Arterial hypertension remains the leading modifiable cause of cardiovascular morbidity and mortality resulting in characteristic changes in cardiac structure and function. Contemporary hypertension clinical guidelines increasingly emphasise prevention and early detection of hypertension-mediated organ damage, yet they differ in how blood pressure is categorised and when further investigation is recommended. Within this prevention-focused landscape and alongside a broader cardio-renal-metabolic framework, this review provides a practical overview on the role of echocardiography in arterial hypertension by integrating contemporary hypertension guidelines with imaging consensus documents. We outline when echocardiography is most likely to add value in hypertension and review echocardiographic assessment of left ventricular structure and geometry, systolic and diastolic function and filling pressures, atrial remodelling, right ventricular assessment, valvular heart disease and the aorta. Practical indications for scanning and transoesophageal echocardiography considerations are discussed. Finally, we highlight future directions including prevention-focused pathways, scalable echocardiography strategies, routine inclusion of contemporaneous blood pressure in reports, artificial intelligence-enabled quantification and selective multimodality imaging within specialist hypertension services.

AIMS:Vascular ageing is characterized by vessel stiffening, with increased deposition of extracellular matrix (ECM) proteins including collagens. Oxidative DNA damage occurs in vascular ageing, but how it regulates ECM proteins and vascular stiffening is unknown. We sought to determine the relationship between oxidative DNA damage and ECM regulatory proteins in vascular ageing. METHODS AND RESULTS:We examined oxidative DNA damage, the major base excision repair (BER) enzyme 8-Oxoguanine DNA Glycosylase (Ogg1) and its regulators, multiple physiological markers of ageing, and ECM proteomics in mice from 22 to 72 w. Vascular ageing was associated with increased oxidative DNA damage, and decreased expression of Ogg1, its active acetylated form, its acetylation regulatory proteins P300 and CBP, and the transcription factor Foxo3a. Vascular stiffness was examined in vivo in control, Ogg1-/-, or mice with vascular smooth muscle cell-specific expression of Ogg1+ (Ogg1) or an inactive mutation (Ogg1KR). Ogg1-/- and Ogg1KR mice showed reduced arterial compliance and distensibility, and increased stiffness and pulse pressure, whereas Ogg1 expression normalized all parameters to 72 w. ECM proteomics identified major changes in collagens with ageing, and downregulation of the ECM regulatory proteins Protein 6-lysyl oxidase (LOX) and WNT1-inducible-signaling pathway protein 2 (WISP2). Ogg1 overexpression upregulated LOX and WISP2 both in vitro and in vivo, and downregulated Transforming growth factor β1 (TGFb1) and Collagen 4α1 in vivo compared with Ogg1KR. Foxo3a activation induced Lox, while Wnt3 induction of Wisp2 also upregulated LOX and Foxo3a, and downregulated TGFβ1 and fibronectin 1. In humans, 8-oxo-G increased with vascular stiffness, while active OGG1 reduced with both age and stiffness. CONCLUSION:Vascular ageing is associated with oxidative DNA damage, downregulation of major BER proteins, and changes in multiple ECM structural and regulatory proteins. Ogg1 protects against vascular ageing, associated with changes in ECM regulatory proteins including LOX and WISP2.

