American Journal of Hypertension最新文献

Endothelial cells (ECs) are a highly specialized and heterogeneous population that plays a fundamental role in maintaining vascular homeostasis, immune regulation, and blood flow control. Beyond serving as a physical barrier, ECs exhibit remarkable plasticity, undergoing phenotypic transitions, including endothelial-to-mesenchymal (EndMT), endothelial-to-hematopoietic (EndHT), endothelial-to-osteoblast (EndOT) and endothelial-to-immune-cell-like (EndICLT). These transitions allow ECs to adapt to developmental, physiological, and pathological conditions. Advances in single-cell RNA sequencing (scRNA-seq), and associated technologies, have provided deeper insights into the molecular diversity of ECs across different vascular beds and stages of development, revealing their transcriptional heterogeneity and specialized functions. For example, ECs within the aortic arch display distinct phenotypic variations depending on their location, reflecting adaptations to regional differences in blood flow and shear stress. Activated EndMT has been implicated in the progression of various cardiovascular diseases, including hypertension, atherosclerosis, and vascular malformations by contributing to endothelial dysfunction, vascular wall inflammation, and remodeling. Recent therapeutic approaches aim to mitigate EndMT-associated vascular damage through interventions such as endothelial reprogramming, statins, and autophagy enhancers. Partial reprogramming of ECs has shown promise in restoring endothelial function, reducing vascular stiffness, and lowering blood pressure in hypertensive models. Understanding the complexity of EC heterogeneity and plasticity is critical for developing targeted therapies to prevent and treat cardiovascular diseases. By leveraging emerging genomic technologies and reprogramming strategies, future research may offer novel regenerative medicine approaches to restore vascular health and improve clinical outcomes for patients with cardiovascular diseases.

Background: The objective of our case-control study was to evaluate the determinants of childhood cardio-vagal baroreflex failure and exaggerated orthostatic pressor response, which are risk factors for subsequent hypertension.

Methods: Four groups of children were matched for sex and age: 12 with congenital central hypoventilation syndrome (autonomic nervous system dysfunction), 12 with chronic kidney disease (frequently abnormal blood pressure [BP]), 12 with sickle cell disease (frequently abnormal orthostatic BP), and 24 control children (preterm birth with normal BP). The children underwent tonometry evaluation (aortic systolic BP) and continuous BP and ECG measurements in supine and standing positions, allowing ambulatory BP monitoring and the computation of heart rate variability indices, baroreflex sensitivity (BRS), and orthostatic systolic BP response.

Results: Supine and standing BRS correlated significantly with aortic systolic BP (ρ= -0.34, ρ= -0.52, respectively), daytime systolic BP (ρ= -0.33, ρ= -0.54, respectively), LF power in similar body positions (supine: ρ= 0.68, standing: ρ= 0.65), and HF power (ρ= 0.78, ρ= 0.76, respectively). Orthostatic BP response correlated significantly with standing BRS (ρ= -0.38) and standing HFnu (ρ= -0.46). In multivariate analyses, only supine and standing HF power remained independently associated with the respective BRS, while standing HFnu and standing BRS were independently associated with the orthostatic pressor response.

Conclusions: Defective parasympathetic modulation's detrimental effect on baroreflex sensitivity and the orthostatic pressor response in childhood is evident, regardless of the underlying pathology.

Introduction: Evidence on left ventricular (LV) mechanics, assessed by speckle tracking echocardiography (STE), in children and adolescents with elevated blood pressure (BP)/hypertension is scanty.

Aim: The aim of the present meta-analysis was to provide an updated information on LV systolic function phenotyped by global longitudinal strain (GLS) and LV ejection fraction (LVEF) in the setting of pediatric hypertension.

Methods: Following the PRISMA guidelines, systematic searches were conducted across bibliographic databases (Pub-Med, OVID, EMBASE and Cochrane Library) to identify eligible studies from inception up to November 30th 2024. Clinical studies reporting data on LV mechanics in pediatric hypertension and controls were included. The statistical difference of the echocardiographic variables of interest between groups such as LVEF and GLS was calculated by standardized mean difference (SMD) with 95% confidence interval (CI) using random-effects models.

Results: Eight studies including 719 individuals with elevated BP/hypertension and 1653 age-matched healthy controls were considered for the analysis. Pooled average LVEF values were 72.4±1.6% in the healthy control group and 72.5±1.8% in the elevated BP/hypertensive group (SMD: 0.08±0.15,CI: -0.21/0.36, p=0.60); the corresponding values of GLS were -19.6±1.1% and 18.5±0.9% (SMD:-0.96±0.25, CI: -1.46/-0.47, p< 0.0001). A parallel impairment of global circumferential strain (GCS) also emerged from pooled data of 3 studies (SMD: -0.96±0.25, CI: -1.46/-0.47, p< 0.0001).

