Background: To investigate the relationships of plasma renin, angiotensin, and aldosterone levels to blood pressure variability and target organ damage in children with essential hypertension. Methods: A case-control study was conducted on 132 children diagnosed with essential hypertension (103 males and 29 females with the mean age of 11.8 ± 2.4 years). The plasma RAAS levels were measured using the enhanced chemiluminescence method, the ambulatory blood pressure was monitored for 24 h, and then the average real variability (ARV) was calculated. Data on indicators were used for assessing cardiac and renal damages. The correlations of plasma renin, angiotensin, and aldosterone (RAAS) levels to blood pressure variability (BPV) and target organ damage (TOD) were studied. A comparison between the groups was conducted using SPSS 20. Results: Among the 132 children, 55 cases had target organ damage. The 24-h ARV and the daytime ARV of the systolic blood pressure of the high angiotensin II (AT II) group was significantly higher than that of the normal AT II group (t = 2.175, P = 0.031; t = 2.672, P = 0.009). Plasma AT II and aldosterone levels were significantly associated with the left ventricular mass index (r = 0.329, P = 0.0001; r = 0.175, P = 0.045). Linear regression analysis showed that AT II [β ± s.e. = 0.025 ± 0.006, 95% CI (0.013–0.038), P = 0.0001] and aldosterone [β ± s.e. = 0.021 ± 0.007, 95% CI (0.008–0.034), P = 0.002] were risk factors for LVH. Conclusions: The AT II level in children with essential hypertension affected the variability of the 24-h and the daytime SBP. Plasma AT II and aldosterone levels were associated with cardiac damage. Results from this study indicated that AT II and aldosterone are risk factors for LVH in childhood hypertension and are of great significance for improving the clinical prognosis of pediatric patients with hypertension.

Objective: To explore the association of dipping pattern and blood pressure load with left ventricular hypertrophy (LVH) in pediatric essential hypertension.Materials and Methods: Through an echocardiography monitor and an ambulatory blood pressure monitor of 425 children and adolescents diagnosed with essential hypertension with no treatment received, we identified 140 cases of LVH. Grouping patients according to LVH (LVH, N = 140; n-LVH, N = 285), we further evaluated their ambulatory blood pressure monitoring (ABPM) parameters by comparing dipping patterns between groups. A multivariable logistic regression analysis was used to determine the effect of blood pressure load on LVH.Results: No significant difference was found in systolic or diastolic blood pressure dipping patterns between groups (P = 0.161, P = 0.139). However, compared to the n-LVH group, the LVH group presented significant elevated nighttime systolic blood pressure (SBP) (P < 0.05), while nighttime DBP remained stable (P = 0.391), resulting in higher daytime and nighttime SBP loads, higher nighttime DBP load, and higher 24-h SBP load (P < 0.05). Notably, our multivariable logistic regression has shown that this trend of 24-h SBP load acts independently as a critical risk factor for LVH.Conclusion: Collectively, we observed a correlation between BP load and LVH in pediatric hypertension. Our data demonstrated that SBP load has a more significant weight in LVH progression, and 24-h SBP load, in particular, acts as a critical early prognostic parameter for LVH in pediatric hypertension.

The mechanism of hypertension in children remains elusive. The objective of this study was to analyze plasma metabolomics characteristics to explore the potential mechanism of hypertension in children. Serum samples from 29 control children, 38 children with normal body mass index and simple hypertension (NBp), 8 children overweight with simple hypertension (OBp), 37 children with normal body mass index and H-type hypertension (NH) and 19 children overweight with H-type hypertension (OH) were analyzed by non-targeted metabolomics. A total of 1235 differential metabolites were identified between children with hypertension and normal controls, of which 193 metabolites including various lipids were significantly expressed. Compared with the control group, 3-dehydroepiandrosterone sulfate, oleic acid and linoleic acid were up-regulated, and gamma-muricholic acid was down-regulated in the NBp group; 3-dehydroepiandrosterone sulfate, 4-acetamidobutanoate and 1-hexadecanoyl-2-octadecadienoyl-sn-glyero-3-phosphocholine were up-regulated in the OBp group, whereas adenosine and 1-myristoyl-sn-glyero-3-phosphocholine were down-regulated; in the NH group, 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine, phenol and 3-methoxytyramine were up-regulated, while pentadecanoic acid was down-regulated; in the OH group, NG,NG-dimethyl-L-arginine, 1-palmitoyl-sn-glycero-3-phosphocholine and monoethyl phthalate were up-regulated, while phloretin and glycine were down-regulated. The results showed that the children with hypertension had obvious disorders of lipid metabolism (especially in the overweight hypertension group), which led to the occurrence of hypertension. Additionally, the concentration of NO production-related NG, NG-dimethyl-L-arginine, was significantly increased, which may play an important role in H-type hypertension in children.

