The sensitive period during which the adult cardiovascular system is particularly vulnerable to body mass index (BMI) changes remains unclear. This study aimed to examine how rates of BMI change from childhood to adulthood influence the risk of subclinical cardiovascular outcomes in mid-adulthood. This cohort study included 2446 participants from the Hanzhong Adolescent Hypertension Study who had at least two BMI measurements in childhood/adolescence (6–18 years) and at least two in adulthood (≥ 19 years). The BMI growth curve from ages 6 to 52 years was modeled using random-effects mixed models with restricted cubic splines. These models yielded age-specific estimates of BMI levels and rates of change, the latter of which were subsequently residual-adjusted for concurrent BMI levels. Multivariable logistic regression models were used to examine the associations of BMI levels and level-adjusted rates of change from 6 to 52 years with left ventricular hypertrophy (LVH) and arterial stiffness in mid-adulthood. BMI at each age from 10 to 52 years was associated with mid-adult LVH and arterial stiffness, and these associations became stronger with increasing age at BMI measurement. Additionally, age-level–adjusted rates of BMI change at most ages from childhood to adulthood were positively associated with a higher risk of both subclinical cardiovascular outcomes. However, the odds ratios (ORs) for both LVH and arterial stiffness per 1-SD increase in BMI change rate declined with increasing age. For LVH, the ORs decreased from 2.49 (95

Objective To examine the associations between cumulative body mass index (BMI) burden from childhood to adulthood and the risk of adult metabolic multimorbidity. Research Design and Methods This prospective cohort study used data from the Hanzhong Adolescent Hypertension Study (1987-2023). A total of 2,446 participants with at least two BMI measurements in both childhood (6-18 years) and adulthood (19-52 years) were included. Cumulative BMI exposure was quantified using total and incremental area under the curve (AUC). Outcomes included metabolic multimorbidity, defined as the presence of ≥2 or ≥3 metabolic diseases, specifically hypertension, diabetes, dyslipidemia, elevated liver enzymes/bilirubin, and kidney damage. Results Higher total and incremental BMI AUC during childhood, adulthood, and over the life course were consistently associated with an increased risk of adult metabolic multimorbidity (≥2 diseases). For total AUC, odds ratios (ORs) ranged from 1.51 to 2.59 (all P<0.05); for incremental AUC, ORs ranged from 1.94 to 4.33 (all P<0.05). Compared with total AUC, incremental AUC showed a stronger association with metabolic multimorbidity in childhood (OR: 4.33, 95%CI: 2.93-6.40 vs. 1.51, 1.17-1.95, respectively). Conversely, total AUC exhibited a stronger association in adulthood than in childhood (OR: 2.51, 95%CI: 2.08-3.04 vs. 1.94, 1.62-2.31). Furthermore, the associations for adulthood and life-course BMI AUC were significantly stronger in males than in females (P for interaction <0.05). Conclusions These findings highlight the importance of life stage-specific strategies: curbing rapid BMI gain in childhood and maintaining long-term weight control throughout adulthood.

BACKGROUND:Blood pressure (BP) is a dynamic trait associated with cardiovascular disease. We aimed to estimate age-specific BP levels and rates of change from childhood to mid-adulthood and to examine their associations with subsequent subclinical target organ damage. METHODS:We included 2508 participants from the Hanzhong Adolescent Hypertension Study with BP measured ≥4× from 1987 to 2023. Surrogate markers of target organ damage were assessed, including arterial stiffness, left ventricular hypertrophy, and albuminuria. Growth models were used to construct BP trajectories and estimate age-specific BP levels and rates of change (slopes). RESULTS:Rates of change in BP at each age point from childhood to mid-adulthood were positively associated with arterial stiffness and albuminuria in mid-adulthood, independent of corresponding BP levels. The magnitude of the associations rose from childhood, peaked in adolescence, and declined thereafter. For example, odds ratios (95% CIs) per 1 SD increase in systolic BP change rates for arterial stiffness increased from 1.94 (1.69-2.24) at age 6 to 2.11 (1.82-2.44) at age 13, then declined to 1.13 (1.01-1.28) by age 52. Faster BP increases were more strongly associated with arterial stiffness and albuminuria than concurrent BP levels during childhood and adolescence, whereas the opposite trend was observed in young and mid-adulthood. Similar age-dependent trends were identified for left ventricular hypertrophy, with minor variations in the ages at which associations reached statistical significance. CONCLUSIONS:Accelerated BP increases during childhood and adolescence show a stronger association with mid-adult subclinical target organ damage than increases occurring in adulthood.

