People living with HIV have an increased risk of cardiovascular disease, but data on the development and consequences of hypertension remain limited. Using data from REPRIEVE, a global randomised trial of pitavastatin for primary cardiovascular prevention among people with HIV, we evaluated whether pitavastatin reduces the incidence of hypertension among participants without hypertension at baseline and whether incident hypertension is associated with subsequent major adverse cardiovascular events (MACE). We conducted a prespecified secondary analysis of participants without evidence of hypertension at REPRIEVE entry (baseline). REPRIEVE (NCT02344290) was a global, randomised, double-blind, placebo-controlled trial that enrolled adults with HIV aged 40-75 years at low-to-moderate atherosclerotic cardiovascular risk, receiving stable antiretroviral therapy. The primary outcome in this secondary analysis was incident hypertension based on clinical diagnosis according to standard criteria. Included participants were those without hypertension at baseline; excluded were those with documented hypertension, antihypertensive treatment use, systolic blood pressure of 140 mm Hg or higher, or diastolic blood pressure of 90 mm Hg or higher. The association between incident hypertension and a secondary outcome of MACE was evaluated in a time-updated analysis. Analyses used both Cox and Fine-Gray proportional hazards models and Poisson regression. Of 7769 participants enrolled in REPRIEVE, 4989 (64%) without hypertension at baseline were included (2496 assigned to pitavastatin and 2493 to placebo) in this secondary analysis. The median age was 49 years (IQR 45-54); 1464 (29%) were women and 3525 (71%) men; and the median systolic and diastolic blood pressures at baseline were 102 mm Hg and 76 mm Hg, respectively. Over a median follow-up of 5·0 years (IQR 4·4-5·8), 668 (13%) participants developed hypertension. Participants randomly assigned to pitavastatin showed a modestly lower incidence of hypertension (24·7 per 1000 person-years vs 29·6 per 1000 person-years), corresponding to a 17% relative risk reduction (cause-specific hazard ratio [HR] 0·83, 95% CI 0·71-0·97; p=0·017). Risk factors of incident hypertension included old age, high BMI, metabolic syndrome, reduced estimated glomerular filtration rate (eGFR), and Black race in high-income regions. Among participants with incident hypertension, 581 (87%) initiated antihypertensive therapy. Of 213 who initiated antihypertensive therapy after diagnosis of hypertension, 159 (74·6%) were controlled 4 years after diagnosis. Incident hypertension was associated with a higher risk of MACE during follow-up (subdistribution HR 2·16, 95% CI 1·32-3·52) in modelling adjusted for baseline cardiovascular risk score. These findings suggest additional cardiovascular benefits of pitavastatin on hypertension among people with HIV targeted for primary cardiovascular prevention. National Institutes of Health, Kowa Pharmaceuticals America, Gilead Sciences, ViiV Healthcare, Instituto de Salud Carlos III, and the European Regional Development Fund.
Although an unhealthy lifestyle is an established risk factor for hypertension, the underlying association through this effect is not fully delineated. This study aimed to examine the potential mediating role of the TyG index in the association between lifestyle and hypertension. A cross-sectional study was analyzed among 8,201 residents of Jilin Province. A lifestyle risk score was derived from five lifestyle factors. The TyG index was calculated using fasting blood glucose and triglyceride levels. Hypertension was defined by the guidelines of the WHO and blood pressure measurements. The associations were examined using logistic regression and mediation analyses, with sensitivity and subgroup analyses employed to test the robustness. The study included 8,201 participants (37.8% with hypertension). Each 1-point increase in lifestyle risk score raised hypertension odds (OR 1.25, 95% CI 1.20-1.31). Mediation analysis showed TyG accounted for 39.8% of the association. All sensitivity analyses demonstrated robustness of the findings. Subgroup analysis revealed that the mediating association was statistically significant across all demographic groups, with significant effect modification by age for the TyG-hypertension association (P = 0.0007). The TyG index plays a significant mediating role in the association between lifestyle and hypertension (significant for all age and gender subgroups). Notably, age significantly modifies the TyG-hypertension association, suggesting that the link between insulin resistance and hypertension may be stronger in adults aged ≤ 60 years. This finding implies that interventions targeting insulin resistance could have differential effects on hypertension prevention across age groups.
