
GRAPHICAL ABSTRACT:https://links.lww.com/HJH/D83.
Hypertensive disorders of pregnancy (HDP) remain a leading cause of maternal and perinatal morbidity and mortality worldwide, especially in low- and middle-income countries. Moreover, HDP are directly linked to an increased risk of long-term cardiometabolic and kidney disease in mothers and offspring. Since prevention, diagnosis, and treatment of HDP remain suboptimal globally, enhanced understanding and implementation of current guidelines on HDP present a substantial opportunity to significantly reduce maternal and fetal morbidity and mortality. This position paper by the International Society of Hypertension reviews current knowledge in the field, identifies knowledge gaps and provides recommendations on the care of women with HDP and lifelong care, thereafter.
OBJECTIVE:Foam rolling reduces vascular resistance and enhances peripheral blood flow; however, its ability to attenuate pressure wave reflection remains purely hypothetical. Given the positive correlation between skeletal muscle mass and flow-mediated vasodilation, the present study investigated the acute effects of foam rolling on pressure wave reflection and explored whether skeletal muscle index moderates this response. METHODS:Twenty-six men and women (age, 22-62 years) completed 20 min of foam rolling and sham control on separate days in a randomized controlled crossover design. Skeletal muscle index was calculated as skeletal muscle mass/height2 (bioelectrical impedance analysis), and the BMI as body weight/height2. Carotid pressure waveforms were recorded to derive time to reflection, reflection magnitude, and aortic augmentation index at baseline, and at 10 and 30 min postintervention. RESULTS:Foam rolling elicited reductions in aortic augmentation index at 10 min (P < 0.001) and 30 min (P = 0.021) postintervention. Reflection magnitude decreased 10 min after foam rolling (P < 0.001), whereas the time to reflection remained unchanged. Skeletal muscle index correlated negatively with reductions in augmentation index (r = -0.45, P = 0.021) and reflection magnitude (r = -0.41, P = 0.049) at 10 min, even after adjusting for age, sex, and BMI (both P < 0.05). CONCLUSION:Foam rolling acutely attenuated aortic pressure augmentation by reducing the magnitude rather than the timing of peripheral wave reflections. Moreover, individuals with greater muscle mass may derive more substantial cardiovascular benefits from foam rolling.
AIMS:Marinobufagenin (MBG), the endogenous cardiotonic inhibitor of the transmembrane adenosine triphosphatase sodium-potassium pump, is a steroid hormone with divergent effects on blood pressure and cardiovascular (CV) system. In response to sodium load, MBG stimulates natriuresis to compensate for body fluid overload but, in condition of sustained high sodium intake, its excessive production promotes a maladaptive pro-hypertensive effect. Since the role of MBG on the cardiac alterations frequently affecting hypertensive patients has been poorly investigated, we focused on gaining insight into this relationship in essential hypertension. METHODS:We studied the relationships between MBG, LV mass and geometry and investigated whether diuretic therapy modifies these associations in 180 incident-prevalent patients with essential hypertension. RESULTS:Serum MBG levels were significantly lower in hypertensive patients than in normotensive individuals (P = 0.005) and strongly associated with the mass and muscle component of the left ventricle. On multivariable linear regression models, left ventricular mass index and the cardiac measurements posterior wall thickness, interventricular septal thickness, mean wall thickness, relative wall thickness increased in parallel with the decrease in serum MBG levels (P ≤ 0.01). Coherently, in a multivariable logistic model, the odds of having cardiac remodeling/hypertrophy increased by 9% for each 0.1 nmol/l MBG reduction (odds ratio: 1.09, 95% confidence interval: 1.01-1.18, P = 0.03). Furthermore, diuretic therapy modified the link between MBG and cardiac biomarkers by acting as an amplifier of the harmful effect of low MBG levels on these measures. CONCLUSIONS:In patients with essential hypertension, lower circulating levels of MBG are associated with alterations in myocardial morphology whose severity is modified by the diuretic therapy that amplifies the noxious effect of low MBG levels. GRAPHICAL ABSTRACT:https://links.lww.com/HJH/D96.