The associations of long-term body mass index (BMI) exposure, including both cumulative burden and increasing trends from childhood to adulthood, with subclinical cardiovascular outcomes remain incompletely understood, especially across distinct life stages. This study aimed to examine these associations and evaluate the potential mediating roles of established cardiovascular risk factors. We analyzed data from 2,446 participants in the Hanzhong Adolescent Hypertension Study, all of whom had at least four BMI measurements over a 36-year follow-up period. Cumulative burden and increasing trends of BMI were quantified using total and incremental areas under the curve (AUCs). Multivariable logistic regression and exploratory multiple-mediator analyses were used to examine associations and potential indirect-effect patterns, respectively. Higher total and incremental BMI AUCs during childhood, adulthood, and across the life course were significantly associated with an increased risk of arterial stiffness in mid-adulthood. For childhood, the odds ratios (ORs) with 95

BackgroundLimited data exists on how early-life weight changes relate to metabolic syndrome (MetS) risk in midlife. This study examines the association between long-term trajectories of body mass index (BMI), its variability, and MetS risk in Chinese individuals.MethodsIn the Hanzhong Adolescent Hypertension study (March 10, 1987–June 3, 2017), 1824 participants with at least five BMI measurements from 1987 to 2017 were included. Using group-based trajectory modeling, different BMI trajectories were identified. BMI variability was assessed through standard deviation (SD), variability independent of the mean (VIM), and average real variability (ARV). Logistic regression analyzed the relationship between BMI trajectory, BMI variability, and MetS occurrence in midlife (URL: https://www.clinicaltrials.gov; Unique identifier: NCT02734472).FindingsBMI trajectories were categorized as low-increasing (34.4%), moderate-increasing (51.8%), and high-increasing (13.8%). Compared to the low-increasing group, the odds ratios (ORs) [95% CIs] for MetS were significantly higher in moderate (4.27 [2.63–6.91]) and high-increasing groups (13.11 [6.30–27.31]) in fully adjusted models. Additionally, higher BMI variabilities were associated with increased MetS odds (ORs for SDBMI, VIMBMI, and ARVBMI: 2.30 [2.02–2.62], 1.22 [1.19–1.26], and 4.29 [3.38–5.45]). Furthermore, BMI trajectories from childhood to adolescence were predictive of midlife MetS, with ORs in moderate (1.49 [1.00–2.23]) and high-increasing groups (2.45 [1.22–4.91]). Lastly, elevated BMI variability in this period was also linked to higher MetS odds (ORs for SDBMI, VIMBMI, and ARVBMI: 1.24 [1.08–1.42], 1.00 [1.00–1.01], and 1.21 [1.05–1.38]).InterpretationOur study suggests that both early-life BMI trajectories and BMI variability could be predictive of incident MetS in midlife.FundingThis work was supported by the National Natural Science Foundation of China No. 82070437 (J.-J.M.), the Clinical Research Award of the First Affiliated Hospital of Xi'an Jiaotong University of China (No. XJTU1AF-CRF-2022-002, XJTU1AF2021CRF-021, and XJTU1AF-CRF-2023-004), the Key R&D Projects in Shaanxi Province (Grant No. 2023-ZDLSF-50), the Chinese Academy of Medical Sciences & Peking Union Medical College (2017-CXGC03-2), and the International Joint Research Centre for Cardiovascular Precision Medicine of Shaanxi Province (2020GHJD-14).

