Clinical and Experimental Hypertension最新文献

Objective: This study aimed to evaluate the diagnostic performance, risk assessment, and treatment-guiding value of coronary computed tomographic angiography (CCTA) in patients with coronary heart disease (CHD).

Methods: The diagnostic value of CCTA for CHD was assessed by analyzing key parameters including sensitivity, specificity, accuracy, positive predictive value, and negative predictive value. Additionally, the diagnostic relevance of specific CCTA-derived metrics was explored. Patients with confirmed CHD underwent percutaneous coronary intervention (PCI), and the occurrence of major adverse cardiovascular events (MACE) within one year after PCI were recorded. Differences in CCTA parameters between patients with and without MACE were compared. Multivariate logistic regression was conducted to identify independent risk factors for post-PCI MACE.

Results: CCTA demonstrated high diagnostic value for CHD. Compared to the control group, patients with CHD exhibited significantly greater plaque length, total plaque volume, calcified plaque volume, lipid plaque volume, plaque burden, and coronary diameter stenosis, along with a smaller minimum lumen area. These imaging features were predictive of CHD. Relative to the non-MACE group (n = 69), the MACE group (n = 56) had higher plaque length, total plaque volume, plaque burden, and coronary diameter stenosis rate, and smaller minimum lumen area. Multivariate logistic regression analysis identified plaque burden, coronary diameter stenosis, and hypertension serve as independent predictors for adverse cardiovascular events following PCI in CHD patients.

Conclusion: CCTA is a valuable noninvasive modality for the diagnosis of CHD, risk assessment, and optimization of treatment strategies, particularly in predicting adverse outcomes following PCI.

Background: Mitochondrial dysfunction of pulmonary vascular endothelial cells is one of the important pathogenesis of pulmonary arterial hypertension (PAH). Anthocyanin can protect mitochondrial function, but whether anthocyanin can prevent PAH and its related mechanism has not been reported.

Methods: Using rodent PAH models induced by chronic hypoxia for 21 days, we investigated the changes of hemodynamics, histopathology and vascular endothelial function after anthocyanin treatment for 21 days.

Results: We found that anthocyanin treatment improved pulmonary endothelial function, vascular remodeling and associated right heart failure. Mechanistically, we found that anthocyanin treatment promoted the nucleus translocation of Nrf2 and improved the impaired mitochondrial function. The beneficial effects of anthocyanin on regulation of mitochondrial function were abolished by inhibition of Nrf2. Finally, in Nrf2 deficient mice, the protective effects of anthocyanin on PAH were largely vanished.

Conclusions: Collectively, we showed that anthocyanin attenuated PAH and associated right heart failure via improving mitochondrial function through Nrf2-dependent mechanism, suggesting that anthocyanin may represent a novel therapeutic potential for PAH.

Background: Pyroptosis is a novel kind of programmed cell death and Caspase-1 plays key roles in driving pyroptosis. The current study aims to elucidate the molecular mechanism affecting cardiomyocyte pyroptosis in myocardial ischemia/reperfusion (I/R) injury, both in vivo and in vitro.

Methods: A murine model of myocardial I/R injury was established and then treated with lentivirus-mediated shRNA targeting Caspase-1 to evaluate the effect of Caspase-1 on myocardial I/R injury. Further, Caspase-1 was silenced in the cardiomyocytes following hypoxia-reoxygenation (H/R) to detect the function of Caspase-1 in mitochondrial homeostasis and cardiomyocyte pyroptosis.

Results: Knockdown of Caspase-1 inhibited the secretion of interleukin-1 beta (IL-1β), improved cardiac dysfunction and decreased pyroptosis in vivo. The cardio-protective effect was verified in the H/R-induced cardiomyocyte model. Recombinant IL-1β protein reversed the inhibitory effect of Caspase-1 knockdown on pyroptosis.

Conclusion: Overall, activating the Caspase-1/IL-1β axis by myocardial I/R injury causes mitochondrial homeostasis imbalance, pyroptosis, and the consequent cardiomyocyte injury.

Objective: This study aims to identify risk factors for adverse pregnancy outcomes in primipara with gestational diabetes mellitus (GDM) combined with pregnancy-induced hypertension syndrome (PIH) and to develop a predictive model for such outcomes.

Methods: A total of 120 primipara with GDM and PIH, admitted from January 2019 to May 2023, were divided into two groups: the adverse group (n = 57) and the good group (n = 63), based on pregnancy outcomes. Multivariate logistic regression analysis was used to identify independent risk factors for adverse outcomes. A nomogram was constructed based on these factors, and its efficacy was validated through internal evaluation.