BACKGROUND:Visit-to-visit variability (VVV) of blood pressure (BP) has been linked to adverse cardiovascular and kidney outcomes in various populations, but results in those with chronic kidney disease (CKD) have been inconsistent. METHODS:We evaluated VVV in Chronic Renal Insufficiency Cohort (CRIC) participants, using the coefficient of variation (CoV = standard deviation of SBP/mean SBP) calculated from BP measurements obtained at baseline visit through year 5 of the study. Cox proportional hazards models were used to assess the association of CoV with a composite cardiovascular outcome (myocardial infarction, stroke, peripheral artery disease, heart failure) and a composite kidney outcome (50% reduction in estimated glomerular filtration rate or end-stage kidney disease). RESULTS:Among 3891 participants (44% women, mean age 63 ± 10 years, mean CoV 10.3 ± 5.2%), 757 cardiovascular and 920 kidney events occurred during a median follow-up of 5.4 and 4.5 years, respectively. In unadjusted analyses, the upper tertile of CoV was associated with increased risk of both cardiovascular [hazard ratio 2.04, 95% confidence interval (CI) 1.70-2.43] and kidney outcomes (hazard ratio 1.62, 95% CI 1.38-1.89) compared to the lowest tertile. However, after adjustment for clinical and sociodemographic factors, higher CoV was significantly associated with cardiovascular outcomes (adjusted hazard ratio 1.25, 95% CI 1.04-1.52) but not kidney outcomes (adjusted hazard ratio 0.95, 95% CI 0.80-1.15). CONCLUSION:In this large CKD cohort, higher visit-to-visit BP variability was independently linked to adverse cardiovascular, but not kidney, outcomes.
OBJECTIVES:Activation of the intrarenal renin-angiotensin system (RAS) has been implicated in chronic kidney disease (CKD) pathophysiology. Although urinary angiotensinogen (AGT) is a noninvasive surrogate marker of intrarenal RAS activity, whether urinary AGT is associated with incident CKD remains unclear. We investigated the association between urinary AGT and incident CKD in community-dwelling adults without CKD. METHODS:We conducted a prospective cohort study of community-dwelling adults without CKD. Urinary AGT, urinary N-acetyl-β-d-glucosaminidase (NAG), urinary β2-microglobulin (β2-MG), urinary albumin-to-creatinine ratio (ACR), and estimated glomerular filtration rate (eGFR) were assessed at baseline. Incident CKD was defined according to established criteria based on eGFR and urinary ACR during follow-up. Associations between urinary AGT levels and incident CKD were examined using multivariable-adjusted Cox proportional hazards models. RESULTS:Among 197 participants without CKD at baseline, 22% developed incident CKD during a median follow-up of 4.9 years. Weak to moderate correlations were observed between urinary AGT levels and kidney-related markers at baseline, including an inverse correlation with eGFR (ρ = -0.21) and positive correlations with urinary ACR (ρ = 0.44), urinary NAG (ρ = 0.35), and urinary β2-MG (ρ = 0.56). Higher baseline urinary AGT levels were significantly associated with an increased risk of incident CKD [adjusted hazard ratio per 1-SD increase, 1.48; 95% confidence interval (CI), 1.02-2.16] after multivariable adjustment. CONCLUSION:Higher urinary AGT levels were associated with incident CKD in individuals with preserved kidney function, suggesting that urinary AGT may serve as a marker of early CKD risk.