Aim – GLP-1 and glucagon dual receptor agonists are under clinical development for a range of metabolic conditions including as type 2 diabetes and obesity. The cardiovascular actions of GLP-1 and glucagon receptor agonism are well studied, however less is known about their combination. The aim of this study was to explore the haemodynamic effects of dual agonism at the GLP-1 and glucagon receptor. Methods – Healthy male participants attended a series of randomised, saline-controlled intravenous infusion studies using glucagon [low] (25 ng/kg/min), glucagon [high] (50 ng/kg/min), exenatide (loading dose 50 ng/min for 30 minutes then 25 ng/min) and exenatide:glucagon co-infusion for 120 minutes (Part A, glucagon dose-ranging study), or 60 minutes (Part B, dual-agonism study). Results – In Part A (n=7, 25±7 years), glucagon dose-dependently increased heart rate by 3 bpm with glucagon [low] (p=0.407) and 11 bpm with glucagon [high] (95% CI 4-17 bpm, p<0.01). In Part B (n=12, 25±3 years), exenatide increased heart rate by 4 bpm (95% CI 2-6 bpm, p<0.001). Glucagon [low] increased heart rate by 4 bpm (95% CI 1-7 bpm, p<0.001). Co-infusion increased heart rate by 7 bpm (95% CI 4-9 bpm, p<0.001). There were no differences in stroke volume, cardiac output, blood pressure, or heart rate variability. Conclusion – With the exception of an increase in heart rate, no concerning haemodynamic signals have been detected in studies with GLP-1 and glucagon dual receptor agonists. Our data are consistent with these findings, showing dual agonism acutely increases heart rate in healthy male participants.

OBJECTIVE:To investigate the prevalence of hypertension and cardiovascular dysfunction 1 year postpartum in Black African women who experienced pre-eclampsia in a low-resource setting in Uganda. DESIGN:Prospective cohort study. SETTING:Tertiary referral hospital in urban Uganda. POPULATION:Pregnant women who developed pre-eclampsia between 2019 and 2021, matched to normotensive controls with maternal and gestational age. METHODS:Sociodemographic, clinical and laboratory data were collected at recruitment and 1 year postpartum. Baseline characteristics and incidence rate ratios were calculated to assess risk factors for developing hypertension. Multivariable conditional Poisson regression adjusted for matched study design was used to analyse outcomes. MAIN OUTCOME MEASURES:The primary outcome was hypertension (≥ 140/≥ 90 mmHg) at 1 year postpartum. Secondary outcomes included aortic pulse wave velocity, left ventricular mass index, and left ventricular ejection fraction at 1 year postpartum. RESULTS:At one-year postpartum, hypertension prevalence was higher among women with pre-eclampsia than controls (36.4% (96/264) versus 4.5% (12/264); aIRR 1.26, 95% CI 1.16-1.36, p < 0.001). Postpartum median aortic pulse wave velocity was increased in women with pre-eclampsia (6.45 ± 0.76 m/s vs. 5.67 ± 0.22 m/s, p < 0.001). Left ventricular mass indexed to body surface area was increased in women with pre-eclampsia (71.7 ± 19.6 g vs. 76.5 ± 23.2 g, p < 0.01). Left ventricular ejection fraction was not influenced by pre-eclampsia (p = 0.35). CONCLUSIONS:In this low-resource setting, black African women with pre-eclampsia had increased cardiovascular risk markers at one year postpartum. Over one-third of women with pre-eclampsia developed hypertension at one year postpartum, emphasising the need for postpartum blood pressure monitoring and early intervention to mitigate long-term cardiovascular risk in this high-risk population.

Specialised pro-resolving mediators (SPMs) are endogenously produced lipid mediators that regulate the propagation of inflammation and promote tissue repair. We hypothesised that SPM production is dysregulated in COPD; and associated with disease severity, defined by patients with stable COPD (no exacerbations)versuspatients with frequent exacerbations.MethodsLipid mediators were measured in plasma samples from patients with COPD (stable and frequent exacerbators) and age, sex, BMI-matched healthy controls using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Lipid mediator (LM) profiles were compared between controls and stable COPD patients, and stable COPD patients compared with frequent exacerbators. Exploratory association with ever occurrence of severe exacerbation over 4.1 years of follow up was examined. Data are presented as mean±semin pg·mL−1for LMs, or mean±sd.ResultsForty-nine stable COPD patients had increased levels of pro-inflammatory mediators and some SPMs compared with 28 controls (prostaglandin (PG)D2: 13.97±2.44versus0.53±0.13, p<0.001, lipoxins: 226.83±23.84versus59.84±20.25, p<0.01, respectively). Fifty-two frequent exacerbators had lower PGD2(3.07±0.97versus13.97±2.44, p<0.01) and SPMs (D-resolvins: 8.73±1.25versus34.53±8.95, p<0.01, lipoxins: 53.93±9.23versus226.83±23.84, p<0.01, respectively) compared with stable COPD patients, despite a higher neutrophil count (5.28±2.16versus4.28±1.60×109/L, p=0.004).In exacerbators, D-resolvins levels were independently, inversely associated with occurrence of severe exacerbation (OR:0.88 (95%CI: 0.79,0.97), p=0.03, over follow-up.ConclusionThese findings demonstrate distinct LM profiles of stable COPD and frequent exacerbator patients. In exacerbators, D-resolvins were downregulated compared with stable COPD patients and associated with future risk of severe exacerbations over follow up. Further work is needed to understand these findings.

