Blood pressure (BP) fluctuates with an annual cycle, with BP levels generally lower in summer and higher in winter. In this narrative review with a quasi-systematic literature search, we aim to summarise current evidence from a wide variety of research fields on seasonal BP variability, and to present our findings to stimulate interest in this largely unexplored area. Environmental temperature would be the key driver of seasonal BP variation, while other external and internal factors mediate this variation; quantifying these effects is difficult because of the various factors and their interactions. Self-measured home BP would be the most favorable information for evaluating long-term seasonal BP changes. Nocturnal home BP reduction is lower in summer than in winter, leading to a higher prevalence of a riser BP pattern in summer; we need to pay attention to the various risk factors associated with higher BP across seasons. Temperature obviously affects BP; therefore, it seems reasonable to assume that seasonal BP changes linearly contribute to seasonal mortality variation. However, our patients database showed that there are >10% of patients whose home BP is higher in summer than in winter, and the cardiovascular risk was significantly higher in patients with such inverse seasonal variation as well as those with contrarily large-sized seasonal variation in home BP (≥9.1 mm Hg in systolic or ≥4.5 mm Hg in diastolic measurements) than in those with the other small- to middle-sized seasonal variation. The inverse seasonal BP pattern is not rare in patients under antihypertensive drug treatment, and the mechanisms warrant investigation. Although the importance of BP level as a dominant and modifiable risk factor should be emphasized, assessing seasonal BP variation through long-term BP measurement, particularly based on home BP monitoring, has clinical benefits and should be widely promoted.

Salt-sensitivity of blood pressure (SSBP) is associated with immune-metabolic dysfunction, yet the mechanism that coordinates sodium exposure, mitochondrial remodeling, and blood pressure response remains undefined. Phenome-wide and laboratory-value association studies (PheWAS and LabWAS) in the All of Us Research Program identified fluid, electrolyte, and acid-base balance disorders and renal phenotypes as the strongest disease associations. At the same time, hypertension was linked to reduced serum potassium, chloride, and eGFR, corroborating the centrality of renal-electrolyte physiology in blood pressure regulation. Using a within-subject sodium challenge in humans, we show that sodium loading reorganizes circulating tricarboxylic acid (TCA) cycle intermediates in proportion to the individual blood pressure response. Transcriptomic profiling of immune cells under high sodium revealed suppression of oxidative phosphorylation, induction of HIF1α-dependent glycolytic gene networks, and rebalancing of the pyruvate dehydrogenase complex. Single-cell chromatin accessibility profiling demonstrated that HIF1α motif activity in circulating immune cells correlates with changes in systolic blood pressure and pulse pressure in salt-sensitive individuals. High sodium induced mitochondrial fragmentation with increased organelle mass and glycolytic capacity. Pharmacological HIF1α inhibition reversed fragmentation while only partially normalizing metabolic output, indicating structural and metabolic remodeling are partially dissociable downstream of HIF1α. Renal HIF1α gain-of-function in mice recapitulated the glycolytic transcriptional response with medullary specificity. Concordantly, Drosophila melanogaster subjected to a high-salt diet exhibited impaired locomotor performance, mitochondrial dysmorphology, intestinal barrier disruption, and cardiac remodeling, establishing evolutionary conservation of sodium-induced end-organ dysfunction independent of an adaptive immune system. Together, these findings identify a HIF1α-dependent axis of mitochondrial metabolic adaptation providing a mechanistic basis for SSBP.

Background/Objective: Continuous blood pressure (BP) monitoring is essential in clinical settings, where rapid hemodynamic changes influence patient management. While intra-arterial measurement remains the reference standard, non-invasive volume-clamp systems offer a potential alternative. We assessed the accuracy of finger-cuff-based continuous BP monitoring compared to invasive measurement in patients with pulmonary hypertension (PH). Methods: This post hoc analysis from a crossover RCT included PH patients who underwent repetitive hemodynamic assessments at rest and during exercise. The participants had simultaneous invasive BP monitoring via the radial artery and a non-invasive finger-cuff device (Finapres[®] NOVA Basic). The mean blood pressure (mBP) was compared at rest, 50% of the maximal workload, and at the end of exercise using Bland-Altman and Taffé analysis. Results: In the study, 24 patients (seven female; 59 ± 14 years) contributed 385 paired mBP measurements. The invasive and non-invasive methods showed similar values at rest (96.1 ± 16.7 vs. 96.4 ± 17.2 mmHg) and during maximal exercise (106.8 ± 18.6 vs. 111.8 ± 21.6 mmHg). The overall Bland-Altman bias was 2.8 mmHg with wide limits of agreement (-39.6 to 45.3 mmHg), which remained broad across all exercise intensities. The Taffé analysis revealed a non-uniform, directionally dependent bias: the non-invasive system overestimated the mBP at low pressures and underestimated it at higher pressures. The measurement variability was substantially greater for the non-invasive method than for the invasive reference. Conclusions: In PH patients, finger-cuff-based continuous BP monitoring demonstrated acceptable group-level agreement but insufficient individual-level accuracy for clinical decision-making.