OBJECTIVE:In previous studies involving older hypertensive adults, geriatric conditions with potential prognostic impact and outcomes of geriatric relevance (e.g., disability) remained largely unexplored. This study investigated predictors of all-cause mortality and incident disability in a real-world sample of older hypertensive outpatients undergoing comprehensive geriatric assessment. METHODS:We analyzed data from the longitudinal HYPER-FRAIL pilot study, involving hypertensive outpatients ≥75 years undergoing comprehensive geriatric assessment, office, ambulatory and home blood pressure (BP) measurements. Predictors of long-term all-cause mortality and incident disability in basic activities of daily living (BADL) were assessed using multivariate Cox and logistic regression analyses, respectively. RESULTS:Among 112 participants (mean age 81.2 years, 58% women, median follow-up 55 months), mortality was 25.9%. Baseline BADL disability, impaired physical performance and frailty independently predicted mortality. Stratified analyses showed that higher BP was associated with increased mortality risk only in patients with preserved autonomy in instrumental activities of daily living (IADL). Among those with IADL disability, office diastolic BP <80 mmHg and ambulatory 24 h systolic BP <130 mmHg were associated with increased mortality. Among 78 participants with baseline BADL autonomy, disability incidence was 39.7%. Predictors included baseline IADL and physical impairment, cognitive decline and ambulatory daytime hypotension. The association with hypotension was independent of falls or syncope, but not of dementia. CONCLUSIONS:Disability, impaired physical performance and frailty predicted all-cause mortality in older hypertensive outpatients. The association between BP and mortality varied by functional status, suggesting a modifying - possibly reversing - effect. Ambulatory hypotension was associated with incident disability. GRAPHICAL ABSTRACT:https://links.lww.com/HJH/D93.
In 2024, the European Society of Cardiology (ESC) hypertension guidelines introduced an "elevated blood pressure" category (120-139 and/or 70-89 mmHg), lowering the diastolic threshold from 85 to 70 mmHg. Its relevance for cardiovascular risk stratification in low-risk primary prevention remains uncertain. We conducted a cross-sectional study of 1394 adults undergoing standardized preventive health assessment in France, with office blood pressure (BP) measured using a validated oscillometric device. Participants were classified by ESC/ESH 2018 and ESC 2024 definitions. We quantified category shifts and compared the clinical, lifestyle and biological profile of individuals reclassified from 2018 optimal to 2024 elevated on the basis of diastolic BP ≥70 mmHg (systolic BP < 120 mmHg) vs. those remaining nonelevated. SCORE2, available in 61% of participants, was used as a supporting risk estimate. ESC 2024 classified 10.0% as nonelevated, 64.2% as elevated and 25.8% as hypertensive; 70% of previously "optimal" individuals became "elevated." Compared with nonelevated peers, the diastolic-only reclassified group differed only in age (45.5 vs. 42.7 years; P = 0.007), with no difference in sex, body mass index, lifestyle, cardiovascular history or biomarkers. Their slightly higher SCORE2 was attributable to higher systolic BP and age, and was no longer significant after adjustment for systolic BP. By contrast, individuals reclassified from normal to elevated had a less favorable cardiometabolic profile. Lowering the diastolic threshold to 70 mmHg produced substantial reclassification but did not identify an independent higher-risk phenotype when systolic BP remained < 120 mmHg, questioning the relevance of such a low diastolic threshold for elevated BP in the new ESC 2024 classification. Prospective outcome studies are needed.
BACKGROUND:The aim of this study was to characterize hypertension-associated cardiac damage in the blood pressure (BP) phenotypes sustained normotension (SNT), white coat hypertension (WCHT), masked hypertension (MHT) and sustained hypertension (SHT). METHODS:In a population-based study, 4115 individuals were examined with office and home BP measurement, computed tomography, coronary computed tomography angiography and echocardiography. The odds ratios of hypertension-associated cardiac damage in the BP phenotypes were analysed with SNT and SHT as references, respectively, for coronary artery calcium score (CACS) at least 100 and at least 300, Segment Involvement Score (SIS) at least 4, any significant (>50%) coronary stenosis, left ventricular ejection fraction (LVEF) less than 50%, E/e΄ ratio (E/e΄) at least 14, and global longitudinal strain (GLS) greater than -17 (men) or greater than -18 (women). RESULTS:The odds of having hypertension-associated cardiac damage were significantly higher for WCHT than for SNT [LVEF < 50%: OR 1.83 (1.17-2.86), CACS ≥ 100: OR 1.58 (1.19-2.11)], and for SHT than for SNT [LVEF < 50%: OR 2.34 (1.53-3.57), CACS ≥ 100: OR 1.52 (1.14-2.02)]. The odds of having hypertension-associated cardiac damage were also significantly higher for MHT than for SNT (LVEF < 50%: OR 2.68 (1.41-5.10), CACS ≥ 100: OR 2.15 (1.37-3.38) and CACS ≥ 300: OR 2.34 (2.21-4.52)]. CONCLUSION:The prevalence of hypertension-associated cardiac damage was higher in WCHT and in MHT compared to SNT. WCHT and MHT should therefore be considered when assessing cardiovascular risk, and BP should be measured both in the office and at home when diagnosing and monitoring hypertension.