Hypertension is common among patients with type 2 diabetes mellitus (T2DM) and represents a major contributor to cardiovascular and renal morbidity. Real-world data from primary care are essential to characterise associated clinical profiles and cardiometabolic multimorbidity patterns in routine clinical practice. To assess the prevalence of hypertension among patients with T2DM managed in primary care, to characterise associated clinical profiles, and to explore sex-related differences using real-world data. A cross-sectional study was conducted including 680 adults with T2DM receiving routine care in primary care settings. Clinical, sociodemographic and laboratory data were obtained from electronic health records, direct clinical assessment, and structured patient interviews. Hypertension was defined as a previously recorded clinical diagnosis, current antihypertensive treatment, or blood pressure ≥ 140/90 mmHg. Comparisons were performed according to sex. Factors independently associated with hypertension were analysed using bivariate analyses and multivariable logistic regression models adjusted for age, sex, duration of T2DM, pharmacologically treated dyslipidaemia, and established cardiovascular disease. The mean age of participants was 69.8 ± 13.3 years and the mean duration of diabetes was 9.9 ± 4.6 years; 52.1% were men. Overall hypertension prevalence was 84.3%, with no significant difference between men (85.9%) and women (82.5%). Hypertension prevalence increased with age in both sexes. Women had lower educational and socioeconomic levels, higher abdominal obesity, and higher lipid concentrations, whereas men showed higher fasting glucose, serum creatinine, and markers of renal damage. In multivariable analysis, hypertension was independently associated with older age (OR 1.04 per year; 95% CI 1.02-1.06), pharmacologically treated dyslipidaemia (OR 1.83; 95% CI 1.17-2.86), established cardiovascular disease (OR 2.03; 95% CI 1.16-3.55), and longer duration of T2DM (OR 1.06 per year; 95% CI 1.00-1.12). Sex was not independently associated with hypertension after adjustment. Hypertension was common among patients with T2DM in primary care and was associated with older age, longer diabetes duration, and established cardiovascular disease. Sex-related differences in clinical profiles were observed but should be interpreted as descriptive. This cross-sectional secondary analysis has limitations, including the lack of blood pressure control data and the potential for residual confounding.
Hypertension increases the risk of cardiovascular diseases and is prevalent worldwide, especially in low- to middle-income countries. Globally, it is poorly controlled, especially in Sub-Saharan Africa, and patients experience several challenges in adhering to recommended interventions. The study aimed at exploring and describing the support needs expressed by patients with hypertension in an urban primary care setting in Ghana to inform the development of a psychoeducational programme to support the management of hypertension. A qualitative descriptive design was employed in this study. Face-to-face interviews were conducted using a semi-structured interview guide. Thirty-five participants were purposively sampled. Each interview lasted for 30-60 min until data saturation was achieved. Inductive content analysis was used to analyse the data. Ethics committee approval was secured for this study. Four main themes and ten sub-themes emerged from the study. The main themes: (i) health information needs from healthcare providers, (ii) lifestyle modifications, (iii) Patient self-care, and (iv) psychosocial support. Sub-themes include blood pressure monitoring and interpretation, the mechanism of medications, side effects of medications, complications of hypertension, dietary modifications, stress management, the importance of exercise, medication adherence, attending regular checkups, and emotional and psychological support. The findings identify patient-expressed needs that can guide the design of future psychoeducational interventions for hypertension management.
