referred to a Hypertension Center for blood pressure (BP) evaluation. SUPERNOVA status was defined based on cf-PWV values lower than the age-expected averages derived from European population. Clinical, laboratory, and ambulatory BP measurements were recorded. From a total cohort of 829 participants, 37.2

Background/Objectives: Aortic stiffness is a strong independent factor in cardiovascular outcomes. The method of choice for evaluating aortic stiffness is the measurement of aortic pulse wave velocity (PWV). Endovascular aortic repair (EVAR) increases aortic rigidity and thus aortic stiffness. The aim of this study is to investigate the correlation between endograft length and post-operative increases in PWV in patients with abdominal aortic aneurysms (AAAs) subjected to EVAR. Methods: A prospective observational study enrolling 107 patients from February to December 2025 was conducted. Patient demographics and comorbidities were recorded. The length of the endografts was calculated by studying computed tomography angiograms (CTAs) and digital subtraction angiographies (DSAs) of the patients. PWV was measured pre-operatively and post-operatively during the first 24 h after EVAR, and the difference in PWV (dPWV) was calculated. Results: The mean age of the patients was 72 ± 7.5 years, and 93.5% of them were males. The mean transverse AAA diameter was 5.7 ± 1.1 mm, and the mean endograft length was 169.7 ± 26.9 mm. An extension to the external iliac artery was deployed in 10 patients (9.3%). A strong positive correlation was observed between dPWV and endograft length, indicating that each additional 1 mm in graft length corresponded to a 0.541% increase in dPWV. Patients with an extension to external iliac arteries exhibited a significantly higher mean dPWV (9.95 ± 2.08% vs. 27.12% ± 12.15%, t = -4.463, p = 0.002). No statistically significant differences in dPWV between the different endograft types were found (p = 0.74). Conclusions: Endograft length is strongly related to PWV elevation during the immediate post-operative time after EVAR, especially when the endograft is extended to the external iliac arteries.

Understanding the impact of early vascular aging (EVA) on acute ischemic stroke (AIS) outcomes may provide new insights for improving prognostic assessments and developing targeted therapeutic strategies. This study aimed to validate the EVA ambulatory score (EVAAs) in AIS patients, assessing its association with stroke type, severity, and prognosis. Among the 2,730 AIS patients with a mean age of 72.0 ± 14.4 years, 83.4

OBJECTIVE:Blood pressure (BP) phenotypes and day-night variability have been associated with acute ischemic stroke (AISTR). The aim of this study was to analyze the BP phenotypes and day-night variability during the first 3 days of an AISTR and their correlation with 10-year cardiovascular death (CVD). METHODS:Eighty-five volunteers (49.9% men, 77.3 ± 6 years), diagnosed for AISTR, were included in the study. Twenty-four hour ABPM was performed during the first 3 days of AISTR symptoms. A follow-up visit was performed through phone call, 10 years after the AISTR event. RESULTS:There is a reproducible nocturnal circadiac rhythm, with the nondipping status to be the most prevalent (89.3%, 89.2%, 88.3% for Days 1, 2, 3 accordingly, P > 0.05), compared to dipping status ( P < 0.05), but not a reproducible BP phenotype, except the hypertensive one (50%, 45.8%, 51.6% for Days 1, 2 and 3 accordingly, P > 0.05). The mean follow-up was 509.6 ± 10 weeks. 37.1% had died (41.2% from MACE). Cox regression analysis revealed that age [odds ratio (OR):1.15, confidence interval (CI): 1.01-1.17, P < 0.05], sex (male, OR: 1.92, CI: 1.07-3.82, P < 0.05), diabetes mellitus (OR: 1.55, CI: 1.06-3.14, P < 0.05), early vascular ageing (OR: 2.01, CI: 1.19-3.74, P < 0.05), transient ischemic attack (OR: 2.32, CI: 1.02-5.34, P < 0.05), sustained hypertension (OR: 2.78, CI: 1.13-6.83, P < 0.05), day-night SBP ratio (OR: 0.98, CI: 0.96-0.99, P < 0.05) and day-night DBP ratio (OR: 0.96, CI: 0.94-0.99, P < 0.05) were significant predictors for CVD. CONCLUSION:Hence, patients with AISTR present a reproducible nocturnal circadian rhythm, but not a reproducible BP phenotype, except sustained hypertension. These parameters found also to be determinants for 10-year CVD.

Blood pressure (BP) measuring devices must demonstrate clinical accuracy proven by proper validation testing in the intended population, following recommendations published by scientific organizations. This review aims to evaluate out-of-office validated BP measuring devices in children and adolescents and discuss their accuracy based on current validation standards. Only successful, validated studies for out-of-office BP measuring devices were included. Studies for office blood pressure measuring (OBPM) devices or devices that failed validation were excluded. Based on the eligibility criteria, 17 validation studies on BP measuring devices were included, 8 for home blood pressure measurement (HBPM), and 9 for ambulatory blood pressure measurement (ABPM). The accuracy of validated devices and the quality of the eligible studies were evaluated using the AAMI/ESH/ISO Universal Standard (ISO 81060-2:2018). The systematic search was conducted through three search engines (PubMed, Scopus, and CENTRAL (Cochrane Central Register of Controlled Trials)). When assessing on AAMI/ESH/ISO 2018 validation criterion 1, HBPM devices showed significantly lower accuracy than ABPM devices, in terms of absolute mean difference (MD, in mmHg) for systolic blood pressure (SBP) (1.35, 95