The genetic architecture of cardiovascular traits is poorly characterised in non-European populations, limiting our understanding of disease aetiology and contributing to health disparities. Here, we analyse the genetic architecture of four cardiovascular traits (systolic and diastolic blood pressure, pulse rate, and maximum heart rate) using multi-trait analysis of genome-wide association studies and local genetic correlation analysis in 459,327 European (EUR) and 6654 African (AFR) ancestry individuals from the UK Biobank. Our analysis identifies 957 and 45 novel variants in the EUR and AFR cohorts, respectively, but reveals a profound divergence in the pleiotropic architecture of blood pressure. We identify 181 genomic loci with significant local genetic correlation between systolic and diastolic blood pressure (SBP-DBP) in the European sample, whereas such signals are completely absent in the African ancestry cohort. This marked disparity in local genetic correlation structure highlights that pleiotropic mechanisms can be highly ancestry-specific, underscoring the limitations of transferring genetic risk models across populations and the critical need for inclusive genomic research.

GLP-1 receptor agonists (GLP-1 RAs) are increasingly evaluated for cardiovascular outcomes, including heart failure (HF), due to their weight-reducing and anti-inflammatory effects. Individual trials in HF have reported heterogeneous results, which appear to differ by HF subtype. No prior quantitative synthesis has systematically compared GLP-1 RA effects in heart failure with preserved (HFpEF) versus reduced ejection fraction (HFrEF) across a wide range of clinically relevant outcomes. This meta-analysis addresses this gap by evaluating subtype-specific efficacy across clinical, functional, biochemical, and hemodynamic domains to guide therapy and inform future research. Eight randomized controlled trials enrolling 11,234 patients were included following a systematic search of major databases per PRISMA 2020 guidelines. Risk of bias was assessed using the Cochrane ROB 2.0 tool. Data were pooled using random-effects models with Hartung-Knapp adjustment. Sensitivity analyses assessed robustness and certainty of evidence was rated using GRADE. In HFpEF, GLP-1 RAs significantly reduced HF worsening events (HR 0.67, 95% CI 0.50-0.89; I[2] = 9.9%, high-certainty) and improved NT-proBNP (ratio 0.85), six-minute walk distance (+17.6 m), Kansas City Cardiomyopathy Questionnaire score (+7.4 points), and systolic blood pressure (-3.6 mmHg). The composite of HF worsening events or cardiovascular death was also reduced (HR 0.76, 95% CI 0.64-0.90). In HFrEF, no benefit was observed for HF worsening events (HR 1.23, 95% CI 0.89-1.69; I[2] = 0%, moderate-certainty) or secondary outcomes. Gastrointestinal adverse events were the most frequent cause of drug discontinuation (RR 3.12, 95% CI 1.28-7.63). In conclusion, GLP-1 RAs improve clinical, functional, and biomarker outcomes in HFpEF but not in HFrEF, highlighting subtype-specific efficacy. Gastrointestinal intolerance remains a key limitation, emphasizing the need for careful patient selection to optimize adherence. PROSPERO Registration: CRD420251138529.

Lasers operating in the 2.1 μm band are important beam sources with a wide range of applications. However, previous investigations have primarily focused on quasi-continuous-wave and Q-switched regimes with nanosecond pulse durations. In this work, a 1064 nm laser with a pulse-width of 491 ps was used to pump high-pressure nitrogen, and a 2111 nm Raman laser (second Stokes, S2) was generated. Through systematic optimization of the experimental parameters, a maximum output energy of 67.9 mJ at 2111 nm was achieved, the pulse-width was estimated to be narrower than 387 ps, and peak power was expected to be more than 175.5 MW, and the beam quality was measured to be Mx2=2.82, My2=2.96. This work presented a novel, to the best of our knowledge, approach for generating high peak power sub-nanosecond 2.1 μm lasers with good beam quality.

A wide range of vascular pathologies can lead to upper extremity ischemia, including atherosclerotic disease, complications following arterial bypass graft, steal from hemodialysis fistula or graft, trauma including iatrogenic injury, vascular compression syndromes, collagen vascular disorders and vasospasm. Non-invasive vascular laboratory testing can be helpful in diagnosis as well as follow-up to assess disease progression and response to therapy. In this article, the technique and interpretation of physiological testing studies such as the wrist brachial index, digital brachial indices, segmental pressure measurements and pulse volume recordings are reviewed. Demonstrative clinical cases are provided with Doppler ultrasound, CT angiography, and angiography correlation.