BackgroundLipid management with a low-density lipoprotein cholesterol (LDL-C) goal of < 1.4 mmol/L is recommended for patients with acute coronary syndrome (ACS) and diabetes mellitus (DM) due to a high risk for adverse cardiovascular events. This study evaluated the lipid-lowering treatment (LLT) pattern and the LDL-C goal attainment rate in this special population.MethodsDM patients were screened from the observational Dyslipidemia International Study II-China study which assessed LDL-C goal attainment in Chinese ACS patients. The baseline characteristics between the LLT and no pre-LLT groups were compared. The proportions of patients obtaining LDL-C goal at admission and at 6-months, the difference from the goal, and the pattern of the LLT regimen were analyzed.ResultsTotally 252 eligible patients were included, with 28.6% taking LLT at admission. Patients in the LLT group were older, had a lower percentage of myocardial infarction, and had decreased levels of LDL-C and total cholesterol compared to those in the no pre-LLT group at baseline. The overall LDL-C goal attainment rate was 7.5% at admission and increased to 30.2% at 6 months. The mean difference between the actual LDL-C value and LDL-C goal value dropped from 1.27 mmol/L at baseline to 0.80 mmol/L at 6 months. At 6 months, 91.4% of the patients received statin monotherapy, and only 6.9% received a combination of statin and ezetimibe. The atorvastatin-equivalent daily statin dosage was moderate during the study period.ConclusionThe low rate of lipid goal attainment observed was in line with the outcomes of other DYSIS-China studies.

BackgroundThis study aimed to identify the subgroups of individuals sharing similar blood pressure (BP) trajectories from childhood to youth and explore the associations of these trajectories with arterial stiffness in adulthood.MethodsA group-based trajectory model was used to identify BP trajectories among 2,082 individuals in the Hanzhong adolescent hypertension cohort by using BP values repeatedly measured at four visits from childhood (6–15 years) to youth (14–23 years). The brachial–ankle pulse wave velocity (baPWV) was examined 30 years after the baseline survey. Mixed linear regression models were used to examine the associations of these trajectories with adult baPWV.ResultsAmong the 2,082 individuals, three trajectory groups of systolic BP were identified as follows: the low-level group (n = 889), medium-level group (n = 1,021), and high-level group (n = 172). The baPWV in adulthood was higher in medium-level and high-level groups compared with the low-level group (1271.4 ± 224.7 cm/s, 1366.1 ± 249.8 cm/s vs. 1190.1 ± 220.3 cm/s, all p < 0.001). After adjustment for potential confounding factors, the association between baPWV and systolic BP trajectories was statistically significant (adjusted β = 49.4 cm/s; p < 0.001 for the medium-level group and β = 107.6 cm/s; p < 0.001 for the high-level group compared with the low-level group). Similar results were obtained for the association of baPWV with the trajectories of diastolic BP and mean arterial pressure (MAP), except for pulse pressure.ConclusionOur investigation demonstrates different BP trajectories from childhood to youth and shows the trajectories of systolic BP, diastolic BP, and MAP are significant predictors of arterial stiffness in adulthood.

目的 利用生物信息学方法探究扩张型心肌病潜在的生物标记物和相关富集通路.方法 搜索GEO数据库中与扩张型心肌病相关的数据集,提取人心肌细胞的两张芯片GSE42955和GSE1869,然后利用R语言进行差异基因分析、蛋白互作网络分析、鉴定差异表达的核心基因和核心模块并进行基因本体数据库(GO)富集、京都基因与基因组百科全书(KEGG)通路分析.搜索ArrayExpress数据库与扩张型心肌病相关的数据集,提取出人心肌细胞芯片E-TABM-480,验证核心基因和模块在其中的表达情况.结果 共验证出10个差异表达基因,即DZIP3、FBXO32、BTBD6、FBXL5、ASB8、COMMD1、LTN1、FBXO21、RCHY1、ARIH2,核心差异基因为DZIP3,经GO和KEGG,上述差异基因的生物学过程主要集中在泛素和蛋白酶体相关的生物学过程和通路中.结论 生物信息学分析显示,泛素-蛋白酶系统在扩张型心肌病发病中具有重要作用,其机制尚待进一步研究.

