Elevated blood pressure (BP) is the most significant modifiable risk factor for cardiovascular morbidity and mortality. However, the optimal systolic BP target in hypertensive patients remains unclear. We conducted a meta-analysis of randomized controlled trials (RCTs) comparing intensive (≤120 mmHg) versus standard (≤140 mmHg) systolic BP control. A systematic search of three databases identified six RCTs including 39 811 patients (mean age 64.8 years). Intensive BP control significantly reduced the risk of stroke [risk ratio (RR) 0.81; 95% confidence interval (CI) 0.74-0.90], myocardial infarction (RR 0.83; 95% CI 0.73-0.95), cardiovascular death (RR 0.73; 95% CI 0.58-0.91), and all-cause mortality (RR 0.87; 95% CI 0.76-0.99). No significant differences were observed in bradycardia (RR 1.12; 95% CI 0.70-1.77) or symptomatic hypotension (RR 2.25; 95% CI 0.61-8.24), though syncope occurred more frequently with intensive control (RR 1.54; 95% CI 1.23-1.92). Intensive systolic BP control may offer substantial cardiovascular benefits with minimal adverse effects and should be considered in clinical practice.

Target trial emulation (TTE) is a demanding framework for causal inference using observational data, yet its use in hypertension research is limited. This scoping review maps current TTE applications, highlights methodological strengths and gaps, and suggests future directions. Following Joanna Briggs Institute (JBI) and Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines, we screened multiple databases and included 14 of 1352 articles. Common methods for confounding adjustment included inverse probability weighting (50%) and the g-formula (21.5%), often alongside regression models. Time-varying confounders were inconsistently addressed, and loss to follow-up was typically handled via simple censoring. Residual confounding remained a concern; although unobserved confounders were noted, only five studies (36%) used negative controls or e-values. Subgroup analyses were frequent, but causal machine learning for heterogeneous treatment effect (HTE) estimation was not reported. Although still in its early stages, TTE in hypertension research shows promise for addressing key challenges, including HTE, long-term outcomes, and dynamic treatment strategies.

Diabetic lower extremity arterial disease (LEAD) is a manifestation of diabetic lower extremity vascular complications. This study aimed to screen the key single nucleotide polymorphism (SNP) gene signature in patients with type 2 diabetes mellitus (T2DM) and LEAD.

Pregnancy-induced hypertension (PIH) is a significant health concern affecting both maternal and fetal well-being, with limited effective interventions currently available. The objective of this study is to examine the relationship between stable blood pressure and changes in gut microbiota in pregnancy-induced hypertension (PIH) rats following treatment with probiotic-fermented buffalo milk (PBM).

Clevidipine emulsion injection is an ultra-short-acting, intravenous calcium-channel blocker that produces a rapid and transient antihypertensive effect.

Carotid-femoral pulse wave velocity (PWV), a marker of arterial stiffness, is a recognized cardiovascular disease risk factor. As measuring PWV is time-consuming, reliable estimation methods have been developed, but their ability to inform cardiovascular risk prediction beyond what is achievable with current clinical risk tools is uncertain.

Hypertension is closely associated with autonomic dysfunction. The role of the structural integrity of the central autonomic network (CAN) of the brain is insufficiently explored. Large-scale imaging data were used to investigate the relationship between the microstructural properties of the CAN with blood pressure (BP) and hypertension.

Proteinuria is a key marker of renal damage and is often associated with hypertension and increased cardiovascular risk. This study reviews and brings the potential involvement of renal nerves in the pathophysiology of proteinuria and renal impairment in clinical and experimental studies. Studies have highlighted that increased activation of renal sympathetic and sensory nerves activity either alone or in combination with the renin-angiotensin-aldosterone system (RAAS) contributes to the development of proteinuria and the decline in renal function. This phenomenon may occur through mechanisms that alter glomerular and/or tubular function. Additionally, interventions aimed at disrupting renal nerve activity, including pharmacological agents and surgical denervation, or RAAS blockade demonstrated a significant reduction in proteinuria and improved renal and cardiovascular outcomes. Here, we highlight the potential roles of renal nerves beyond their traditional effects on renal function, such as albumin reabsorption, glomerular function, and renal damage, in the onset and maintenance of cardiovascular disease and hypertensive nephropathy.

The magnitude of the association between fibromuscular dysplasia (FMD) and spontaneous cervical artery dissection (sCeAD) remains uncertain, since data available derive from uncompleted vascular screening. This study aims to assess the frequency and types of cervical and extra-cervical arterial lesions, particularly of the FMD type, in patients with sCeAD.