Fibromuscular dysplasia (FMD) is a rare cause of ischemic stroke. It is an important element of differential diagnosis that should be considered, especially in patients who do not have common cardiovascular risk factors. A 65-year-old man was admitted with transient left arm weakness and drooping of the mouth, asting about 3 minutes, followed by left-sided paresthesia. A similar episode had occurred a week earlier. On admission, the patient was alert and oriented. Neurological exam showed subtle flattening of the left nasolabial fold and a tendency to a positive ipsilateral Babinski sign, with no other abnormalities. Brain MRI revealed a subacute ischemic lesion in the anterior deep structures and a hyperacute focus at the right temporo-occipital border. CT angiography showed bilateral internal carotid artery changes suggestive of FMD, critical stenosis of the right MCA (M1), and aneurysmal dilation of the left ophthalmic artery origin. Digital subtraction angiography (DSA) confirmed a wide-neck saccular aneurysm of the left internal carotid artery (ICA). Rehabilitation and multidisciplinary consultations were undertaken. The patient was discharged in good condition without significant neurological deficits. Regular blood pressure control, atherosclerotic diet, physical activation and taking medications (antihypertensive drugs, acetylsalicylic acid and statin) regularly were recommended. Due to the diagnosis of a saccular aneurysm of the left ICA, a referral was issued to the neurosurgery department. The described case illustrates the need for a comprehensive and interdisciplinary approach to a patient with stroke in order to determine the etiology of the stroke and implement secondary prevention.

The focus of this study is to investigate the role of diffusion tensor imaging along the perivascular space (DTI-ALPS) index in brain aging. To address this, we first examined the association of DTI-ALPS with aging hallmarks among 40,488 UK Biobank (UKB) participants. Next, we developed normative brain age models incorporating the DTI-ALPS index from 12,401 healthy UKB adults and validated in UKB-ADNI and UKB-TALENT datasets. Finally, we explored the relationship between brain age gap (BAG) with peripheral organ function, chronic diseases, proteomics, and genetics, while identifying modifiable factors in a longitudinal cohort. The findings revealed that DTI-ALPS index correlated with chronological age, telomere length, brain structure, and cognition. A brain age model integrating the DTI-ALPS index achieved good accuracy in the UKB (r = 0.756) and replicated well in two independent datasets (UKB-ADNI: r = 0.766; UKB-TALENT: r = 0.724), with choroid plexus volume emerging as an additional contributor. Musculoskeletal health was a key driver for brain aging in females, while pulmonary metrics prevailed in males. Neurodegenerative and metabolic disorders increased BAGs, imparting increased mortality risk. Protein-wide and genome-wide analysis identified 154 BAG-related proteins and 11 loci. Modifiable factors, particularly systolic blood pressure below 120 mmHg, were strongly associated with reduced BAGs. Overall, the DTI-ALPS index is a promising brain aging biomarker, offering insights into links between brain and peripheral health, and highlighting sex-stratified therapeutic strategies. Aggressive blood pressure control may mitigate brain aging and promote long-term brain health.

Background : Obstructive Sleep Apnea (OSA) is a pervasive cardiovascular risk factor linked to accelerated aging and systemic inflammation. Intermittent hypoxia (IH)-a hallmark of OSA-induces cardiovascular decline, yet the underlying tissue-specific and systemic epigenetic mechanisms and the role of cellular senescence in the pathophysiology of OSA and associated cardiovascular disease (CVD) remain poorly understood. Methods : C57BL/6J male mice were exposed to IH or room air (RA) for durations ranging from 7 to 210 days. Genome-wide DNA methylation profiling was conducted on left cardiac ventricle and peripheral blood mononuclear cells (PBMCs) samples. Differentially methylated positions (DMP; q<0.05) were identified between IH and RA groups and the impact of IH duration was studied using regression models. Epigenetic age acceleration (EAA) was calculated using a multi-tissue epigenetic clock. Furthermore, p16-reporter and targeted ablation mouse models (p16-Cre ERT2 -DTR-tdTomato) were utilized to assess the role of p16 Ink4a -mediated senescence in IH-induced vascular dysfunction. Results : Chronic IH exposures significantly increased systolic and diastolic blood pressure and altered endothelial function. Epigenetic analysis identified 5,747 and 1,307 DMLs in the left cardiac ventricle and PBMCs, respectively, with minimal overlap between tissues (n=163, p=8.03 x 10 -8 ; Fisher's Exact Test), indicating a highly tissue-specific epigenetic response. Both tissues exhibited an early peak in EAA at 7 days of exposure, differing in the trajectory in longer exposures. Pathway analysis linked these epigenetic changes to cardiac dysfunction and cellular senescence, specifically highlighting Cdkn2a gene, which encodes the p16 protein, a marker of cellular senescence. Immunofluorescence confirmed increased p16 expression in aortic endothelial cells following IH. Remarkably, systemic ablation of p16-expressing cells (i.e., p16 high cells), reversed IH-induced hypertension and restored coronary flow reserve to control levels. Conclusions : IH induces duration-dependent, tissue-specific epigenetic dysregulation and accelerated biological aging. Our findings provide initial evidence that p16 Ink4a -mediated cellular senescence is a primary driver of OSA-induced cardiovascular morbidity and that targeting the senescent endothelium can revert vascular dysfunction, thereby establishing a novel mechanistic framework for cellular senescence as a therapeutic target in OSA.