White-coat Uncontrolled Hypertension (WUH) is characterized by elevated office blood pressure but normal out-of-office levels, and it has shifted from a phenomenological concept to a precision diagnosis model centered on ambulatory and home monitoring. This study provides a comprehensive review of the evolution of definitions, epidemiology, pathophysiology, and risk evidence, and compares the diagnostic value of Office Blood Pressure Monitoring (OBPM), Ambulatory Blood Pressure Monitoring (ABPM), and Home Blood Pressure Monitoring (HBPM). Within this analytical framework, the investigation examines cardiovascular and metabolic risks, interventions in special populations, and ongoing controversies in treatment. These findings are significant for integrating both Chinese and international guidelines with emerging digital monitoring trends. The study further proposes an integrated “home–clinic–cloud platform” model to support individualized hypertension management. This framework offers a more nuanced understanding of evolving paradigms in hypertension diagnosis and treatment. Based on current guideline-supported evidence, we emphasize ABPM/HBPM-based confirmation, risk stratification, and long-term surveillance to avoid misclassification and overtreatment. Emerging directions—including psycho-physiological modeling, multi-scenario monitoring, and digital-twin-enabled simulation—should be regarded as conceptual or research-oriented frameworks that require prospective validation and outcome data before clinical implementation.

ABSTRACT Objective This study aimed to compare the metabolic and inflammatory profiles of dipper and non-dipper hypertensive patients versus healthy controls, specifically evaluating the Triglyceride-glucose (TyG) index's association with nocturnal blood pressure patterns. Methods This retrospective, cross-sectional study included 325 participants (110 normotensive controls, 106 dipper hypertensive, and 109 non-dipper hypertensive). Circadian blood pressure phenotypes were defined using 24-hour ABPM according to the 2024 ESC Hypertension Guidelines. Inflammatory indices (NLR, LMR, and HALP score) and the TyG index were calculated from fasting blood samples. Results Hypertensive groups had higher BMI and waist circumference than controls (p < 0.001). HALP, NLR, and LMR did not differ between the cohorts (p > 0.05). The TyG index showed the greatest intergroup variation and was strongly associated with the non-dipper phenotype (OR = 3.6, p = 0.004). TyG was positively correlated with nocturnal SBP/DBP and negatively correlated with nocturnal SBP decline. It showed significant diagnostic performance for hypertension and non-dipper status (AUC 0.667–0.696, p < 0.001), but limited accuracy for classifying hypertensive subgroups (AUC = 0.573, p = 0.064). Conclusion The TyG index serves as a significant independently associated with the non-dipper hypertension phenotype, reflecting predominant metabolic and cardio-renal stress rather than cellular inflammation. These findings suggest that clinical management should extend beyond blood pressure control to include early optimization of insulin resistance and atherogenic lipid imbalance. Ultimately, the TyG offers a practical and cost-effective clinical tool for multidimensional cardiometabolic and cardio-renal risk assessment.

Hypertension, one of the most prevalent chronic conditions worldwide, stands as a principal risk factor for cardiovascular and cerebrovascular diseases, including coronary heart disease and stroke. Recent advances have clarified a graded, dose–response relationship in which higher blood pressure is consistently associated with increased vascular event risk, with relative risks commonly ranging from modest elevations (~1.2) at the lower end of above-optimal blood pressure to substantially higher levels (>3.0) in more severe hypertension categories. This review synthesizes current evidence on how hypertension influences the incidence and progression of cardiovascular and cerebrovascular diseases, emphasizing its interplay with comorbid conditions such as obesity, metabolic syndrome, pregnancy-induced hypertension, and sleep apnea. Additionally, it explores the impact of blood pressure management targets on the prevention of adverse vascular events and evaluates the safety and efficacy of pharmacological treatments in diverse patient populations. Environmental contributors and their role in modulating disease risk are also addressed. By integrating epidemiological data with clinical research findings, this article aims to provide a comprehensive theoretical framework and practical guidance for the prevention and management of cardiovascular and cerebrovascular complications in hypertensive patients.