Conclusions: Our data suggest that LVEF is unable to detect early alterations in systolic function in pediatric hypertension, and the implementation of STE may be highly useful in unmasking systolic dysfunction in this setting.

Background: Primary aldosteronism (PA) is the main cause of secondary arterial hypertension. In this study, we present the medical treatment of Hispanic patients with PA followed for up to 5 years, highlighting the complete cure with pharmacological treatment in one of our patients.

Methods: We studied 32 PA patients, followed every 6 months after starting MRA. A clinical response was the normalization of blood pressure (BP) in the absence of other antihypertensive drugs. The biochemical response was considered with normalization of potassium and renin. Responses to treatment were compared using the defined daily dose (DDD). The effect of MRA was evaluated in vitro. The HAC15 cells were cultured and stimulated with aldosterone and spironolactone for 24-72h, and the apoptotic cell death was measured.

Results: At 12 months posttreatment with MRA, 68% of the patients had a total clinical response, and 67% had a total biochemical response. Response to MRA treatment reduced DDD by an average of 74%. Additionally, we observed one PA patients treated with spironolactone after three years, he presented a pharmacological cure with normalization of aldosterone and renin without treatment with spironolactone. The in vitro study shows that spironolactone increased early apoptosis in a 60% and late apoptosis in a 50%.

Conclusion: These results suggest the importance of timely diagnosis of PA and specific treatment with MRA, especially in patients with a poor response to treatment. Moreover, remission of PA may occur in some patients after spironolactone treatment due to its suggestive role as an apoptotic agent.

Background: During laboratory testing, participants rest quietly in a supine posture with little movement. However, it is rather common for participants to display various behaviors. The extent to which these common encounters influence cardiovascular measures is unknown.

Methods: Fifty-five adults (36 ± 15 years) were studied during the following seven randomized conditions in the supine position: (i) quiet stationary rest (control), (ii) while drowsy, (iii) while and (iv) after talking to investigators, (v) while and (vi) after cell phone use for texting, and (vii) lying on the side.

Results: Heart rate was greater when the participants were talking to investigators (+4 bpm) and texting on cell phones (+5 mm Hg) compared with quiet rest. Systolic blood pressure (BP) increased by 4 mm Hg and diastolic BP by 3 mm Hg while talking to investigators. Systolic BP was 6 mm Hg and diastolic BP was 5 mm Hg lower in the "side lying" position compared with quiet rest. In the side-lying condition, carotid-femoral pulse wave velocity (PWV) was not able to be measured in 38% (n = 16) of the participants while brachial-ankle PWV was not affected. Brachial-ankle PWV was greater while (+65 cm/s) and after (+29 cm/s) the participants were talking to investigators whereas carotid-femoral PWV was not able to be measured during talking. The drowsy behavior did not influence any of the BP and PWV measures.

Conclusions: Talking during the testing period significantly increases all the cardiovascular measures but cell phone use prior to the measures does not appear to influence them.

Background: Guidelines advise automated office blood pressure (AOBP) with an initial 5-minute delay and multiple measurements at least 60 seconds apart. Recent studies suggest that AOBP may be accurate with shorter delays or intervals, but evidence in clinical settings is limited.

Methods: Patients referred to 1 hypertension (HTN) center underwent 24-hour ambulatory blood pressure monitoring (ABPM) and 1 of 4 nonrandomized, unattended AOBP protocols: a 3- or 5-minute delay with a 30- or 60-second interval, i.e., 3 min/30 s/30 s, 3/60/60, 5/30/30 and 5/60/60 protocols. HTN was defined as systolic blood pressure (SBP) ≥140 or diastolic blood pressure ≥90 mm Hg.

Results: We compared differences in mean blood pressure and HTN classification between average AOBP and awake-time ABPM by t-tests and Fisher's exact test. Among 212 participants (mean 58.9 years, 61% women, 25% Black), there was substantial overlap in the probability distributions of awake-time ABPM and each of the 3 AOBP measures. SBP means were similar between the 5/60/60 and 3/30/30 protocols and 5/30/30 and 3/60/60 protocols. The 5/30/30 was associated with a higher proportion of systolic HTN, while the 3/60/60 protocol was associated with a higher proportion of diastolic HTN. There were no significant differences in systolic or diastolic HTN between 5/60/60 and 3/30/30 protocols with respect to awake-time ABPM.

