American Journal of Hypertension最新文献

Background: Hypertension and diabetes mellitus are both known risk factors for atrial fibrillation (AF). Whether coexisting hypertension exacerbates AF risk among individuals with diabetes remains unclear. This study aims to investigate the association between hypertension and incident AF in this population.

Methods: We studied participants in the prospective Kailuan Study, including 18,084 adults diagnosed with diabetes between 2006 and 2011 and free of AF at baseline. Hypertension was defined by a previous diagnosis, use of antihypertensive medications, or systolic/diastolic blood pressure ≥140/90 mmHg. Incident AF was identified via biennial ECGs and hospital records. Cox proportional hazards models adjusted for demographic, lifestyle, metabolic, and clinical covariates were used to estimate hazard ratios (HRs).

Results: Over a median follow-up of 14.8 years (IQR 12.7-16.8), 275 participants with diabetes developed AF, and 5,265 died from any cause. Hypertension was associated with a higher risk of AF (adjusted HR, 1.48; 95% confidence interval [CI], 1.05-2.07) compared to those without hypertension. Compared to participants with normal blood pressure, the adjusted HRs for AF were 1.54 (95% CI, 1.11-2.13) for grade 1 hypertension and 1.61 (95% CI, 1.06-2.44) for grade 2 hypertension. Among those with hypertension, target organ damage-particularly prior myocardial infarction or ischemic stroke-further elevated AF risk (HR, 2.66; 95% CI, 1.26-5.60).

Conclusions: Hypertension independently increases AF risk in individuals with diabetes, especially with higher blood pressure levels and target organ damage. Early hypertension control is crucial for the prevention of AF in this high-risk population.

Background: Preeclampsia (PE) is a pregnancy-specific condition characterized by hypertension and multi-organ dysfunction that can lead to severe maternal and perinatal complications. The miR-127-3p is down-regulated in PE, but the mechanism of action in PE is not yet clear.

Methods: The study enrolled 113 PE patients and 93 healthy controls. The expression level of miR-127-3p was evaluated by qPCR, its correlation with clinical indicators of PE was analyzed by correlation analysis, and the diagnostic value of miR-127-3p in PE was evaluated by the ROC curve. In vitro, HTR8/SVneo cells were treated with hypoxia/reoxygenation (H/R) and transfected with miR-127-3p mimics/inhibitors. The regulatory effects of miR-127-3p on the H/R-induced HTR8/SVneo model were verified by cell counting kit-8 (CCK-8), Transwell, and enzyme linked immunosorbent assay (ELISA). The interaction between KIF3B and miR-574-3p was confirmed through dual-luciferase reporter assays.

Results: The miR-127-3p expression was significantly down-regulated in PE patients and correlated with the severity and outcomes of PE. ROC analysis showed that miR-127-3p had a significant diagnostic value in PE. In vitro, miR-127-3p overexpression could restore trophoblast proliferation and invasion ability, and suppress pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) in HTR8/SVneo cells induced by H/R. KIF3B was confirmed as a downstream gene of miR-127-3p, and the regulatory relationship between miR-127-3p and KIF3B was confirmed.

Conclusion: In PE, downregulated miR-127-3p expression correlating with PE severity and outcomes could be used as a biomarker for PE auxiliary diagnosis. In vitro, miR-127-3p overexpression enhances trophoblast function and inhibits the inflammatory responses.

Background: Nocturnal hypertension (NH) is a significant risk factor for target organ damage and all-cause mortality. Post-saline infusion test plasma aldosterone concentration (post-SIT PAC) serves as an indicator of autonomous aldosterone secretion level, but its link to NH is uncertain. This study aims to explore the association between post-SIT PAC levels and NH in patients with suspected primary aldosteronism (PA).

Methods: Participants were classified into three groups after a saline infusion test (SIT): negative (post-SIT PAC < 5 ng/dL, n = 86), borderline (post-SIT PAC 5-10 ng/dL, n = 180), and positive (post-SIT PAC > 10 ng/dL, n = 75). Restricted cubic spline plots (RCS) were used to explore the dose-response relationship between post-SIT PAC and NH, while multivariable logistic regression models adjusted for potential confounders.