ObjectiveRenalase, a novel secretory flavoprotein with amine oxidase activity, is secreted into the blood by the kidneys and is hypothesized to participate in blood pressure (BP) regulation. We investigated the associations of renalase with BP and the risk of hypertension by examining renalase single nucleopeptide polymorphism (SNPs), serum renalase levels, and renal expression of renalase in humans.Methods① Subjects (n = 514) from the original Baoji Salt-Sensitive Study cohort were genotyped to investigate the association of renalase SNPs with longitudinal BP changes and the risk of hypertension during 14 years of follow-up. ② Two thousand three hundred and ninety two participants from the Hanzhong Adolescent Hypertension Study cohort were used to examine the association of serum renalase levels with hypertension. Renalase expression in renal biopsy specimens from 193 patients were measured by immunohistochemistry. ③ Renalase expression was compared in hypertensive vs. normotensive patients.Results① SNP rs7922058 was associated with 14-year change in systolic BP, and rs10887800, rs796945, rs1935582, rs2296545, and rs2576178 were significantly associated with 14-year change in diastolic BP while rs1935582 and rs2576178 were associated with mean arterial pressure change over 14 years. In addition, SNPs rs796945, rs1935582, and rs2576178 were significantly associated with hypertension incidence. Gene-based analysis found that renalase gene was significantly associated with hypertension incidence over 14-year follow-up after adjustment for multiple measurements. ② Hypertensive subjects had higher serum renalase levels than normotensive subjects (27.2 ± 0.4 vs. 25.1 ± 0.2 μg/mL). Serum renalase levels and BPs showed a linear correlation. In addition, serum renalase was significantly associated with the risk of hypertension [OR = 1.018 (1.006–1.030)]. ③ The expression of renalase in human renal biopsy specimens significantly decreased in hypertensive patients compared to non-hypertensive patients (0.030 ± 0.001 vs. 0.038 ± 0.004).ConclusionsThese findings indicate that renalase may play an important role in BP progression and development of hypertension.

目的 研究高盐饮食对盐敏感性高血压大鼠肾脏组织损伤的影响.方法 将20只实验大鼠按照大鼠品系分为对照组(SS-13BN大鼠,n=10)与盐敏感性高血压大鼠模型组(Dahl/SS大鼠,n=10),通过喂食盐含量为8％的高盐饲料构建盐敏感性高血压大鼠模型,分析两组大鼠肾脏组织损伤程度及肾脏组织中白介素-6(IL-6)、白介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的表达情况.结果 模型组大鼠的收缩压为(183.82±3.87)mmHg,对照组为(129.03±3.94)mmHg,差异有统计学意义(P<0.05).模型组大鼠肾脏组织中Nephrinuria含量为(12.12±0.92)mg/d、肾损伤程度评分为(1.93±0.52)分、TNF-α含量为(623.14±43.12)pg/mg,均高于对照组,差异有统计学意义(P<0.05).模型组大鼠肾脏组织中IL-6 mRNA的相对表达量为(2.25±0.81)、IL-1βmRNA为(2.89±0.86),均高于对照组,差异有统计学意义(P<0.05).模型组大鼠肾脏组织中IL-6蛋白相对表达量为(1.71±0.08)、IL-1β为(2.23±0.13),均高于对照组,差异有统计学意义(P<0.05).结论 高盐摄取会对盐敏感大鼠的肾脏造成严重的损伤,引起炎症反应,从而影响肾小球等肾脏器官的正常功能.

目的 探索急性心肌梗死患者甲状腺功能对心脏射血分数的影响. 方法 采用队列研究法,对2013-01～2016-12我院心内科收治345名急性心肌梗死患者的甲状腺功能及心脏超声心脏射血分数进行数据收集及分析,对患者心血管事件及死亡进行2年的随访记录.采用单元及多元线性回归模型分析甲状腺功能与患者心脏射血分数的相关性.采用Kaplan-Meier生存分析的方法探索甲状腺功能对心血管事件的预测作用. 结果 急性心肌梗死患者中,血浆T3(R square =0.04,P＜0.001)、FT3 (R square =0.05,P＜0.001)及TSH(R square =0.01,P＜0.05)水平与患者心脏射血分数显著相关.随访结果提示血浆T3、FT3和TSH对患者心血管事件预后无显著预测作用. 结论 急性心肌梗死患者中血浆T3、FT3及TSH水平与心脏射血分数显著相关,但对患者心血管事件无显著预测作用.