Background Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a promising therapy for ischemic cardiomyopathy, which is often secondary to hypertension but remain functionally immature. We investigated whether exosomes from human cardiac fibroblasts (hc-FB-EXOs) promote hiPSC-CMs maturation and improve their reparative efficacy after myocardial infarction (MI). Methods hc-FB-EXOs were isolated from cultured fibroblasts. hiPSC-CMs were treated with hc-FB-EXOs or vehicle and assessed for morphology, sarcomeric organization, metabolism, and electrophysiology. RNA sequencing and Western blotting were used to explore mechanisms. In a mouse MI model, left ventricular function, infarct size, wall thickness, and graft density were evaluated after intramyocardial injection of hiPSC-CMs with or without hc-FB-EXOs. Results hc-FB-EXOs induced adult-like features in hiPSC-CMs, including increased cell size and sarcomere length, fetal-to-adult isoform switching of myosin and troponin, enhanced mitochondrial respiration, and a shift toward fatty acid-based oxidative metabolism. Electrophysiological maturation was evidenced by a higher peak sodium current density, faster upstroke velocity, and more mature action potential and field potential profiles. Transcriptomic and biochemical analyses identified activation of AMP-activated protein kinase (AMPK) signaling, with the modulation of downstream regulators of fatty acid oxidation. In vivo, co-delivery of hc-FB-EXOs with hiPSC-CMs improved the left ventricular ejection fraction, reduced the infarct size, and increased the graft density compared with those of hiPSC-CMs alone. Conclusion hc-FB-EXOs promote the maturation of hiPSC-CMs via AMPK-mediated metabolic reprogramming and enhance their therapeutic benefit after MI. Cardiac fibroblast-derived exosomes may serve as a practical adjunct to optimize hiPSC-CMs-based therapy for ischemic cardiomyopathy.

Background Atherosclerosis (AS) is a complex cardiovascular disorder driven by endothelial cell dysfunction and immune microenvironment dysregulation. We identified novel endothelial-related diagnostic biomarkers through multi-omics integration and machine learning approaches. Methods Single‑cell atlas of AS was constructed from scRNA-seq data using the Seurat. Endothelial cell‑specific co‑expression modules and hub genes were identified via high-dimensional WGCNA (hdWGCNA), and key endothelial‑associated differentially expressed genes (DEGs) were obtained by integrating these modules with differential expression analysis. Diagnostic genes were screened using LASSO regression and SVM-RFE using glmnet and caret packages, respectively. Their correlations with immune cell infiltration were assessed by single-sample GSEA (ssGSEA) and the CIBERSORT algorithm. Finally, the binding capacity of the encoded proteins to potential therapeutic agents was evaluated through drug-target prediction using the Enrichr platform and the DSigDB database, followed by molecular docking simulations. Results A total of 66 endothelial cell-associated DEGs were identified, from which four core feature genes (ANXA2, DBN1, ZNF385D, and IL6ST) were screened using machine learning approaches. Immune infiltration analysis revealed a global increase in immune cell infiltration (e.g., activated B cells, T cells, and macrophages) in atherosclerotic lesions, with the four genes showing significant correlations with specific immune subsets, while single-cell data further confirmed T cells, macrophages, and B cells as the predominant cellular components in the plaque microenvironment. Molecular docking results demonstrated strong binding capabilities of ANXA2 with thalidomide and IL6ST with resveratrol, with binding energies of −6.7 kcal/mol and −7.4 kcal/mol, respectively. Conclusion Our findings provided new insights for the targeted AS therapy.