Results: The adverse group had higher proportions of elderly parturients, higher pre-pregnancy BMI, and more weight gain during pregnancy. Additionally, the adverse group showed a higher incidence of family history of diabetes, and more severe types of PIH. Biochemical markers such as HbA1c and total cholesterol (TC) were higher in the adverse group, while high-density lipoprotein cholesterol (HDL-C) was lower (p < .01, p < .05). Multivariate logistic regression revealed that advanced maternal age, pre-pregnancy BMI, family history of diabetes, preeclampsia/chronic hypertension complicated by preeclampsia, and elevated HbA1c were independent risk factors for adverse pregnancy outcomes (p < .01). A nomogram prediction model was developed, with an AUC of 0.821. Bootstrap internal validation confirmed the model's robust discriminative ability.

Conclusion: Advanced maternal age, pre-pregnancy BMI, family history of diabetes, preeclampsia, and elevated HbA1c are significant risk factors for adverse pregnancy outcomes in GDM combined with PIH. The nomogram model provides an effective tool for predicting such outcomes.

Objective: This study explored miRNA-126 and HIF-1α levels in patients with OSAHS-related hypertension. To analyze the relationship between miRNA-126 and OSAHS-related hypertension and explore the pathogenic mechanisms of miRNA-126 and the HIF-1α pathway.

Materials and methods: The 120 participants were assigned to four groups based on their apnea-hypopnea index (AHI) and the presence of hypertension: healthy control group, hypertension group, non-hypertensive OSAHS group, and OSAHS-related hypertension group, with 30 objects in each group. All subjects underwent overnight sleep monitoring and 24-hour (h) ambulatory blood pressure. Their blood samples were analyzed for the following parameters: triglycerides (TG), fasting blood glucose (GLU), total cholesterol (TC), HDL, uric acid (UA), and LDL, hypoxia-inducible factor-1 alpha (HIF-1α), VEGF, C-reactive protein (CRP), IL-6 and tumor necrosis factor alpha (TNF-α). The relative expression levels of miRNA-126 were assessed by RT-qPCR and Western blotting, and dual-luciferase reporter assays were conducted to verify the association between miR-126-3p and HIF1-α.

Results: Results indicated that HIF-1α is a target gene of miRNA-126 and is negatively regulated by miRNA-126; Levels of miRNA-126 were significantly lower in OSAHS and hypertension patients relative to healthy controls, with the lowest levels observed in the OSAHS-related hypertension group(p < .05). miRNA-126 levels were negatively correlated with HIF-1α, VEGF, TNF-α, CRP, IL-6, TG, TC, LDL, GLU and UA levels (p < .01), while it showed positive correlation with HDL level (p < .01).

Conclusion: The level of miRNA-126 in patients with OSAHS-related hypertension is lower than that in patients with OSAHS alone and those with hypertension alone.

This study investigated the safety and efficacy of the HyperQure™ extravascular renal denervation (RDN) system in a swine model of mild hypertension. Ten female pigs were fed a 3% salt diet to induce hypertension and underwent either extravascular RDN using the HyperQure™ RDN system (n = 7) or a sham procedure (n = 3). Blood pressure (BP) was continuously monitored using implanted transmitters, and safety assessments were conducted via computed tomography angiography (CTA) at 28 days post-procedure. The primary endpoint was the change in systolic blood pressure (SBP) at four weeks, while secondary endpoints included changes in diastolic BP (DBP), mean arterial pressure (MAP), and histological evaluation of renal nerve and artery integrity. At four weeks, SBP decreased by 11.8 ± 5.2 mmHg in the RDN group compared to an increase of 6.4 ± 4.2 mmHg in controls, resulting in a mean difference of 18.2 mmHg (p < .05). Similar improvements were observed in DBP and MAP, with mean differences of 15.4 and 16.2 mmHg, respectively (both p < .05). CTA revealed no significant renal artery or intraperitoneal organ injury. Histological analysis confirmed effective nerve ablation, as evidenced by reduced tyrosine hydroxylase staining, without intimal damage. No postoperative complications were observed during the 28-day study period. These findings demonstrate the safety and efficacy of the HyperQure™ extravascular RDN system in reducing BP, providing a promising alternative for patients with resistant hypertension or those ineligible for intravascular RDN. Further clinical trials are warranted to validate these results.

Objective: To investigate the significance of blood lipids and pro-inflammatory in chronic obstructive pulmonary disease (COPD) patients in stable and acute exacerbations (AECOPD) with or without coronary heart disease (CAD).