Colchicine has been incorporated into major clinical guidelines for the secondary prevention of cardiovascular disease (CVD). However, recent randomized trials have presented contradictory results. We aimed to synthesize the current evidence on colchicine in secondary CVD protection, using a cumulative-dose approach. We conducted a meta-analysis incorporating all randomized controlled trials (RCTs) globally. RCTs directly comparing colchicine versus placebo/standard care for the secondary prevention of cerebrovascular or coronary vascular disease were included. Odds ratios (OR) were derived for the primary outcome, defined as the prospective occurrence of major adverse cardiovascular events (MACE). Secondary outcomes included mortality, individual components of MACE, C-reactive protein, and adverse effects. In total, 14 RCTs including 31,397 participants were included. Colchicine significantly reduced MACE (OR 0.80; 95

Introduction Black ethnic cohorts, when compared with white cohorts, have disproportionately higher rates of essential hypertension and related complications. Ethnic differences in the renin-angiotensin-aldosterone system have been identified in black ethnic cohorts displaying a low-renin, salt-sensitive phenotype in comparison to white individuals. Studies have highlighted lower levels of aldosterone in black cohorts compared with white cohorts. However, when renin is considered, in the form of the aldosterone-renin ratio (ARR), the ARR is higher in black cohorts. The Framingham study highlighted that people in the upper quartile for baseline aldosterone were more likely to have a higher blood pressure and develop hypertension at 4 year follow-up. Therefore, the inappropriately suppressed aldosterone may be contributing to the ethnic differences in hypertension prevalence and prognosis.Methods and analysis Four databases will be searched (MEDLINE, Embase, Scopus and Cochrane Library) to identify eligible studies from database creation to August 2025. Two investigators will independently review the search results and document reasons for full-text exclusions. The main outcomes are to assess if there are ethnic differences in baseline aldosterone, baseline plasma renin activity (PRA) and ARR. We will also look at ethnic differences in regulatory mechanisms of aldosterone, such as serum potassium and 24 hour urinary electrolytes, that may explain the potential differences in aldosterone and ARR in black and white ethnic cohorts. Studies looking at normotensive and hypertensive individuals will be included. Studies in paediatric populations (<18 years) will be excluded. We will include studies without language restriction. Risk of bias assessment will be completed with a modified Newcastle-Ottawa scale. Subgroup analysis and sensitivity analyses will be completed to verify the accuracy of the study results and the consistency of the inferences.Ethics and dissemination As this review will involve analysis of previously published data, ethical approval is not required. The results will be submitted to a peer-reviewed journal.PROSPERO registration number CRD420251025642.