Hypertension is a major global public health challenge, and effective management of antihypertensive treatment response is crucial. This study aimed to analyze the demographic, clinical, and lifestyle factors influencing treatment response in hypertensive patients receiving Valsartan monotherapy or Valsartan/Hydrochlorothiazide (HCTZ) combination therapy. This prospective cohort study included 354 adult patients with hypertension who were on stable antihypertensive therapy for at least 6 months prior to enrollment and were initiated on or switched to Valsartan monotherapy (80 mg) or Valsartan/HCTZ combination therapy (80/12.5 mg or 160/12.5 mg) based on clinical indication. Baseline blood pressure inclusion criteria were 140-179 mmHg systolic and/or 90-109 mmHg diastolic. Demographic, clinical, and lifestyle data were collected. The primary outcome was achievement of target blood pressure (< 140/90 mmHg) after 3 weeks of treatment; the secondary outcome was reduction in systolic (SBP) and diastolic (DBP) blood pressure. Statistical analysis included repeated measures ANOVA, multivariable logistic regression, and post-hoc comparisons with Bonferroni correction. The sample consisted of 58.0% females and 42.0% males. Baseline mean SBP was 157.50 ± 17.23 mmHg and DBP was 103.23 ± 10.17 mmHg. After three weeks of treatment, mean SBP decreased to 131.44 ± 20.40 mmHg and mean DBP to 85.08 ± 12.54 mmHg (p < 0.001). Target BP achievement at Week 3 was 82.6% for Valsartan 80 mg, 70.5% for Valsartan/HCTZ 80/12.5 mg, and 56.4% for Valsartan/HCTZ 160/12.5 mg. These unadjusted rates reflect baseline differences in hypertension severity and comorbidity burden rather than differential regimen efficacy. Younger age, shorter hypertension duration, and absence of diabetes were independently associated with better treatment response in multivariable analysis. Younger age and shorter disease duration are key predictors of successful initial blood pressure control with Valsartan-based therapy in this short-term assessment. Longer-term studies are needed to confirm whether these early predictors translate to sustained blood pressure control and reduced cardiovascular events. Treatment should be individualized based on patient age, comorbidity profile, and duration of hypertension, with dose adjustment as needed to achieve optimal outcomes.
Hypertension is a major global health concern and a leading risk factor for cardiovascular diseases, including stroke, myocardial infarction, and heart failure. A hallmark of hypertension is elevated total peripheral vascular resistance, often driven by sustained and abnormal vasoconstriction. Calcium ions (Ca²⁺) play a central role in vascular smooth muscle cell (VSMC) contraction, and their intracellular concentration is tightly regulated by multiple signaling pathways. Among these, the inositol 1,4,5-trisphosphate receptor (IP3R) and the transient receptor potential canonical type 3 (TRPC3) channel are critical mediators of Ca²⁺ signaling. IP3R activation triggers Ca²⁺ release from the endoplasmic reticulum, while TRPC3 channels facilitate Ca²⁺ and Na⁺ influx across the plasma membrane. Several studies have shown that both IP3Rs and TRPC3 channels are upregulated in hypertensive animal models. Human studies have also demonstrated elevated TRPC3 expression in the context of pulmonary arterial hypertension (PAH). This review provides a comprehensive overview of the structural domains and membrane microdomains that facilitate IP3R-TRPC3 coupling and Ca²⁺ influx. IP₃ and endothelin-1 stimulate TRPC3 channels and promote their molecular coupling to IP3Rs, leading to activation of nonselective cation currents in artery myocytes. Increased expression and/or activity of IP3Rs and TRPC3 channels amplifies this signaling, contributing to the increased vascular tone characteristic of the hypertensive state. Understanding the molecular interplay between IP3Rs and TRPC3 channels offers new insight into the dysregulated Ca²⁺ signaling underlying hypertension. Targeting this coupling mechanism may represent a novel therapeutic strategy to restore vascular homeostasis and reduce blood pressure in affected individuals.
Portopulmonary hypertension (PoPH) may coexist with hepatopulmonary syndrome (HPS), a condition characterized by intrapulmonary vascular dilatations (IPVDs) and hypoxemia. While pulmonary arterial hypertension (PAH) therapies are commonly used to treat PoPH, their effects on gas exchange remain insufficiently characterized. What are the effects of pulmonary arterial hypertension (PAH)-specific therapies on gas exchange and the development of IPVDs in patients with PoPH? A retrospective cohort of PoPH patients was used to assess changes in the alveolar-arterial oxygen gradient (A-aDO2) following initiation of PAH therapy. A prospective cohort underwent systematic screening for IPVDs to assess their prevalence at baseline and incidence during treatment. The retrospective cohort included 107 patients (70% male, mean age 55 ± 8 years) with a baseline mean A-aDO2 of 37.1 ± 13.0 mmHg. Eighty-three patients received initial oral monotherapy and 24 dual oral therapy. After a median follow-up of 4 months, A-aDO2 remained stable overall (mean change -0.92 mmHg; 95% CI -3.2 to +1.3; P=0.42), with substantial interindividual variability. Changes in A-aDO2 were not associated with variation in 6-minute walk distance or WHO/NYHA functional class. Baseline A-aDO2 and cardiac output (CO) were independently associated with subsequent improvement in A-aDO2. Treatment-induced reductions in mPAP and increases in CO correlated with greater A-aDO2 improvement. In the prospective cohort (n=28), HPS was present in 39% of newly diagnosed PoPH patients. Baseline IPVDs did not influence A-aDO2 evolution; however, 4 patients developed new IPVDs within the first year after PAH therapy initiation. PAH therapy was not associated with overall deterioration in gas exchange in PoPH, despite substantial individual variability. Changes in oxygenation were linked to baseline and treatment-induced hemodynamic parameters. The development of new IPVDs in some patients warrants careful longitudinal monitoring.