Metoprolol therapy for paediatric vasovagal syncope (VVS) has yielded inconsistent results, necessitating predictive markers. We aimed to develop and validate models to identify paediatric VVS patients likely to benefit from metoprolol. 478 metoprolol-treated paediatric patients with VVS were enrolled from three syncope units and divided into retrospective training (March 2017-March 2023, n = 323) and prospective validation cohorts (April 2023-March 2024, n = 155). Fourteen patients (2.9%) were excluded for lacking follow-up data. Patients were classified as responders or non-responders based on symptom improvement after 1-3 months of metoprolol therapy. Univariate analysis and logistic regression were used to select the candidate predictors. A nomogram and a scoring model were established to predict treatment efficacy. The model values were analysed using a receiver operating characteristic (ROC) curve. Consistency was evaluated using the Hosmer-Lemeshow (H-L) test, calibration curve, and concordance index (C-index). The clinical utility of model was assessed through the decision curve analysis (DCA). Internal validation was performed using the bootstrap approach. The predictive model derived from the training cohort was validated in the validation cohort to assess its accuracy and feasibility. Increased heart rate during positive response in head-up tilt test (ΔHR), corrected QT interval dispersion (QTcd), and standard deviation of all normal-to-normal intervals (SDNN) were selected as independent predictors to develop a predictive model. A nomogram model was built (AUC: 0.900, 95% CI: 0.867-0.932); the H-L test and calibration curves showed a strong alignment between predicted and actual results. The scoring model was established in the training cohort (AUC: 0.941, 95% CI: 0.897-0.985), yielding a sensitivity of 82.8% and a specificity of 96.5%, with a cut-off value of 2.5 points. In the external validation cohort, the scoring model achieved a sensitivity, specificity, and accuracy of 93.6%, 80.9%, and 87.7%, respectively. The nomogram and scoring model were constructed to predict the efficacy of metoprolol for children with VVS, which will greatly assist paediatricians in the individual management of VVS in children and adolescents. This research was funded by National High-Level Hospital Clinical Research Funding (Clinical Research Project of Peking University First Hospital, grant number 2022CR59).

Fibroblast growth factor 23 (FGF 23), an endocrine hormone regulating the homeostasis of phosphate and vitamin D, has been shown to play a role in cardiovascular disease. Increased blood FGF 23 is found to be associated with elevated blood pressure in adults. However, measurement of FGF 23 in hypertensive children has not been documented. In this study, a total of 98 children with primary hypertension and 37 controls were recruited, and blood FGF 23 was comparatively investigated. Additionally, FGF 23 levels were compared between the subgroups of patients after hypertensive children were sub-grouped according to their cardiac geometry, hypertension stages, insulin levels, and weight. The case group had a FGF 23 level of 48.99 (16.42), expressed as the median (the interquartile range), significantly higher than the 41.72 (7.05) from the control group (p = 0.0002). While no remarkable differences were observed in FGF 23 levels between non-obese and obese hypertensive children, between patients with stage 1 and stage 2 hypertension, or between patients with normal and high insulin levels; hypertensive children with abnormal cardiac geometry had significantly higher levels of FGF 23 than patients with normal cardiac geometry (p = 0.0085). Our data revealed for the first time that hypertensive children have higher levels of FGF 23. Further studies are needed to examine if lowering FGF 23 improves the cardiac geometry in hypertensive children with higher FGF 23.