Background Abnormal circadian blood pressure variation, particularly a non-dipper pattern, is associated with increased cardiovascular risk. Naples Prognostic Score (NPS) is a laboratory-based score that reflects the immune-inflammatory and nutritional status. Nevertheless, data regarding the relationship between NPS, circadian blood pressure patterns, and arterial stiffness in patients with newly diagnosed hypertension are limited. This study aimed to evaluate the relationship between blood pressure dipping status, the NPS, and arterial stiffness assessed by pulse wave velocity (PWV). Methods This retrospective study included 297 newly diagnosed, untreated hypertensive patients who underwent 24-hour ambulatory blood pressure monitoring. Patients were classified as dipper (n = 145) or non-dipper (n = 152) according to nocturnal blood pressure decline. Laboratory parameters were recorded, NPS was calculated, and PWV was measured using a validated oscillometric device. Multivariate logistic regression analysis was performed to identify factors independently associated with non-dipper hypertension. Results Non-dipper patients had significantly higher median NPS values compared with dippers [2 (0–4) vs. 1 (0–4), p < 0.001] and a higher prevalence of high NPS (score 3–4: 42.8% vs. 13.8%, p < 0.001). Median PWV was also significantly higher in the non-dipper group [7.70m/s (4.70–12.90) vs. 7.00m/s (4.40–11.20), p = 0.005]. After adjustment for clinically relevant covariates, both NPS (OR 1.71, 95% CI 1.19–2.47; p = 0.004) and PWV (OR 1.37, 95% CI 1.12–1.68; p = 0.002) were independently associated with non-dipper hypertension. Conclusion In patients with newly diagnosed hypertension, a non-dipper blood pressure pattern is independently associated with higher systemic inflammatory burden and increased arterial stiffness. The NPS may serve as a simple and clinically applicable marker for early cardiovascular risk stratification in this population.

Background The carotid body (CB) is a key regulator of sympathetic tone, and its overactivity is implicated in the pathogenesis of neurogenic hypertension. While structural enlargement of the CB may reflect chronic autonomic dysregulation, its association with early markers of hypertension-mediated organ damage (HMOD) remains insufficiently characterized. Objective This exploratory study investigated whether carotid body size is associated with subclinical cardiac remodeling and peripheral vascular resistance in hypertensive patients. Methods We analyzed 49 patients with hypertension who underwent carotid computed tomography angiography (CTA) and comprehensive cardiovascular phenotyping. CB diameter was measured via CTA, and patients were categorized into Group 1 (CB < 2.5 mm, n = 22) and Group 2 (CB ≥ 2.5 mm, n = 27). Cardiac mechanics were assessed using two-dimensional speckle-tracking echocardiography (2DSTE), and hemodynamic parameters were evaluated via oscillometric pulse wave analysis. Results Despite similar peripheral systolic and central blood pressure levels, Group 2 demonstrated significantly impaired left atrial (LA) mechanics and higher vascular resistance. Specifically, Group 2 had lower LA global peak atrial longitudinal strain (PALS) (23.88 ± 7.70% vs. 30.84 ± 11.40%, p = 0.014) and higher total vascular resistance (TVR) (1.56 ± 0.49 vs. 1.22 ± 0.18 s⋅mmHg/mL, p < 0.001) compared to Group 1. Augmentation index normalized to 75 bpm (AIx@75) was also elevated in the CB enlargement group (31.11 ± 7.91% vs. 24.36 ± 11.77%, p = 0.021). In multivariate linear regression analysis, LA diameter, TVR, and urinary microalbumin-to-creatinine ratio were independent determinants of CB size (Adjusted R2 = 0.429, p = 0.022). Conclusion Carotid body enlargement is associated with impaired left atrial strain parameters and increased peripheral vascular load in patients with hypertension. These findings suggest that CB morphology may serve as a potential marker for early subclinical cardiovascular and renal alterations, reflecting a distinct neurovascular phenotype in hypertension.

