Hypertension Research最新文献

Large Language Models (LLMs) demonstrate considerable potential in enhancing the retrieval of health information. However, the hallucinatory they produce poses a security challenge. This study aimed to improve the accuracy and reliability of LLMs in hypertension education through the integration of integrating Retrieval-Augmented Generation (RAG) technology. We constructed a hypertension supplement knowledge base, and subsequently integrated it into a RAG technology, resulting in the development of the HEART (Hypertension Enhancing Answer Retrieval Tool) framework. A set of 50 commonly asked questions related to hypertension was used to evaluate the performance of four base LLMs-ChatGPT-4o, Claude-3.5, Gemini-2.5, and Llama-3.3-as well as their corresponding HEART-enhanced versions. Clinical experts assessed each response in terms of accuracy, completeness, consistency, robustness, security, and overall quality. The integration with the HEART framework led to a significant improvement in the performance of all four LLMs across five key evaluation dimensions: accuracy, completeness, consistency, security, and robustness (all P < 0.05). The average overall quality scores for all models increased significantly: from 3.57 (SD 0.72) to 4.20 (SD 0.41) for Llama-3.3, from 3.92 (SD 0.70) to 4.38 (SD 0.42) for Claude-3.5, from 3.91 (SD 0.73) to 4.32 (SD 0.39) for ChatGPT-4o, and from 4.03 (SD 0.69) to 4.38 (SD 0.41) for Gemini-2.5 (all P < 0.001). This study highlights the importance of combining high-quality, domain-specific medical data with advanced artificial intelligence techniques to enhance accuracy and reduce misinformation in healthcare applications.

Pulmonary arterial hypertension (PAH) is a rare disease characterized by a progressive increase in pulmonary arterial pressure, leading to right heart failure. In clinical practice, reduced exercise tolerance is commonly observed in patients with PAH. Several studies have identified skeletal muscle abnormalities and muscle weakness as factors contributing to impaired exercise capacity in these patients. Recently, peak expiratory flow rate (PEFR) has been shown to correlate with skeletal muscle mass. Given that PEFR can be easily and noninvasively measured using respiratory function tests, we investigated the relationship between PEFR and prognosis in patients with PAH. We enrolled consecutive untreated patients diagnosed with PAH at Kagoshima University Hospital between July 2005 and July 2024. A total of 85 patients were included and divided into the preserved PEFR group and the reduced PEFR group. There were no significant differences in hemodynamic parameters between the two groups; however, the 6-minute walk distance was significantly shorter (p = 0.0062) in the reduced PEFR group. Kaplan-Meier analysis revealed that the cumulative event-free rate was significantly lower in the reduced PEFR group (Log-rank p = 0.0048). Reduced PEFR was independently associated with poorer outcomes after adjusting for age, plus each of right atrial pressure, cardiac index, and pulmonary vascular resistance. In conclusion, PEFR, a method for measuring skeletal muscle, was associated with poor prognosis in patients with PAH when assessed at the time of diagnosis. PEFR can be easily and repeatedly measured, making it potentially useful for prognostic prediction and exercise rehabilitation in these patients.

Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all cases of heart failure and is associated with poor outcomes. Large clinical trials have demonstrated that sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce hospitalizations for HFpEF and are now recommended as foundational therapy; these benefits have been authenticated in established HFpEF populations (EMPEROR-Preserved, DELIVER), whereas mechanistic and imaging studies have provided insights into the earlier pathogenesis of the disease. However, the precise mechanisms underlying their benefits in HFpEF remain incompletely understood. HFpEF represents a heterogeneous clinical syndrome encompassing multiple phenotypes, including obesity-related, amyloid, and congestion-predominant phenotypes. Among them, interstitial rather than intravascular fluid retention has emerged as a convergent mechanism particularly relevant to HFpEF in which congestion is the main symptom, driving myocardial stiffness, pulmonary congestion, and renal venous hypertension. Moreover, endothelial glycocalyx degradation and lymphatic dysfunction, often associated with comorbidities such as hypertension, diabetes, and obesity, further promote interstitial fluid accumulation, linking systemic inflammation and comorbidities to maladaptive cardiorenal interactions. Unlike conventional diuretics, SGLT2 inhibitors preferentially remove interstitial fluid while preserving plasma volume, potentially through enhanced lymphatic drainage and maintenance of capillary permeability, thereby improving diastolic function and alleviating pulmonary and renal congestion. However, although SGLT2 inhibitors alone provide sustained decongestion with good tolerability, their combination with loop or thiazide diuretics may result in greater interstitial fluid clearance and offer additional benefits in patients with overt congestion. Therefore, by targeting interstitial fluid retention-one of several key mechanisms contributing to HFpEF-SGLT2 inhibitors improve outcomes through integrated modulation of hemodynamic, renal, and molecular pathways. Targeting interstitial fluid retention and cardiorenal interactions in HFpEF: the role of SGLT2 inhibitors.