Conclusions: In this quality improvement study, the shortest AOBP protocol did not differ significantly from the longest protocol. The time savings of shorter protocols may improve AOBP adoption in clinical practice without meaningfully compromising accuracy.

Background: Preeclampsia is associated with higher levels of asymmetric (ADMA) and symmetric (SDMA) dimethylarginines. Dimethylarginines are inhibitors of nitric oxide, a uterine smooth muscles relaxant. Women with preeclampsia experience a shorter labor duration compared with normotensive women. However, very little is known about the possible biochemical mechanisms behind these differences. We aimed to investigate if women with preeclampsia had higher levels of arginines (ADMA, SDMA, and l-arginine) at labor than controls and also investigate the association between arginines and labor duration.

Methods: The study was based on data from the Swedish, Uppsala County population-based, prospective cohort BASIC, 2009-2018. Arginines were analyzed by ultra-high-performance liquid chromatography using plasma samples taken at labor from women with preeclampsia (n = 47) and normotensive pregnancy (n = 90). We also analyzed inflammation markers such as C-reactive protein, tumor necrosis factor (TNF)-R1, TNF-R2, and growth differentiation factor (GDF-15).

Results: Women with preeclampsia had higher levels of ADMA (P < 0.001), SDMA (P < 0.001), l-arginine (P < 0.001), TNF-R1 (P < 0.001), TNF-R2 (P = 0.03), and GDF-15 (P < 0.01) compared with controls. Furthermore, ADMA and SDMA, not inflammation markers, were negatively correlated to labor duration in preeclampsia. No correlations were observed when comparing arginines and inflammation markers.

Conclusions: Among women with preeclampsia, our novel findings of higher level of arginines, negative correlation of arginines to labor duration, and absence of correlation of arginines to inflammation markers might support the theory that it is not inflammation but arginines which could be associated with shorter labor duration in preeclampsia.

Transmural pressure and shear stress are mechanical forces that profoundly affect the smooth muscle cells (SMCs) comprising the vascular wall and the endothelial cells (ECs) lining the lumen. Pressure and flow are detected by mechanosensors in these cells and translated into appropriate responses to regulate blood pressure and flow. This review focuses on the role of the transient receptor potential (TRP) superfamily of cation channels in this process. We discuss how specific members of the TRP superfamily (TRPC6, TRPM4, TRPV1, TRPV4, and TRPP1) regulate the resting membrane and intracellular Ca2+ levels in SMCs and ECs to promote changes in vascular tone in response to intraluminal pressure and shear stress. Although TRP channels participate in vascular mechanotransduction, little evidence supports their intrinsic mechanosensitivity. Therefore, we also examine the evidence exploring the force-sensitive signal transduction pathways acting upstream of vascular TRP channels. Understanding the interplay between mechanosensors, force-induced signaling cascades, and TRP channels holds promise for the development of targeted therapies for diseases caused by vascular dysfunction.

Background: The 24-h activity cycle (24H-ACT) (sleep, sedentary behavior, light physical activity, and moderate to vigorous physical activity) may have deleterious or beneficial associations with 24-h blood pressure (24H-BP).

Purpose: Estimate the short-term associated changes in 24H-BP with acutely replacing 30 min/d from one behavior of the 24H-ACT to other behaviors in employed adults.

Methods: Participants (N = 659) wore an ambulatory blood pressure monitor and two accelerometers (waist and wrist) to measure 24H-BP and the 24H-ACT.

Results: Replacing 30 min of sedentary behavior with 30 min of sleep was associated with lower 24-h mean systolic [ß = -0.32 mm Hg per 0.5 h (95% CI: -0.58, 0.06)] and diastolic [ß = -0.31 mm Hg per 0.5 h (95% CI: -0.50, -0.12)] blood pressure. Replacing 30 min of light physical activity with 30 min of sleep was associated with lower 24-h mean systolic [ß = -0.30 mm Hg per 0.5 h (95% CI: -0.62, 0.03,)] and diastolic blood pressure [ß = -0.34 mm Hg per 0.5 h (95% CI: -0.58, -0.11)]. No other time reallocations between 24H-ACT behaviors were associated with changes in 24H-BP.

Conclusion: Replacing time in sedentary behavior or light physical activity with sleep may provide small short-term reductions in that day's 24H-BP.