Journal of Hypertension最新文献

Background: Increased activity of the sympathetic nervous system (SNS) is a critical factor in the pathophysiology of hypertension. Centrally acting sympatholytic agents (CASA) and renal denervation (RDN) represent two distinct therapeutic strategies targeting the SNS.

Aims: This study explored whether the blood pressure (BP)-lowering effect of RDN is influenced by the presence of CASAs.

Methods: Patients from the Global Symplicity Registry (GSR) were categorized into two groups based on whether or not their antihypertensive medication regimen prior to RDN included CASAs. Changes in systolic and diastolic 24-h ambulatory BP from baseline to 3-, 6, 12 and 24-month follow-up were compared between groups with crude and adjusted ANCOVAs.

Results: A total of 2712 patients had medication data available at baseline, of whom 1036 (38.2%) were on CASAs, and 1676 (61.8%) were not. Systolic 24-h ambulatory BP lowering at all time points after RDN was consistently more pronounced in the non-CASA compared to the CASA group (P < 0.001). DBP lowering was greater in the non-CASA group at 3- and 6-month follow-up, but not at later time points.

Conclusion: Patients not treated with CASAs prior to RDN demonstrated a more pronounced ambulatory SBP reduction over 24 months compared to those on CASA treatment. These findings corroborate the notion that the RDN-induced BP reduction is at least in part mediated via modulation of central sympathetic outflow. Even in the presence of CASAs, RDN still results in significant BP lowering, yet to a lesser degree. These findings have implications for managing patient expectations prior to RDN.

The regulation of blood pressure is closely linked to sympathetic activity. This retrospective study analyzed 142 hypertensive patients undergoing computed tomography (CT)-guided O 2 -O 3 neurolysis targeting intervertebral foramina or lumbar paravertebral ganglia for pain management. Results demonstrated significant reductions in both postoperative in-hospital blood pressure and office blood pressure during follow-up alongside decreased antihypertensive medication use. Notably, blood pressure reduction showed independence from pain relief but exhibited strong anatomical correlation with renal sympathetic innervation, specifically with the lower thoracic vertebral level (T9-T12) and the upper lumbar vertebral level (L1-L2). The findings suggest that modulation of thoracolumbar sympathetic pathways through minimally invasive gas neurolysis may represent a novel therapeutic strategy for hypertension management, potentially offering a targeted approach for renal sympathetic denervation. Further prospective studies are warranted to validate these observations.

Objective: The aim of this study was to identify which blood pressure (BP) measurement method - ambulatory (ABPM), home (HBPM), office (OBPM) - provides the highest accuracy according to the categorization of patients across different obesity assessment tools.

Methods: All participants performed ABPM, HBPM and OBPM. Participants were categorized based on BMI: underweight, normal, overweight, obese, waist circumference: as having normal waist circumference, increased and greatly increased, and waist to hip ratio: normal and increased.

Results: The study population consisted of 281 participants (39.9% men), 56.9 ± 15.8 years old. OBPM presented the best accuracy (78.9%), sensitivity (86%) and specificity (72.9%) in obese BMI, in greatly increased waist circumference (accuracy 79%, sensitivity 80.6% and specificity 77.1%) and increased waist to hip ratio (accuracy 78.4%, sensitivity 80.2% and specificity 76%), while the accuracy was reduced as BMI, waist circumference and waist to hip ratio were lowered. HBPM presented the best accuracy in overweight BMI (accuracy 75.8%, sensitivity 86%, specificity 58.8%) and in increased waist circumference (accuracy 81.5%, sensitivity 91.7%, specificity 73.3%), while the accuracy was reduced in the other categories. HBPM presents same accuracy, sensitivity and specificity in both waist to hip ratio categories.

Conclusion: This study shows a different accuracy of BP measurement methods across different categories of obesity assessment tools. OBPM emerges as an alternative to ABPM in patients with obesity, greatly increased waist circumference and increased waist to hip ratio, while HBPM in patients overweight or with increased waist circumference.

Refractory hypertension (RfH) is the most difficult-to-control form of hypertension and carries the highest cardiovascular risk. It is estimated to account for 0.5-1% of all forms of hypertension. Sleep apnea syndrome (OSA), defined as the repeated partial or complete interruption of the airway flow during sleep, is highly prevalent, with almost one billion people worldwide suffering from it. Both diseases share a pathophysiological mechanism: the hyperactivation of the sympathetic nervous system. In recent years, a clinical relationship between RfH and OSA has been demonstrated. 80-90% of patients with RfH suffer from OSA, which could partly explain the refractoriness to treatment. Treatment of OSA with continuous positive airway pressure (CPAP) significantly reduces blood pressure by 8-10 mmHg in patients with RfH.

Objective: Rarefaction in capillary density is a hallmark of hypertension-mediated microvascular damage. This study aimed to assess the association between clinically accessible inflammatory markers, including the systemic immune-inflammation index (SII), and retinal capillary density, as well as other indicators of microvascular damage.