Results: In this retrospective study, the overall prevalence of NH was 70.4%. A positive, nonlinear association was identified between post-SIT PAC and NH (P-nonlinear < 0.05). After adjustment for multiple variables, post-SIT PAC remained significantly correlated with NH (OR = 1.08; 95% CI: 1.01-1.15; P < 0.05), while basal PAC was not. Additionally, guideline-defined subgroups with elevated post-SIT PAC demonstrated a higher prevalence of NH (P < 0.05). Specifically, NH prevalence was 81.3% (n = 75) in the positive subgroup, 72.2% (n = 180) in the borderline subgroup, and 57.0% (n = 86) in the negative subgroup.

Conclusions: The level of autonomous aldosterone secretion, rather than the basal aldosterone level, is relevant to potential PA patients at risk for NH. NH prevalence increases nonlinearly with higher post-SIT PAC levels.

Background: Hypertension is a major risk factor for cardiovascular and renal diseases, significantly contributing to morbidity and mortality. The COVID-19 pandemic has heightened concerns about the impact of hypertension on severe COVID-19 outcomes.

Methods: We analyzed 2020-2021 data from the MarketScan Commercial and Health and Productivity Management databases, focusing on adults aged 18-64 years with continuous employer-sponsored private insurance, excluding pregnancy or capitated plans. We compared medical costs, healthcare utilization (emergency department [ED] visits, inpatient admissions, outpatient visits, and outpatient prescription drugs), and productivity losses (sick absences, short-term disability [STD], and long-term disability) between individuals with and without hypertension, stratified by COVID-19 diagnosis. We used multivariable regression models, including an interaction term for hypertension and COVID-19 diagnosis, to estimate differences in outcomes, adjusting for demographics and comorbidities.

Results: Among 1,296,596 adults, 21% had hypertension. Those with hypertension were older, less likely female, less likely urban residents, and had more comorbidities. Excess medical costs associated with hypertension were $8,572 per patient over the 2-year period (95% CI $8,182-$8,962). Patients with vs. without hypertension had 0.200 (95% CI, 0.195-0.205) more ED visits, 0.081 (95% CI, 0.077-0.085) more inpatient admissions, 5.984 (95% CI, 5.892-6.075) more outpatient visits, and 20.25 (95% CI, 20.09-20.41) more prescriptions per patient over the 2-year period. They also had more sick absences (1.13 days; 95% CI 0.93-1.34) and STD occurrences (3.88 days; 95% CI 3.56-4.20) per patient. Among those with hypertension, individuals with vs. without COVID-19 had $3,495 (95% CI, $2,135-$4,856) higher medical costs and 2.588 (95% CI, 1.112-4.065) more STD days per patient over the 2-year period.

Conclusions: Hypertension was associated with higher medical costs, healthcare utilization, and productivity losses, exacerbated by COVID-19.

Background: Thoracic aortic dissection (TAD) is a potentially fatal condition. It has been linked with hypertension, and guidelines recommend antihypertensives.

Methods: Electronic searches were conducted in MEDLINE and EMBASE with the following search strategy: (("thoracic aortic dissection"[Mesh]) AND ("antihypertensive agents"[Mesh] from database inception to August 2024.

Results: Hypertension is associated with a significant risk of TAD with a hazard ratio (HR) of 2.51 (95% CI: 1.75-3.60). Beta-blocker treatment produces a significant (P < 0.01) lower risk of an MACE HR of 0.55 (95% CI = 0.39-0.77). Angiotensin receptor blockers (ARBs) or ACE inhibitors also lower the risk of a major adverse cardiac event with a HR of 0.67 (95% CI = 0.58-0.78). Calcium channel blockers (CCB) significantly (P =0.0007) lowered MACE outcomes with a HR of 0.66 (95% CI = 0.53-0.84). A network meta-analysis was performed to evaluate the relative risk of aortic events associated with commonly prescribed antihypertensive agents, using beta-blockers (BB) as the reference comparator. Compared to BB, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (ACE/ARB) were associated with a non-significant increase in risk (HR 1.28, 95% confidence interval (CI): 0.91-1.81). CCB also demonstrated a non-significant reduction in risk (HR 0.68, 95% CI: 0.33-1.40) to BBs.