Background Malignant hypertension (mHTN) is a severe hypertensive emergency, often associated with renal deterioration. Kidney length may be of useful to identify patients with renal dysfunction. Whether kidney length in mHTN patients is associated with renal prognosis is unclear. Methods The study enrolled 280 mHTN patients with renal thrombotic microangiopathy (TMA) who underwent renal biopsy between 2008 and 2023. Linear regression was used to explore patient characteristics of kidney length. The association between kidney length and ≥15% increase in estimated glomerular filtration rate (eGFR), and end-stage renal disease (ESRD) was analyzed using Cox regression and logistic regression, respectively. Kidney length was analyzed in tertiles, using the first tertile as reference. Results Patients with larger kidney length had higher levels of body mass index (BMI) and eGFR, but lower levels of urea nitrogen, serum creatinine, uric acid, global sclerosis ratio, and tubular atrophy/interstitial fibrosis ratio. Kidney length was strongly positively correlated with BMI, and negatively related to tubular atrophy/interstitial fibrosis ratio. During the follow-up, 72 patients experienced a ≥15% increase in eGFR and 172 patients progressed to ESRD. Patients in the third tertile of kidney length had a better renal recovery outcome of ≥15% increase in eGFR and lower odds of ESRD. Conclusions In mHTN patients with renal TMA, large kidney length is associated with better renal function improvement of ≥15% increase in eGFR, and lower risk of ESRD. In clinical practice, the measurement of kidney length may serve as a non-invasive indicator to assess renal prognosis and inform timely treatment interventions in mHTN patients.

ABSTRACT Background Renal denervation (RDN) has emerged as a potential therapeutic option for resistant hypertension (HT), which remains a major clinical challenge due to poor blood pressure (BP) control despite optimized pharmacotherapy. This study aimed to assess the safety and effectiveness of catheter-based RDN in resistant hypertension patients, based on our center’s experience. Methods This retrospective, single-center study included 120 patients with resistant HT who were eligible for RDN and underwent the procedure using the Symplicity Spyral system between January 2023 and December 2024. Office systolic and diastolic BP were assessed at baseline and 6 months after RDN. The primary endpoint was the reduction in BP, while secondary endpoints included changes in the number of antihypertensive medications. Results At 6 months, office systolic BP decreased significantly from 156 ± 7.7 mmHg to 143 ± 3.7 mmHg, while diastolic BP declined from 93.5 ± 5.5 mmHg to 90 ± 3.9 mmHg (both p < 0.001). Median per-patient reductions were 13 mmHg systolic and 3.5 mmHg diastolic. The mean number of antihypertensive medications decreased from 4.88 ± 0.9 to 4.47 ± 1.1 (p < 0.001). Minor adverse events included acute kidney injury in two patients (1.7%) and femoral artery injury in one patient (0.8%). Conclusion Catheter-based RDN using the Symplicity Spyral system was safe and effective in reducing BP and medication burden in patients with resistant HT. These results support RDN as a potential therapeutic option in appropriately selected patients.

Background Circulating microRNA-210-3p (miR-210-3p) is a hypoxia-related regulator implicated in placental maladaptation. Its longitudinal behavior across hypertensive disorders of pregnancy (HDP), and whether low-dose aspirin modifies its trajectory, remain insufficiently understood. Methods This prospective case-control study was conducted between October 2021 and November 2024. Circulating miR-210-3p was measured in the first trimester and at delivery. Aspirin use followed routine clinical practice for preeclampsia prevention. Longitudinal trajectories were examined using generalized estimating equations (GEE) as the primary analytic approach and linear mixed effects models (LMM) as a secondary method. Results Ninety-four women were enrolled, including 73 controls, 11 with gestational hypertension, and 10 with preeclampsia. miR-210-3p increased significantly from the first trimester to delivery in gestational hypertension (p = 0.003) and preeclampsia (p = 0.006), with no significant change in controls. In the first trimester, gestational hypertension exceeded controls (p = 0.006), and preeclampsia exceeded both groups (both p < 0.001). At delivery, gestational hypertension and preeclampsia remained higher than controls (both p < 0.001), and preeclampsia exceeded gestational hypertension (p = 0.036). GEE demonstrated a significantly slower rise in miR-210-3p among aspirin users with gestational hypertension (p = 0.042), and this association strengthened in sensitivity analysis (p = 0.001). LMM showed a similar, non-significant trend. Conclusion miR-210-3p exhibited disorder-specific longitudinal patterns across HDP. Aspirin-associated changes were observed in gestational hypertension but not in preeclampsia, suggesting differences in molecular expression trajectories between the two conditions over the course of gestation, while the underlying biological mechanisms remain to be clarified.