BACKGROUND:Essential hypertension is often treated as a uniform condition. However, it encompasses distinct patterns of blood pressure elevation such as isolated systolic, systolic diastolic, and isolated diastolic hypertension, which vary in prevalence according to age and sex. We hypothesized that different hemodynamic mechanisms account for the age- and sex-related differences in these hypertensive phenotypes. METHODS:In this cross-sectional analysis of the ACCT (Anglo-Cardiff Collaborative Trial), 5371 individuals (2402 male), aged 18 to 92 years, free of cardiovascular disease and medication were included. Blood pressure, cardiac output, stroke volume, peripheral vascular resistance (PVR), and aortic pulse wave velocity were measured. Within each sex, subjects were stratified according to age (<30, 30-60, and >60 years), and blood pressure phenotype based on clinic (seated) blood pressure. RESULTS:Isolated systolic hypertension was the most common hypertensive phenotype in young men and characterized by an elevated cardiac output and stroke volume. In contrast, systolic diastolic hypertension and isolated diastolic hypertension were more common in younger females, with systolic diastolic hypertension associated with elevated PVR and aortic pulse wave velocity, and isolated diastolic hypertension with increased PVR. Systolic diastolic hypertension was the most common phenotype in middle age and accompanied by increased PVR in both sexes. Isolated systolic hypertension was again the most common phenotype in older individuals. However, in contrast to younger adults, isolated systolic hypertension affected both men and women equally (~1:1) and was characterized by elevated aortic pulse wave velocity and PVR. CONCLUSIONS:Different hypertensive phenotypes are characterized by distinct hemodynamic mechanisms in an age- and sex-dependent manner. Targeting therapy toward primary hemodynamic abnormalities could lead to more effective interventions in essential hypertension.

In this position statement the British and Irish Hypertension Society (BIHS) present a review of the current evidence for blood pressure (BP) treatment thresholds and targets. The BIHS recommend initiating pharmacological antihypertensive therapy, irrespective of cardiovascular disease risk, following a confirmed diagnosis of hypertension (sustained out-of-office BP ≥ 135/85 mmHg despite diet and lifestyle advice). The BIHS recommend an on-treatment BP target < 130/80 mmHg or as low as reasonably achievable without causing unacceptable side-effects, within 6-months of initiating treatment, for all adults. Possible subgroups to whom this may not apply are those who are frail and/or have limited life expectancy where higher targets may be appropriate based on clinical judgement and the individuals’ tolerance to treatment. The BIHS believe that this simple 2-step approach will facilitate practitioners deliver evidence-based best practice, discourage therapeutic inertia around BP lowering and improve heath outcomes for all adults living with high BP.

INTRODUCTION:Normal pregnancy is associated with cardiovascular changes that enable adaptation to the pregnancy state. We sought to describe the haemodynamic changes from prepregnancy to very early pregnancy in women planning to conceive in southwestern Uganda. METHODS:In this prospective cohort study, we enrolled women in southwestern Uganda planning to conceive. Brachial and central blood pressure, heart rate, cardiac output, stroke volume, and peripheral vascular resistance were assessed prepregnancy and repeated in very early pregnancy. RESULTS:We studied 86 women with a mean age of 27.8 years (SD ± 4.4). The mean gestational age was 7 (±2) weeks at the time of repeat blood pressure measurement. Brachial systolic and diastolic blood pressure decreased in very early pregnancy (116 ± 11 to 114 ± 8 mmHg and 68 ± 6 to 65 ± 5 mmHg, respectively; P  < 0.001). Central systolic and diastolic blood pressure also decreased (112 ± 10 to 109 ± 8 mmHg, P  = 0.003 and 68 ± 6 to 65 ± 5 mmHg, P  < 0.001, respectively), as did peripheral vascular resistance (1450 ± 581 to 1311 ± 276 dyn/s/cm 5P  = 0.038). There was no significant difference in cardiac output (5.3 ± 1.2 vs 5.5 ± 1.1 l/min P  = 0.146) or stroke volume (64 ± 13 to 66 ± 12 ml, P  = 0.172). CONCLUSION:Significant haemodynamic changes occur in very early pregnancy. Using late first trimester measurements as a baseline for pregnancy induced changes may not be suitable for understanding the full extent of pregnancy induced haemodynamic changes, or provide a reliable substitute for prepregnancy states.

Vitamin D deficiency is common in patients with end stage kidney disease (ESKD) and is a strong predictor of death from cardiovascular disease, infections and cancer. Currently only 68 https://doi.org/10.1186/ISRCTN15087616 ). Recruitment commenced in March 2017.