Backgrounds: The AFIRE (Atrial Fibrillation and Ischemic Events with Rivaroxaban in Patients with Stable Coronary Artery Disease) trial demonstrated that rivaroxaban monotherapy was non-inferior in efficacy and superior in safety compared to rivaroxaban plus single antiplatelet therapy in patients with atrial fibrillation (AF) and stable coronary artery disease (CAD). This study examined whether systolic blood pressure (SBP) affects clinical outcomes and modifies the impact of antithrombotic therapy.

Methods: In this post hoc analysis, participants were stratified based on median SBP at baseline: >126 mmHg (High SBP group, n = 1042) and ≤126 mmHg (Low SBP group, n = 1093). The primary efficacy endpoint was a composite of cardiovascular events and all-cause death. The primary safety endpoint was major bleeding.

Results: The mean SBP was 139 mmHg and 114 mmHg in the High and Low SBP groups, respectively. In the propensity score-matched cohort (n = 1684), the Low SBP group had a significantly higher incidence of the primary efficacy endpoint (hazard ratio [HR], 1.38; 95% confidence interval [CI], 1.01-1.88; p = 0.039), while the primary safety endpoint was comparable between groups. In the Low SBP group, rivaroxaban monotherapy was associated with lower risks of both the primary efficacy (HR, 0.60; 95% CI, 0.41-0.86; p = 0.006) and safety endpoints (HR, 0.40; 95% CI, 0.22-0.74; p = 0.003) compared with combination therapy, whereas no significant differences were observed in the High SBP group.

Conclusions: Lower SBP was associated with increased risk of cardiovascular events and all-cause death. Rivaroxaban monotherapy demonstrated more favorable efficacy and safety outcomes particularly patients with lower SBP.

Although previous studies reported that BP PRS is associated with CVD, it is less explored whether BP PRS and BP are jointly associated with CVD, especially among non-European populations. Therefore, we examined joint associations of BP control and BP polygenic risk score (PRS) with CVD mortality in a Japanese population. Data were obtained from the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study, the multi-centered cohort study with 14 study areas throughout Japan. Of which, we analyzed ~35,000 Japanese individuals (Mean age: 55 years old, Men: 44%) with measured BP data (11,242 and 23,904 participants in subgroup #1 and #2). We developed PRS for systolic blood pressure (SBP) and diastolic blood pressure (DBP) in each subgroup. Participants were followed up from the baseline survey (2005-2014) to the end of 2020. Not elevated BP was defined as SBP ≤ 140 mmHg or DBP ≤ 90 mmHg regardless of antihypertensive medications. During the follow-up period, a total of 381 CVD deaths were observed. Compared with not elevated BP, HRs (95% CI) of CVD mortality were 1.98 (1.37-2.88) for elevated SBP and 2.41 (1.66-3.49) for elevated DBP. Compared to not elevated BP in the lowest PRS tertile, HRs (95% CI) of CVD mortality in the highest PRS tertile were 2.28 (1.17-4.43) for SBP and 3.08 (1.61-5.91) for DBP even though BP was not elevated. These associations in the subgroup #1 were replicated in the subgroup #2. Our findings highlighted the importance of BP PRS to detect a hidden CVD risk strata in addition to laboratory BP measurements.

Preeclampsia comprises early-onset (EOPE) and late-onset (LOPE) subtypes with distinct etiologies, placental pathology, and severity, but cellular/metabolic drivers and early biomarkers remain unclear. We integrated placental single-cell RNA-seq, spatial transcriptomics, and spatial metabolomics from EOPE, LOPE, and matched controls, and performed maternal serum metabolomics in a prospective cohort of 199 pregnancies. The scRNA-seq identified 14 cell types; Hofbauer cells and trophoblasts resolved into 7 and 3 subclusters. EOPE placentas showed increased macrophages and extravillous trophoblasts, reduced oxygen-transporting Hofbauer subtypes (HB_1, HB_6), and trophoblasts with heightened HIF-1, VEGF, and IGF signaling. LOPE preserved cellular composition but exhibited stronger inflammatory transcriptional programs. Spatial analyses indicated disrupted oxygen transport in EOPE and perturbed interferon-γ signaling and exosome secretion in LOPE. Metabolically, trophoblasts and Hofbauer cells displayed subtype-specific lipid-transport defects and mitochondrial dysfunction. Three early-pregnancy serum metabolites-phosphatidylcholine PC(22:5/0:0), 3-hydroxybutyric acid, and L-allothreonine-robustly predicted EOPE (AUC > 0.85). This study delineates preeclampsia as a spectrum of placental immune-metabolic disorders. Hofbauer cells and trophoblasts undergo subtype-specific transcriptional and metabolic remodeling in EOPE vs LOPE. Multi-omics-guided, noninvasive biomarkers enable early EOPE risk prediction, informing timely detection and intervention.