Methods: One hundred and sixty COPD patients were divided into four groups based on whether COPD was in the acute or stable phase and whether comorbid CAD: AECOPD without CAD group, AECOPD with CAD group, stable COPD without CAD group, and stable COPD with CAD group.

Results: The levels of ApoA-I and ApoA-II in the AECOPD group and AECOPD with CAD group were significantly lower than in the stable COPD group, stable COPD with CAD group, and control group. The levels of SAA, TNF-α, and IL-6 was significantly higher in AECOPD group with CAD or without CAD compared with control group. SAA levels were significantly increased in stable COPD with CAD group compared with control group.

Conclusion: The levels of ApoA-I and ApoA-II in the AECOPD without CAD group and AECOPD with CAD group were significantly lower than those in the stable COPD group, stable COPD with CAD group. The change of pro-inflammatory factor TNF-α and IL-6 levels would be an important reason. The SAA level was significantly increased in the AECOPD without CAD group and AECOPD with CAD group, which indicated that the changes in HDL-C components in this group may be an important reason for promoting the progress of CAD.

Background: Recent studies indicate that tenapanor, an inhibitor of sodium/proton exchanger-3 (NHE3), diminishes intestinal phosphorus (Pi) absorption. Given NHE3's pivotal role in sodium (Na+) metabolism, there is a suspected functional link between Na+ and Pi metabolism. High-salt diets (HSD) have been demonstrated to disrupt calcium (Ca2+) metabolism. Since Ca2+ and Pi share analogous metabolic pathways, it is yet to be determined whether HSD also impacts Pi metabolism.

Methods: Male C57 mice were randomly assigned to three groups: a standard diet group, HSD groups for 1 week (HSD-1w) and 4 weeks (HSD-4w). Throughout the study, dietary intake and water consumption were monitored using metabolic cages, and urine and feces were collected. Blood pressure was measured using a noninvasive tail vein sphygmomanometer. Upon completion of the intervention, mice were euthanized under anesthesia for blood collection, and intestinal and renal tissues were harvested for molecular analysis.

Results: Although plasma Pi levels were comparable between HSD groups and the control group, HSD groups exhibited increased urinary Pi excretion and decreased fecal Pi excretion. The HSD-4w group displayed elevated parathyroid hormone levels, reduced fibroblast growth factor 23 levels, and higher renal Cyp27b1 mRNA expression. The expression of sodium-dependent phosphate transporter 2b (Npt2b) and NHE3 was elevated in the intestine of HSD mice.

Conclusion: HSD disrupts Pi metabolism by enhancing urinary Pi excretion and altering hormonal levels. The decrease in fecal Pi excretion, coupled with the upregulation of intestinal Pi transporter expression, suggests that HSD promotes intestinal Pi absorption in mice.

Objectives: We aimed to: (1) explore the effect of oral potassium supplementation on urinary potassium excretion, and (2) evaluate the value of urinary potassium-related indicators in distinguishing primary aldosteronism (PA) from non-PA patients.

Design and methods: A prospective study of 20 patients with hypertension and hypokalemia caused by renal potassium loss between November 2023 and April 2024 was conducted. Demographic features, 24-hour urine collection before and after potassium supplementation were all collected.

Results: The patients had a mean age of 49.38 years and 70% were male. Following a median potassium supplement dose of 8.50 g, serum potassium increased from 3.25 to 3.90 mmol/L (p < .001), and 24-hour urinary potassium (24 h UK) rose from 41.40 to 59.75 mmol/24 h (p = .004). After supplementation, 20% of patients had decreased 24 h UK, while 25%, 25%, and 40% showed increases of 0-10, 10-20, and > 20 mmol/24 h. Urinary-to-serum potassium ratio (USR) decreased in 40% of patients, while it increased by 0-5, 5-10, and > 10 L/24 h in 25%, 25%, and 10% of patients, respectively. Both 24 h UK and USR after repletion predicted PA with moderate-to-high accuracy (AUC = 0.808 for both). The optimal cutoff of 24 h UK and USR after supplementation were 51 mmol/24 h and 17.43 L/24 h. The AUC for 24 h USR and 24 h UK before repletion in predicting PA were 0.788 and 0.652, respectively.

Conclusions: Urinary potassium does not increase proportionally with serum potassium levels or the oral potassium dose, showing individual variability. Post-supplementation urinary potassium has greater diagnostic value for distinguishing PA than pre-supplementation indicators.