AIM:An updated meta-analysis targeting the prevalence of left ventricular hypertrophy (LVH), a cardinal marker of hypertensive heart disease (HHD), over the last 15 years is lacking. Thus, we analyzed the literature in order to provide a comprehensive information on LVH prevalence, as assessed by echocardiography, in the hypertensive setting. METHODS:The PubMed, OVID-MEDLINE, and Cochrane Library databases were analyzed to search English-language articles published from 1 January 2011 up to 31 December 2025. Studies were identified by using MeSH terms and crossing the following search items: 'left ventricular hypertrophy', 'left ventricular mass', 'hypertensive heart disease', 'echocardiography', 'hypertension', and 'subclinical cardiac damage'. RESULTS:A total of 51 studies including 74 632 hypertensive patients were considered. Overall, the prevalence of LVH in the pooled cohort, defined according to criteria recommended by echocardiographic guidelines, was 36.6% (95% CI: 33.4-40%). Data provided by 18 studies ( n = 40 108 patients) showed that the probability of having LVH was lower in men than in women (OR = 0.62, CI: 0.48-0.80, P < 0.0001). Among patients with LVH (17 studies), the risk of concentric LVH was almost twice as high as eccentric (OR = 1.94, CI: 1.52-2.49, P < 0.0001). CONCLUSION:Our meta-analysis suggests that the high contemporary prevalence of LVH reflects the failure of therapeutic strategies worldwide in the prevention and treatment of HHD. From a clinical perspective, these data imply the need for a more aggressive treatment of hypertension and related cardiovascular risk factors leading to LVH, especially in women.
Hypertension in sub-Saharan Africa is escalating, with many cases undiagnosed and poorly controlled, even among children, despite its significant contribution to cardiovascular disease. Poor blood pressure control is largely due to limited national guidelines, underfunded programs, and a shortage of trained health professionals. Simplified protocols for non-physician health workers, who deliver most of the primary care, are essential. Cultural myths and misconceptions further delay care, underscoring the need for community-based education. Early and opportunistic screening, including in schools, markets, and places of worship, is vital across the life course. Sustainable progress depends on tailored strategies, investment in equipment and training, and leveraging existing infrastructure to improve hypertension detection and management. Africa-centred hypertension guidelines are now a priority because international models fail to address the continent's unique clinical, cultural and resource realities. The African Regional Advisory Group of the International Society of Hypertension worked with the Pan African Society of Cardiology to develop simplified protocols for primary care, particularly for non-physician health care workers, by considering the special situation and condition for managing the vast majority of cases within hypertension in Africa.
This study aimed to quantify the effects of exercise on aerobic capacity in people with prehypertension or hypertension and to identify exercise prescription parameters that optimize improvements. A comprehensive search was conducted in PubMed, Web of Science, Embase, Cochrane Library, and Scopus from inception to 24 October 2025. Data were pooled using standardized mean differences (SMDs) with 95% confidence intervals (CI). Fifteen studies met the inclusion criteria. Exercise significantly improved aerobic capacity in people with prehypertension or hypertension (SMD = 0.88; 95% CI: 0.61-1.15; P < 0.00001), with multicomponent training demonstrating superior efficacy. Exploratory subgroup analyses suggest that longer programs (≥12 weeks), lower frequency (<3 sessions/week), 60-min sessions or longer, total weekly exercise less than 180 min, and professional supervision may be associated with better outcomes.