Background: Recognising the importance of patient-reported outcomes in assessing COPD severity, the GOLD ABE assessment tool highlights the clinical priority of exacerbations and in those with infrequent exacerbations, symptoms. It has the potential to identify high-risk individuals with COPD which may be important for disease progression and to guide treatments. However, the GOLD ABE tool has not been validated in clinical research studies. Aim: To evaluate the utility of GOLD ABE assessment to predict severe exacerbations in a UK COPD cohort. Firstly, to evaluate across A-B-E within the cohort and then compare the tool to other established COPD severity indices (GOLD grade and BODE quartiles). Methods:664 participants from the ERICA (Evaluation of the Role of Inflammation in Chronic Airways Disease) COPD cohort with complete data to enable classification based on GOLD ABE, GOLD grade (2-4) and BODE quartiles were selected. The COPD Assessment Test (CAT) score was used to assess symptoms for A-B and repeat analysis with mMRC was also undertaken. NHS hospital episode statistics (HES) data were prospectively collected for a median 4.75 years of follow-up and hospital admissions for acute exacerbations of COPD (severe exacerbations, H-AECOPD) were extracted from hospital episode primary position ICD-10 codes. Cox proportional hazards regression, logistic regression and ROC analyses were undertaken. Models were performed unadjusted and then adjusted for age and sex (and FEV1 for ABE). Data are presented as median (IQR), average±SD, n (%). Results: Out of 664 participants, GOLD ABE stratification was as follows: A=60 participants (9%), B=277 (42%), E=327 (49%), 324 (49%) were on triple inhaled therapy. A total of 225 participants (34%) in the cohort had H-AECOPD over follow up with median time to first H-AECOPD being 525 (205-1071) days. 46% of group E, 25% in group B and 10% in group A had a H-AECOPD over follow-up. Group B had a higher risk of H-AECOPD and time to first H-AECOPD compared with group A (p<0.01 for both), despite both groups being infrequent exacerbators at baseline. Table 1 shows further data for ABE, GOLD grade and BODE quartiles. Conclusion: ABE was not more strongly associated with H-AECOPD than other COPD severity indices. Its utility from these data, however, seems to be across the A-B-E comparison to identify individuals at higher risk for future H-AECOPD. Table 1

Type 2 diabetes (T2D) significantly increases the risk of heart failure, a major cause of hospitalisation and increased morbidity and mortality. Dual and multi-agonist synthetic peptides at the GLP-1 and glucagon receptor are in clinical development as potential new treatments for a range of chronic metabolic conditions including T2D. Here, we aimed to explore the effects of GLP-1 and glucagon dual receptor agonism on myocardial glucose uptake (MGU) and myocardial function in T2D. Eight adults with a mean age of 52 ± 12 years and body mass index 31 ± 4 kg/m2 attended three randomised infusion visits using combinations of 0.9% saline, glucagon (12.5 ng/kg/min) and exenatide:glucagon co-infusion (exenatide loading dose 50 ng/min for 30 min then 25 ng/min). MGU and myocardial function were assessed using 18F-FDG PET-MRI. MGU increased in n = 7/8 (88%) participants from a median of 9.2 × 10-3 µmol/g/min (IQR 0.33-19 × 10-3 µmol/g/min) with saline, to 20 × 10-3 µmol/g/min (5.4-98 × 10-3 µmol/g/min) with exenatide:glucagon, n = 8, z = 2.24, r = 0.79, P < 0.05. Exenatide:glucagon significantly increased the median left ventricular global peak diastolic circumferential strain rate from 0.619 1/s (0.580-0.716 1/s) to 0.686 1/s (0.644-0.737 1/s) n = 8, z = 2.37, r = 0.84, P < 0.05. Left ventricular global longitudinal contraction (as a measure global longitudinal strain) numerically increased by 0.6%, from - 16.0% with saline (-14.0-[-16.7]%) to -16.6% with exenatide:glucagon (-14.1-[-17.6]%), n = 8, z=-1.54, r=-0.54, P = 0.123. Further studies are required to explore whether GLP-1/glucagon dual receptor agonists have a role to play in reducing cardiovascular risk and attenuating heart failure related outcomes in patients with chronic metabolic conditions such as T2D.