Inter-arm blood pressure differences (IABPDs) can be caused by atherosclerosis. We investigated 29 921 men and women aged 50-64 years from the nationwide population-based Swedish CArdio Pulmonary bioImage Study (SCAPIS) to evaluate if IABPD is related to risk factors for atherosclerosis and can be used as a marker of atherosclerosis as evaluated by coronary artery calcium score, arterial segment involvement score on computed tomography, carotid ultrasound, and ankle-brachial index (ABI). The overall prevalence of systolic IABPD at least 10 mmHg was 2110/29 921 (7.1%). Individuals with IABPD at least 10 mmHg were significantly (P < 0.001) older, more often women, had higher BMI, nonhigh-density lipoprotein cholesterol, triglycerides, SBP and DBPs, and were more likely to have diabetes. In unadjusted analyses, IABPD at least 10 mmHg was associated with presence of coronary atherosclerosis, with more carotid arteries with plaque, and with pathological ABI. These associations were largely attenuated after adjustment for cardiovascular risk factors (age, sex, nonhigh-density lipoprotein cholesterol, systolic BP, smoking, diabetes, and the use of BP lowering drugs). Only ABI retained significance after these adjustments. In conclusion, a systolic IABPD of at least 10 mmHg in middle aged men and women is common in the general population, and can be used as a screening tool for subclinical atherosclerotic changes in coronary, carotid, and lower extremity arteries. However, these relationships were largely explained by correlations between IABPD and traditional cardiovascular risk factors.

Arterial hypertension is a complex disorder influenced by extensive genetic variability, which contributes to interindividual differences in drug response by altering metabolism, transport, and receptor interaction. Current antihypertensive therapies effectively control arterial hypertension in only about half of patients, emphasizing the need for precise strategies. Genetic variation plays a crucial role in modulating drug response, and integrating this knowledge into clinical practice could significantly transform the management of hypertension through personalized medicine. This review examines the impact of genetic factors on the efficacy of antihypertensive drug classes, including angiotensin converting enzyme inhibitors and calcium channel blockers. It also examines advances in pharmacogenomic research that can aid in tailoring drug selection and dose adjustment based on genetic profiles. Beyond genomics, this review also highlights the impact of multiomics approaches, such as proteomics, metabolomics, and microbiomics, in advancing precision medicine and enabling a comprehensive, personalized approach to hypertension management. Pharmacogenomics can help refine hypertension care, improve patient outcomes, and reduce the burden of the disease. The future of hypertension treatment lies in precision medicine, where therapy is tailored to individual needs for effective and personalized management.

Gut microbiota is essential in hypertension pathogenesis, and dietary patterns modulate microbial diversity and metabolic function. Specific associations between dietary index for gut microbiota (DI-GM) and hypertension remains unclear.

Isometric exercise is an accessible, time efficient intervention for reducing blood pressure (BP). However, guideline recommendations for its use remain sparse due to safety concerns. This study aimed to determine the proportion of participants whose BP exceeded predefined limits during isometric exercise. Secondary aims were to examine differences in BP responses between sexes and across exercises.

Renal denervation (RDN) has been approved in Europe and the United States and is recommended by the ESH and ESC hypertension guidelines as a therapeutic option for patients with resistant or uncontrolled hypertension. The aim of this study was to evaluate the long-term outcomes of radiofrequency (RF) RDN in a cohort of patients treated at an ESH center of excellence, with a mean follow-up of 8  years, and to review current evidence on the durability and safety of the procedure.

Upon hypoosmotic stimulation, cardiomyocytes undergo a transient positive inotropic effect (Pie) associated with an increase in the amplitude of intracellular Ca2+ transients. However, the underlying mechanisms remain elusive. The Transient Receptor Vanilloid 4 channel (TRPV4) promotes Ca2+ entry and, thus, could contribute to hypotonic swelling-induced Pie. TRPV4 have not been studied in spontaneously hypertensive rats (SHRs). We aimed to determine if TRPV4 contributes to swelling-induced Pie in Wistar rats and if this response is altered in SHR. Cardiomyocytes were isolated from 8 to 12-month-old Wistar and SHR rats. Contractility was assessed by video-edge-detection in myocytes superfused with isotonic (309 mOsm) or hypotonic solution (217 mOsm). TRPV4 expression was assessed by western blot. The slow force response (SFR) was examined in papillary muscles from SHR stretched from 92 to 98% of their maximal length. While TRPV4 inhibition with GSK2193874 (GSK; 300 nmol/l) or HC067047 (1 μmol/l) did not affect the hypotonic solution induced Pie in Wistar myocytes, it was significantly reduced in SHR. Consistently, TRPV4 expression was enhanced in SHR hearts and myocytes. Disruption of caveolae with 5 mmol/l methyl-β-cyclodextrin and inhibition of microtubule polymerization with 10 μmol/l Colchicine, reduced the GSK-sensible component of the hypotonic solution induced Pie. GSK also blunted the SFR in SHR papillary muscles. We conclude that TRPV4 do not contribute to the hypotonic solution induced Pie in Wistar rats but provide Ca2+ entry that amplifies this response in SHR. Intact caveolae and microtubule integrity are required for TRPV4 activation in SHR myocytes. In SHR hearts, TRPV4 can be activated by cardiac stretch contributing to the SFR.

Diagnostic criteria for an exaggerated BP increase in response to standing (ERTS) are still debated making it difficult to interpret data regarding the cardiovascular risk associated with ERTS. The aim of the present study was to identify the ERTS definition that was most strongly associated with cardiovascular disease.