Idiopathic intracranial hypertension (IIH) induces papilledema and can result in progressive visual dysfunction and retinal vascular changes. The purpose of the current study was to determine cross-sectional and longitudinal associations between papilledema severity and retinal vessel tortuosity (RVT) in IIH. Images from 24 eyes of 15 patients diagnosed with papilledema were acquired at two visits. Papilledema severity was graded by Frisen score (FS). Images were analyzed to determine RVT in arteries and veins within the peripapillary region using the first-order derivative method. Inter-visit differences in FS (ΔFS) and RVT (ΔRVT) were calculated. Generalized estimating equation models determined associations of FS and ΔFS with RVT and ΔRVT, respectively. Based on compiled arterial or venous RVT data from both visits, there was no significant association between RVT and FS (p = 0.89), whereas venous RVT (0.31 ± 0.02; N = 48) was significantly higher than arterial RVT (0.24 ± 0.01; N = 48) (p = 0.03). Compared to the ΔFS = 0 group, venous ΔRVT was higher in the ΔFS = 3 group (β = 0.05, p = 0.005), while arterial ΔRVT was higher in ΔFS ≥ 1 (β ≥ 0.04; p ≤ 0.04). The finding of an association between improvement in papilledema and reduction in RVT shows promise for vessel tortuosity as a biomarker for monitoring disease progression and response to therapeutic interventions, as well as advancing knowledge of retinal vascular changes due to papilledema. WHAT IS KNOWN : Idiopathic intracranial hypertension can result in papilledema and visual dysfunction. Papilledema is linked to changes in retinal vascular morphology. Improvement in papilledema severity is associated with a reduction in retinal vessel tortuosity. Retinal vessel tortuosity shows promise as a biomarker for diagnosis and therapeutic intervention for papilledema and intracranial hypertension.
There is increasing recognition of the importance of left ventricular (LV) assessment in pulmonary arterial hypertension (PAH). Hemodynamic patterns derived from hemodynamic force (HDF) analysis is an approach to evaluate hemodynamic patterns and myocardial dysfunction. However, its prognostic value with PAH remains unclear. PAH participants who underwent cardiac magnetic resonance (CMR) between January 2015 and July 2023 were prospectively and consecutively enrolled. LV HDF analysis was performed on the 2-, 3-, and 4-chamber long axis view. The primary endpoint was all-cause mortality. Cox regression analysis and Kaplan-Meier survival analysis were performed to identify the association between parameters and outcomes. The incremental prognostic value of hemodynamic pattern and CMR scores were assessed using χ2 test, net reclassification improvement (NRI) and integrated discrimination improvement (IDI). There were 311 participants (mean age, 38 ± 14 years; 87 men) evaluated. During a median follow-up of 38 months (interquartile range, 16-54 months), 55 participants reached the primary endpoint. Full cardiac cycle (FCC) and diastolic deceleration impulse (DDI) HDF ratios, but not systolic ejection impulse, were significantly lower in PAH patients compared to healthy controls (P= 0.003 and P=0.009, respectively). In multivariable Cox regression analysis, DDI HDF ratios were independent predictors of the primary endpoint in PAH patients and CHD-PAH subgroup (hazard ratio [HR], 0.83, [95% CI: 0.72, 0.96; P= 0.009]; HR, 0.74, [95% CI: 0.56, 0.97; P= 0.03]). Adding the DDI HDF ratio to established clinical models significantly improved risk classification, yielding a continuous NRI of 0.27 (P=0.01) and an IDI of 0.01 (P=0.03) for the overall cohort, with consistent improvements in the CHD-PAH subgroup (NRI 0.30, P=0.04; IDI 0.02, P=0.03). LV hemodynamic patterns derived from CMR-based DDI HDF ratio were identified as independent prognostic predictor in pulmonary hypertension, providing incremental prognostic value beyond established risk scores. This study was registered in the Chinese clinical trial registry (ChiCTR1800019314 and ChiCTR1900025518). URL: https://www.chictr.org.cn/.