BACKGROUND:Mutations in the breast cancer susceptibility gene 2 ( BRCA2 ) are well known to increase the risk of breast and ovarian cancers. Emerging evidence indicates that BRCA2 mutation carriers exhibit increased vascular disorder and may develop endothelial dysfunction, a key mechanism underlying hypertension. Angiotensin II (Ang II), a central effector of the renin-angiotensin system, is a key regulator of blood pressure and a major driver of hypertension, promoting endothelial injury through oxidative stress, inflammation, and impaired nitric oxide (NO) bioavailability. However, the role of endothelial BRCA2 in Ang II-induced endothelial dysfunction remains unknown. METHODS:BRCA2 was silenced in cultured endothelial cells and following Ang II treatment, ROS generation, DNA damage, apoptosis, inflammation, NO production, migration, angiogenic capacity, Ang II receptors and related signaling pathways were assessed. RESULTS:BRCA2 deficiency exacerbated Ang II-induced increases in ROS, DNA damage, and apoptosis, along with impaired functional capacity, including reduced migration and angiogenesis. NO production was suppressed, accompanied by increased micronuclei formation and enhanced c-Jun N-terminal kinase (JNK) activation. In addition, both BRCA2 loss and Ang II treatment upregulated the Ang II receptor AT1R. Pharmacological inhibition of AT1R attenuated Ang II-induced increases in DNA damage and apoptosis in BRCA2 -deficient endothelial cells. CONCLUSION:These findings provide the first pharmacogenomic evidence that BRCA2 deficiency sensitizes endothelial cells to Ang II-induced dysfunction, suggesting that BRCA2 mutation carriers may be at increased risk for hypertension-associated cardiovascular complications.
Aldosterone synthase inhibitors (ASIs) demonstrated significant blood pressure (BP) lowering efficacy in patients with uncontrolled hypertension, but evidence in chronic kidney disease (CKD) remains limited. This meta-analysis explores the effects of selective ASIs on BP levels in CKD. Secondary outcomes were albuminuria (UACR), eGFR change and hyperkalemia incidence. Five RCTs (1,148 patients) were included; 2 used baxdrostat, 2 lorundrostat, and 1 study used vicadrostat. Treatment with ASIs was associated with a significant placebo-adjusted reduction in SBP of-7.9 mmHg [95% confidence interval (CI) -10.0 to -5.9, I2 = 0%] and DBP of -3.1 mmHg (95% CI -5.9 to -0.2, I2 = 62%) and reduced UACR by -31.7% (95% CI -54.5 to -8.9, I2 = 91%). The pooled placebo-adjusted eGFR change was -2.05 ml/min/1.73 m 2 (95% CI -3.15 to -0.95, I2 = 0%). The risk of hyperkalemia was higher with ASIs, but with high heterogeneity (risk ratio, 4.04 [95% CI 0.94 to 17.35], I2 = 76%). In conclusion, selective ASIs present a potential treatment option for BP control and albuminuria reduction in patients with CKD.