Conclusions: Hypertension is strongly associated with a risk of TAD. Beta-blockers are associated with the greatest reduction in MACE and remain the most effective first-line therapy for patients at risk of TAD. ACE inhibitors and ARBs also demonstrate benefit.

Background: High dietary sodium intake is associated with cardiovascular disease. We investigated the influence of sodium intake on the plasma proteome.

Methods: Prospectively recruited normotensive participants underwent 2 controlled dietary sodium interventions to evaluate hormonal and proteomic (1,512 proteins) changes: sodium-restriction resembling ancestral hunter-gatherer intake (~10 mEq/day, ~230 mg/day) and sodium-loading resembling modern industrialized intake (~200 mEq/day, ~4,600 mg/day). Twenty-four hour urine collections were obtained after each diet. Plasma proteomic changes were assessed with correction for false discovery.

Results: Participants achieved a 24-h urinary sodium excretion of 16 mEq/L when sodium-restricted and 249 mEq/L when sodium-loaded. Thirty-eight proteins displayed statistically significant changes with 15 additional proteins exhibiting notable trends that did not reach statistical significance. The most apparent changes were increases in proteins related to fibrosis and the extracellular matrix (ECM) when sodium-loaded, whereas sodium-restriction increased proteins related to immune/inflammatory pathways and the renin-angiotensin system (RAS)-kallikrein-kinin system (KKS)-complement pathway. NT-proBNP, FUMH (fumarate hydratase), LKHA4 (leukotriene A(4) hydrolase), COFA1 (collagen alpha-1(V) chain), COF2 (cofilin-2), BMP-4, and TGF-β RIII had the greatest increases when sodium-loaded, whereas renin, thrombin, apo A-1 (apolipoprotein A-1), FABPA (fatty acid binding protein), and LEAP-1 (hepcidin) had the greatest increases when sodium-restricted.

Conclusions: When compared to a sodium-restricted diet resembling ancestral intake, the modern industrialized dietary sodium intake increased proteins related to fibrosis and the ECM, and decreased proteins related to the RAS, KKS, immunity, and inflammation. These findings in normotensive people provide an atlas of proteomic changes, and biological pathways, that may contribute to hypertension and other sodium-related disorders.

Background: Central blood pressure (CBP) is a better predictor of cardiovascular outcomes than peripheral blood pressure. First- and second-generation beta-blockers have shown poor CBP-lowering effects. However, nebivolol, a third-generation beta-blocker with vasodilatory effects, may be beneficial in lowering CBP. This study compared the CBP-lowering efficacies of nebivolol and telmisartan over a 12-week period in patients with hypertension.

Methods: This prospective, randomized, multicenter, open-label, controlled trial evaluated 98 participants with hypertension. For 12 weeks, participants received either nebivolol (n = 49) or telmisartan (n = 49) for 12 weeks with a target blood pressure of ≤140/90 mmHg for the entire period. The primary endpoint was a change in central systolic blood pressure (cSBP) after 12 weeks.

Results: cSBP reduction at week 12 was significantly less in the nebivolol group than in the telmisartan group (-17.2 vs. -29.3mmHg; between-group difference, 12.7 mmHg; 95% confidence interval [CI], 4.1-21.2; P = 0.004). Central pulse pressure decreased in both groups; however, the difference between the groups was not significant (-8.5 vs. -14.1 mmHg, P = 0.207). The nebivolol group demonstrated a slightly increased augmentation index (AIx), whereas the telmisartan group had a significantly decreased AIx (0.7 vs. -7.3 mmHg; 95% CI, 3.1-13.0; P = 0.002). Heart rate at week 12 was significantly lower in the nebivolol group than that in the telmisartan group (64.2 ± 11 vs. 74.6 ± 11 beats per minute, P < 0.001).

Conclusions: Nebivolol was less effective than telmisartan at reducing cSBP.

Clinical trial registration: NCT05328310.