Methods: We conducted a cross-sectional analysis of data from 132 consecutive patients with established primary hypertension at the Royal Perth Hospital's tertiary hypertension clinic. All patients underwent noninvasive optical coherence tomographic angiography (OCT-A) for the assessment of retinal capillary density in the foveal region (CDF) and blood sampling for inflammatory markers. We examined the association of the SII - calculated as the product of the neutrophil-lymphocyte ratio and platelet count - and its individual components with retinal capillary rarefaction and other markers of microvascular damage, such as the urinary albumin-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR). The results were adjusted for relevant co-variates, including age, sex, 24-h SBP, BMI, antihypertensive medications, lipid levels, and diabetes status.

Results: Retinal capillary rarefaction was associated with increased white cell count, particularly neutrophils, and the SII. Through predictive margin analysis, an optimal cut-off value of 600 x 10 9 /l for SII was determined for median CDF of 34.1 mm 2 . The analysis showed a reduction in CDF of 1.3 mm 2 for every 250 x 10 9 /l increase in SII. Additionally, higher SII levels (≥ 600 x 10 9 /l) were associated with elevated high-sensitivity C-reactive protein (hs-CRP) levels and markers of microvascular damage, such as increased UACR and reduced eGFR.

Conclusion: In patients with primary hypertension, SII and related inflammatory markers were associated with retinal rarefaction and renal indices of microvascular damage. SII may serve as a useful clinical marker of microvascular damage in the retinal and renal vascular bed.

Despite guidelines discouragement, antihypertensive monotherapy (AH-mono) remains widely used. This study assessed AH-mono prevalence and blood pressure control rates based on office and home measurements (OBP/HBPM) using contemporary targets (<130/80 mmHg). Three distinct cohorts undergoing OBP/HBPM assessments between July 2018 and July 2024 were analyzed: cohort 1 ( n  = 63 164) included treated patients with a single OBP/HBPM measurement; cohort 2 ( n  = 5676) comprised treated patients with two OBP/HBPM assessments at different time points; and cohort 3 ( n  = 974) involved individuals with OBP/HBPM measurements before and after initiating antihypertensive therapy. The prevalence of AH-mono was 42.7% in cohort 1, 36.6 and 32.4% in cohort 2, and 50.7% in cohort 3. Among those receiving AH-mono, OBP/HBPM control rates were 8.5% in cohort 1, 6.7 and 7.3% in Cohort 2, and 7.7% in cohort 3. These real-world findings highlight the persistent high prevalence of AH-mono despite its limited efficacy, with less than 10% of patients achieving blood pressure control.

Background and purpose: Myocardial fibrosis is a key pathological feature of hypertension, closely associated with mitochondrial dysfunction and calcium overload. The calcium-sensing receptor (CaSR) has emerged as a potential mediator in this process, but its mechanistic role remains unclear. This study aimed to investigate whether Calhex231, a selective CaSR antagonist, could attenuate myocardial fibrosis in Dahl salt-sensitive (SS) rats by restoring mitochondrial dynamics and intracellular calcium homeostasis.

Methods: Hypertension was induced in Dahl SS rats using an 8% NaCl diet. From week 5, rats were treated with Calhex231 (10 μmol/kg/day) for 6 weeks. In vitro, cardiac fibroblasts (CFs) were stimulated with TGF-β1 (10 ng/ml) and treated with either Calhex231 or Mdivi-1 (a Drp1 inhibitor). Assessments included echocardiography, histological staining (Masson, HE), immunohistochemistry, Western blotting, and fluorescence-based analyses of mitochondrial membrane potential (JC-1), oxidative stress (Dihydroethidium, SOD1/2), intracellular Ca2+ (Fluo-4 AM), and fibrosis markers (α-SMA, Collagen I/III, MMP-2/9).

Results: Calhex231 significantly reduced blood pressure and myocardial fibrosis in hypertensive rats, accompanied by improved cardiac structure and diastolic function. Mechanistically, Calhex231 suppressed mitochondrial fission proteins (Drp1, Fis1) and upregulated fusion proteins (MFN2, OPA1), restoring mitochondrial homeostasis. In TGF-β1-stimulated CFs, Calhex231 alleviated calcium overload, preserved mitochondrial membrane potential, reduced ROS production, and downregulated fibrotic markers. Similar protective effects were observed with Mdivi-1, highlighting the involvement of Drp1-mediated fission in CaSR-induced fibrosis.

Conclusion: Inhibition of CaSR with Calhex231 exerts cardioprotective effects by suppressing Drp1-dependent mitochondrial fission, thereby mitigating oxidative stress and calcium overload. These findings support CaSR as a promising therapeutic target for myocardial fibrosis in salt-sensitive hypertension.