Many primary aldosteronism (PA) patients harbor concomitant mild autonomous cortisol secretion (MACS), termed "Connshing syndrome." The prevalence and cardiometabolic impact of this co-secretion have not been quantitatively synthesized. To determine the pooled prevalence of MACS in PA and evaluate its association with cardiovascular (CV) events, type 2 diabetes mellitus (T2DM), and obesity. PubMed, Embase, Cochrane, Web of Science, and Scopus through January 2026. Following PRISMA 2020 and MOOSE guidelines (PROSPERO: CRD420261334965), studies reporting MACS prevalence [post-1 mg dexamethasone suppression test (DST) cortisol ≥1.8 μg/dl] in PA were included. Prevalence was pooled using random-effects models. Odds ratios (ORs) were calculated for cardiometabolic outcomes. Certainty was evaluated using GRADE. Fourteen studies (2356 patients) were included. Pooled MACS prevalence was 26.2% [95% confidence interval (CI): 24.1-28.4; I2 = 24.2%; prediction interval: 21.6-31.4%], consistent across European (27.0%) and East Asian (25.2%) cohorts ( P = 0.62). MACS + PA patients had higher odds of CV events (OR 1.60; 95% CI: 1.07-2.38; P = 0.021) and T2DM (OR 1.37; 95% CI: 1.00-1.86; P = 0.048), but not obesity (OR 1.10; P = 0.411). Sensitivity analyses confirmed robustness. GRADE certainty was moderate for prevalence and low for CV events. Approximately one in four PA patients has MACS, associated with a 60% higher CV event risk. These findings support routine DST screening in PA and have implications for perioperative management and cardiometabolic risk stratification.
BACKGROUND:The cardiovascular health (CVH) metrics have been reported to play an important role in the development of noncommunicable chronic diseases, yet its link to pulmonary hypertension (PH) risk and the underlying biological mechanisms remain unclear. This study aimed to investigate the association of CVH with PH risk and elucidate the mediating role of plasma proteomic signatures. METHODS:A total of 279 220 participants without PH at enrollment of the UK Biobank were included. Cox regression was used to quantify the association between CVH and incident PH. Proteome-wide association analysis, mediation analysis, and functional enrichment analysis were conducted to identify protein mediators. Key hub proteins were further validated at the transcriptional level through quantitative polymerase chain reaction (qPCR) in an animal model of PH, as well as at the protein level, and by macrophage-specific knockdown of interleukin (IL)-6 and CCL4 to evaluate its impact on rat pulmonary artery smooth muscle cell (PASMC) migration and proliferation. RESULTS:Over a median 13.2-year follow-up, 1325 PH cases occurred. Compared to the lowest CVH, participants with moderate and high CVH had 59% [hazard ratio (HR): 0.41; 95% confidence interval (CI): 0.33-0.49] and 82% (HR: 0.18; 95% CI: 0.14-0.23) lower risk, respectively. Proteomic analyses revealed that this association was significantly mediated by a distinct plasma protein signature. Pathway enrichment analysis indicates that proteins are significantly enriched in inflammatory/immune pathways, and key hub proteins were identified as participating in the central mechanism pathway. In the lung tissue of PH rat models, the mRNA and protein expression levels of IL-6 and C-C motif chemokine ligand 4 (CCL4) were significantly elevated. Furthermore, functional assays demonstrated that knockdown of IL-6 or CCL4 in macrophages significantly attenuated the migration and proliferation of rat PASMCs in vitro. CONCLUSION:High CVH level, defined by Life's Essential 8 (LE8), is significantly linked to a reduced risk of developing PH. This protective effect is primarily mediated by a proteomic signature, revealing the role of signaling pathways such as cytokine-cytokine receptor interaction in the prevention of PH.
The 2025 AHA/ACC blood pressure (BP) management guidelines recommend BP treatment for 10-year cardiovascular disease (CVD) ≥7.5% from the PREVENT equation, replacing the prior pooled cohort equations (PCE). We examined associations between risk in PCE and PREVENT and a composite of CVD or cardiovascular death in SPRINT. Among 1794 participants, 477 (26.6%) were at low risk in both, 119 (6.6%) were high-risk in PREVENT only, 89 (5.0%) were high-risk in PCE only, and 1109 (61.8%) were high-risk in both. Those at high risk in both equations receiving intensive treatment had a lower risk of the primary outcome [hazard ratio (HR): 0.46, 95% confidence interval (CI): 0.24, 0.89]. Intensive treatment did not affect the risk of any outcomes for those at high-risk in PREVENT only or PCE only due to low event rates. These findings confirm the neutrality of the change from PCE to PREVENT for BP treatment recommendations.