Objective To investigate the effect of estrogen-related receptors α (ERRα) on salt sensitivity in salt-sensitive hypertensive rats and its molecular mechanism. Methods Six-week-old male ERRα overexpression and control Dahl salt-sensitive rats were divided into four groups: normal salt control group, normal salt ERRα overexpression group, high salt control group and high salt ERRαoverexpression group. The rats were fed with normal salt (containing 0. 5％ Na Cl) diet per day in normal salt control group and normal salt ERRα overexpression group, and high salt (containing 8％ Na Cl) diet per day in high salt control group and high salt ERRα overexpression group. Rats were fed for 3 weeks and then the blood pressure, blood SOD and MDA levels were measured. The m RNA expression of ERRα and the phosphorylation levels of AKT and SGK1 in thoracic aorta of salt-sensitive hypertensive rats were detected by real-time fluorescent quantitative PCR and Western blot, respectively. Results Compared with normal salt control group, the expression of ERRα was significantly decreased in high salt control group (all P ＜ 0. 01). Compared with high-salt control group, the blood pressure was significantly decreased in high-salt ERRα overexpression group, blood SOD activity was significantly increased, and MDA content was significantly decreased (all P ＜ 0. 01). In addition, the expression of p-AKT and p-SGK1 protein in high salt ERRα overexpression group was significantly higher than that in high salt control group (all P ＜ 0. 01). Conclusion ERRα may inhibit oxidative stress in salt-sensitive hypertensive rats and reduce salt sensitivity in rats via AKT/SGK1 pathway.

目的:对我院住院医师规范化培训运行效果进行评价.方法:选择2015年与2016年期间参与培训的90名住院医师,对他们思想品德素质、临床技能、病历质量等方面的成绩进行考核,深度探究与分析其间存在的问题,提出几点应对措施.结果:应对措施编制与实施以后,除了专业英语之外,90名住院医师2016年其他各项目成绩显著高于2015年,差异有统计学意义(P<0.05).结论:编制确切性培训目标,制定可行性培训规划,建立健全考评体制等对策的编制与实施,能够强化住院医师培训活动运行的规范性,提升住院医师业务能力与职业素养,可见住院医师规范化培训值得推广.

OBJECTIVETo evaluate the effects of dietary sodium intake on QT interval dispersion (QTd) in normotensive healthy subjects and assess the protective effects of dietary potassium. Methods All subjects were sequentially maintained on a protocol with a three-day baseline investigation, seven-day low-salt period (3 g/day (d), NaCL), seven-day salt loading period (18 g/d, NaCL) and a seven-day salt loading with potassium supplementation period (4.5 g/d, KCL). On the last day of each period, 24-hour urine samples were collected, the blood pressure values were measured and an electrocardiogram was recorded. The QT interval, QTd and T peak-T end interval (Tp-Te) were subsequently measured and calculated. Patients Sixty-four normotensive subjects, men and women, ranging from 28 to 60 years of age, were enrolled. Results There were no great fluctuations in heart rate after salt loading, whereas the systolic blood pressure (SBP, mmHg) and diastolic blood pressure (DBP, mmHg) increased and the corrected QT interval (QTc), corrected QT interval dispersion (QTdc) and Tp-Te values were significantly prolonged compared to that observed in the low-salt period (SBP, 118.6 ± 13.5 vs. 111.7 ± 11.3, p<0.01; DBP, 76.9 ± 8.6 vs. 71.7 ± 7.7, p<0.01; QTdc, 60.3 ± 19.4 vs. 55.6 ± 19.4, p<0.05; Tp-Te, 83.0 ± 10.1 vs. 79.8 ± 8.5, p<0.01). Surprisingly, all of these changes were reversed by potassium supplementation (SBP, 114.5 ± 12.3 vs.118.6 ± 13.5, p<0.01; DBP, 72.2 ± 7.9 vs.76.9 ± 8.6, p<0.01;QTd, 42.6 ± 15.1 vs. 47.4 ± 19.0, p<0.05; QTdc, 52.2 ± 18.0 vs. 60.3 ± 19.4, p<0.05; Tp-Te, 79.1 ± 8.5 vs. 83.0 ± 10.1, p<0.01). Conclusion Salt loading prolongs the QT interval, QTd and Tp-Te, while dietary potassium supplementation reverses these alterations. These findings suggest that potassium supplementation may improve variation in the healing time and prevent arrhythmia.