Portal hypertension (PH) is one of the major complications of liver cirrhosis, traditionally assessed using invasive methods such as the hepatic venous pressure gradient (HVPG). Soluble endoglin (sENG), a marker of endothelial dysfunction and fibrosis, has been proposed as a non-invasive biomarker of various liver diseases. This study aimed to evaluate serum sENG concentrations in cirrhotic patients with PH and investigate its relationship with PH severity, alcohol consumption, and smoking. Serum concentrations of sENG were measured in clinically well-examined patients with liver cirrhosis (n = 60, age range 24-82 years) with PH classified as mild, moderate, or severe according to the HVPG values measured invasively using the classical wedge technique. sENG concentrations were also compared to healthy controls (n = 54). Liver enzyme activities, alcohol consumption history, and smoking habits were also recorded to assess their association with sENG. sENG concentrations were significantly higher in patients with PH compared to healthy controls (6.31; 5.14-7.30 vs. 3.70; 3.24-4.20 ng/mL, p < 0.001) but did not correlate with the severity of HVPG-diagnosed portal hypertension. A moderately significant correlation was observed between sENG concentrations and GGT activities (p < 0.001). Alcohol consumption, but not smoking, was associated with higher serum sENG concentrations (p < 0.01). Based on our results, sENG appears to be a non-invasive marker of endothelial dysfunction/fibrosis in cirrhotic patients with PH, particularly in alcohol-related liver disease. Although it does not reflect PH severity and thus cannot be used as a diagnostic tool, it has the potential for early disease detection and risk prediction as a screening component in non-invasive approaches in clinical hepatology.
High-altitude pulmonary hypertension (HAPH), classified as Group 3 pulmonary hypertension, is a significant threat to the health of high-altitude populations. The scarcity of studies in diverse populations has become a research bottleneck, limiting diagnostic and therapeutic advances. In this first proteomic study focusing on the eastern Pamir Plateau (Kizilsu Kyrgyz Autonomous Prefecture, Xinjiang), plasma samples were analyzed using data-independent acquisition (DIA) mass spectrometry. Differential expression analysis in parallel with weighted gene co-expression network analysis was performed to identify core pathways and hub proteins, and gene set enrichment analysis was used for quality assessment. Integrative analysis of the two methods was used to select candidates for validation by enzyme-linked immunosorbent assay (ELISA) in an independent cohort. Among > 1400 detected proteins, 123 were differentially expressed and 45 were identified as hub proteins significantly associated with HAPH. Extracellular matrix (ECM) remodeling- and angiogenesis-related proteins were upregulated, whereas proteins related to enzyme activity, iron metabolism, and inflammatory responses were downregulated. Integrative analysis identified 23 core proteins, with ECM-receptor interaction and TGF-β/Smad signaling identified as key pathways. ELISA confirmed that plasma levels of THBS2, LOXL1, and POSTN were significantly elevated in patients with HAPH (P < 0.05). Among these, THBS2 and LOXL1 levels were positively correlated with mPAP (THBS2: r = 0.389, 95% CI: 0.034-0.657, P = 0.033; LOXL1: r = 0.457, 95% CI: 0.115-0.701, P = 0.011). ECM remodeling is closely associated with HAPH in this indigenous high-altitude population. THBS2, LOXL1, and POSTN show potential as biomarkers and therapeutic targets.
Children with congenital heart disease (CHD) are at increased baseline cardiovascular (CV) risk due to their structural heart disease and social determinants of health may further increase their CV risk. The Child Opportunity Index (COI) is a measure of neighborhood conditions and is associated with cardiometabolic risk in children. However, the impact of COI on children with CHD and associated cardiometabolic risk factors has not been well described. Patients aged 13-17 years with echocardiogram data between 2012 and 2019 were reviewed. COI scores were calculated using geolocation data. Patients were classified into state-normed COI groups into Very Low, Low, Moderate, High, and Very High opportunity groups. Prevalence of obesity, hypertension, and left ventricular hypertrophy (LVH) were determined. A total of 768 patients (mean age 15.49 ± 1.46 years, 57% male (437/768) were included. A high proportion of patients were in the Very Low and Low COI groups (37.5%). There were significant differences in obesity prevalence between COI groups (X2 = 18.52, df = 4, p < 0.001) with the Low group having the highest prevalence (26.4%). There was not a significant difference in hypertension prevalence between groups. There were significant differences in LVH prevalence between groups (X2 = 11.43, df = 4, p = 0.02) with the highest prevalence in the Low COI group (32.3%). Adolescents with CHD had significant differences in prevalence of obesity and LVH by COI with higher prevalence in the more adverse COI groups. This highlights the importance of considering SDoH when risk stratifying children with CHD.
Idiopathic pulmonary arterial hypertension (IPAH) is characterized by irreversible pulmonary vascular remodeling. This pathological remodeling is mainly driven by the aberrant proliferation and migration of pulmonary artery smooth muscle cells (PASMCs). However, the molecular mechanisms underlying these dysfunctions remain incompletely understood. In this study, we integrated single-cell RNA sequencing (scRNA-seq) analysis with in vivo and in vitro validation to identify key driver genes implicated in IPAH. The GSE169471 dataset was acquired from the Gene Expression Omnibus and processed via quality control, clustering, and cell subtype annotation. Further analyses identified dominant cell subtypes, cell-cell communication networks, and differentially expressed genes (DEGs). Hub genes were then screened using multiple bioinformatic algorithms. The selected hub genes were validated in pulmonary arteries from a monocrotaline (MCT)-induced PAH rat model via qPCR and Western blotting. Furthermore, siRNA-mediated knockdown was conducted to investigate the effects of hub gene silencing on HMGB1-induced PASMC proliferation and migration. Our results revealed that SMCs were the dominant communicating cell subtype and were significantly increased in IPAH. A total of 63 upregulated DEGs were identified, primarily enriched in biological processes such as extracellular matrix organization and signaling pathways, including the focal adhesion pathway. Four hub genes (COL1A1, MYL9, COL1A2, and TPM2) were identified, with significantly increased expression observed in the pulmonary arteries of PAH rats. Subsequently, silencing these genes notably reduced HMGB1-induced PASMC proliferation and migration. These findings provide novel insights into the molecular mechanisms of IPAH and highlight these hub genes as potential therapeutic targets.
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Primary aldosteronism (PA) is now recognized as a prevalent disorder that contributes to hypertension and cardiovascular disease. Updated Endocrine Society guidelines recommend universal screening for primary aldosteronism among people with hypertension using a streamlined approach to diagnosis that emphasizes the recognition of renin-independent aldosterone production and de-emphasizes the use of aldosterone suppression tests. Emerging molecular imaging modalities may further transform PA subtyping. Treatment options and efficacy for primary aldosteronism continue to expand, with surgery remaining the gold standard for lateralizing PA, while adrenal or adrenal arterial ablation, steroidal and nonsteroidal mineralocorticoid receptor antagonists, and aldosterone synthase inhibitors offer promising alternatives.
Pulmonary hypertension-induced right ventricular (RV) overload can result in right atrial (RA) remodeling and tricuspid regurgitation (TR), which in turn affects RV function and negatively impacts patient prognosis. This study aimed to clarify the prognostic significance of RA function and TR in patients with chronic thromboembolic pulmonary hypertension (CTEPH). For this retrospective analysis of 97 patients with CTEPH who underwent balloon pulmonary angioplasty (BPA), clinical, hemodynamic, and echocardiographic data were acquired before the first BPA and after the final BPA. The composite end point was hospitalization due to right heart failure and all-cause death. After BPA, patients experienced significant increases in RA reservoir strain (RASr, 26.7 ± 9.1% vs. 35.2 ± 11.3%, P<.001) and conduit strain (15.0[9.6] % vs. 22.6[9.6] %, P<.001), with no significant change in RA contraction strain. TR was significantly improved after BPA, decreasing from 49.5% to 22.7% in patients with significant TR (P<.001). Over a mean follow-up of 24.7 ± 12.4 months, 22 patients met the composite end point. On multivariate Cox regression analysis, Right atrial reservoir strain (RASr) was independently associated with composite clinical outcomes(P=.012). Patients with post-BPA RASr ≥ 29.85% exhibited superior event-free survival compared to those with lower values. Right atrial reservoir and conduit functions were impaired in CTEPH patients and showed significant improvement following BPA. Post-BPA RASr ≥ 29.85% demonstrated an independent association with long-term clinical outcomes. These findings support the inclusion of RA strain in postoperative assessments and long-term follow-up of CTEPH patients treated with BPA. In this study, 2D-speckle tracking echocardiography can be used to better monitor right heart status of patients. To some extent, it can help clinicians to provide better treatment for patients and improve the quality of life of patients.
Mechanotransduction is a process converting mechanical cues into electrochemical signals. Piezo1, a mechanically sensitive cation channel protein, is widely distributed in non-sensory cells of mammals, particularly highly expressed in the endothelial cells (ECs). Piezo1 is implicated in various physiological activities, including the regulation of vascular tone, angiogenesis, and maintenance of the endothelial barrier. Under pathological mechanical forces, Piezo1 is involved in the development of endothelial dysfunction-related diseases, including atherosclerosis (AS), hypertension, heart failure (HF), myocardial infarction (MI), pulmonary arterial hypertension (PAH), acute respiratory distress syndrome (ARDS), and diabetes mellitus (DM). In this review, we focus on the underlying mechanisms of Piezo1 in different endothelial dysfunction-related diseases, highlighting its roles in regulating endothelial function. Moreover, we present some activators and inhibitors targeting Piezo1, and discuss their different effects in distinct contexts. Overall, targeting Piezo1 may open a novel avenue of therapeutic tactic for endothelial dysfunction-related diseases.
Arrhythmia recurrence after atrial fibrillation (AF) catheter ablation remains a substantial clinical challenge, but risk factors of arrhythmia recurrence are not well defined. This study aimed to elucidate baseline clinical risk factors for post-ablation recurrence and variations by AF phenotype and study heterogeneity. We systematically searched eight databases for prospective cohort studies assessing associations between clinical risk factors and post-ablation arrhythmia recurrence up to 31 December 2025. Study quality was evaluated using Newcastle-Ottawa scale. Multivariable-adjusted hazard ratios (aHRs) were pooled through random-effects meta-analyses with subgroup, meta-regression, and sensitivity analyses. Among 152 studies involving 49,919 patients, 16 clinical risk factors were identified. In primary meta-analysis pooling aHRs, the strongest associations were observed for smoking (aHR:2.15 [1.49-3.10)]), periodontitis (aHR:2.04 [1.48-2.83]), metabolic syndrome (aHR:1.71 [1.12-2.62]), sleep apnea (aHR:1.65 [1.31-2.09]) and persistent AF (aHR:1.64 [1.53-1.76]), followed by chronic kidney disease, alcohol consumption, overweight/ obesity, diabetes mellitus, female sex, hypertension, AF history, left atrial enlargement and impaired left ventricular ejection fraction. Untreated sleep apnea (aHR:2.41 [1.51-3.86]) and uncontrolled hypertension (aHR:1.67 [1.12-2.40]) conferred heightened risks. Sensitivity analyses pooling adjusted odds ratios (aORs) additionally identified depression (aOR:2.86 [1.51-5.41]), anxiety (aOR:2.54 [1.59-4.04]). Subgroup analyses revealed no difference across AF phenotypes. Meta-regression identified ablation modality as a significant moderator for AF history, and geographic region for female sex, heart failure and diabetes. Expanded pre-ablation risk profiles with consistent effect across AF phenotypes substantiate personalized risk stratification for ablation candidacy and pre-procedural optimization.