Journal of Hypertension最新文献

Hypertension in children and adolescents is an increasingly prevalent global health concern and a strong predictor of adult cardiovascular and kidney disease. Variability in existing guidelines and limited applicability in low-resource settings hinder effective identification and management. This International Society of Hypertension (ISH) position paper provides practical, harmonized guidance for clinicians globally. To develop evidence-based, clinically relevant recommendations for the evaluation, diagnosis, and management of hypertension in youth, informed by multidisciplinary expertise from 12 countries. An expert panel undertook an iterative, consensus-driven synthesis of current evidence covering epidemiology, risk factors, blood pressure measurement, diagnostic evaluation, target organ injury, lifestyle therapy, pharmacological treatment, and long-term monitoring. Youth hypertension is driven by obesity, adverse childhood experiences, unhealthy lifestyle behaviors, and socioecological factors, with a disproportionately higher burden in low and middle-income countries. Accurate diagnosis requires standardized measurement using validated devices, proper cuff sizing, and out-of-office monitoring, particularly ambulatory blood pressure monitoring. Targeted investigations help distinguish primary from secondary hypertension and identify early organ injury. Lifestyle modification forms the foundation of treatment, while pharmacotherapy is indicated for persistent stage 2 hypertension, comorbid conditions, or evidence of organ damage. Structured transition to adult care is essential to improve long-term adherence and outcomes. Timely recognition and individualized management of youth hypertension are critical for reducing lifelong cardiovascular risk. This ISH position paper offers pragmatic, globally adaptable recommendations to enhance early detection, treatment, and continuity of care for children and adolescents with elevated blood pressure.

Resistant hypertension (RH) affects approximately 10-15% of treated hypertensive adults and up to 50% of individuals with chronic kidney disease (CKD). Defined by persistent elevation of blood pressure despite multidrug therapy, RH reflects inadequate therapeutic control and is associated with accelerated renal function decline, increased cardiovascular morbidity and mortality, and more than US$10 billion in excess annual healthcare costs. Growing evidence indicates that, beyond sodium retention and activation of vasoconstrictor pathways, chronic endothelial dysfunction and maladaptive microvascular remodelling - particularly in CKD-associated RH - are increasingly recognized contributors to disease progression. The vascular endothelium regulates arterial tone through three major vasodilatory systems: nitric oxide (NO), prostacyclin (PGI2), and endothelium-dependent hyperpolarization (EDH). Pharmacologic agents targeting individual pathways have demonstrated short-term vasodilatory effects but have not consistently translated into durable endothelial recovery or microvascular repair in clinical practice. Therapeutic strategies capable of coordinated engagement of all three pathways may therefore be required to modify the vascular abnormalities underlying RH. Human tissue kallikrein-1 (KLK1) and its recombinant analogue, rinvecalinase alfa (DM199), represent a promising approach. In cardiovascular and renal disease models, KLK1 supplementation restores physiological generation of kinin peptides, which, by binding vascular and renal B2 receptors, stimulate NO, PGI2, and EDH signalling pathways, thereby promoting vasorelaxation and natriuresis. Moreover, sustained KLK1 therapy has been associated with improved microvascular integrity and angiogenic signalling through both kinin-dependent and independent mechanisms. Emerging Phase II clinical evidence with DM199 in CKD populations demonstrates blood pressure reduction together with stabilization of renal function and reductions in albuminuria, suggesting potential downstream effects on microvascular structure and function. Importantly, these effects are achieved with a favourable electrolyte and safety profile, supporting investigation in CKD-associated RH where standard therapies often fail. This review integrates contemporary treatment perspectives with mechanistic and clinical evidence supporting KLK1 augmentation as a chronic, endothelial-supportive strategy targeting microvascular remodelling in CKD-associated RH.

Objective: Whether initial systolic blood pressure (SBP) influences blood pressure management in acute ischemic stroke (AIS) and its association with outcome remains inconclusive. We conducted a subgroup analysis of CATIS-2 trial (China Antihypertensive Trial in Acute Ischemic Stroke II) to assess the impact of early vs. delayed antihypertensive treatment in AIS, stratified by baseline SBP.

Methods: CATIS-2 was a multicenter, randomized trial enrolling AIS patients within 24-48 h after onset, presenting with SBP 140-219 mmHg and without reperfusion therapy. Participants were randomized to receive immediate antihypertensive treatment or delayed treatment initiated on day 8. The primary outcome was functional dependency or death (modified Rankin Scale score ≥3) at 90-day. Three prespecified baseline SBP subgroups (<160, 160-179, and ≥180 mm Hg) were analyzed.

Results: 4802 patients (mean age 63.7 years, 65.0% male) were included, with baseline SBP < 160 mmHg (n = 2233), 160-179 mmHg (n = 1849), and ≥180 mmHg (n = 720). Among patients with baseline SBP 160-179 mmHg, early antihypertensive treatment was associated with increased risk of primary outcome compared to delayed treatment [13.3% vs. 10.4%; odds ratio (OR) 1.32, 95% confidence interval (CI) 1.00-1.76]. This finding was not observed in the baseline SBP < 160 mmHg subgroup (OR 1.12, 95% CI 0.84-1.50) or ≥180 mmHg subgroup (OR 0.98, 95% CI 0.66-1.46). No significant differences were found in stroke recurrence or major vascular events between treatment strategies across SBP subgroups.

Conclusion: Early antihypertensive treatment may increase the risk of functional dependency or death in AIS patients with moderately elevated baseline SBP. These findings provide valuable insights into clinical practice regarding individualized blood pressure management in AIS. Further research is warranted.

Registration: ClinicalTrials.gov (NCT03479554).

Objective: Guidelines on the treatment of hypertensive patients usually refer to 'average' patients. However, in clinical practice, individual patient characteristics may differ substantially from the average. Thus, it seems worthwhile to examine the relationship between comprehensive patient profiles and blood pressure responses.

Methods: We divided the patient population from the INSIGHT trial into exploration and validation cohorts and constructed composite patient profiles based on predictors of blood pressure control (age, severity of hypertension, comorbidities, and previous treatment status). Next, we tested in the exploration cohort whether blood pressure control rates and adverse effects after 6 months of therapy across these profiles differed from those in the entire patient group. Finally, we explored whether the results from the exploration cohort could be validated using another cohort.

Results: Logistic regression analysis showed that the odds of achieving blood pressure control differed substantially between patient profiles but not between treatment modalities. Patients with a less favorable profile (e.g. the combination of age above 60 years, baseline systolic pressure above 160 mmHg, and the presence of diabetes) did less well than patients with a low-risk profile (e.g. absence of organ damage). These results were confirmed in the validation cohort.

Conclusion: We conclude that responses to antihypertensive treatment vary in a clinically important manner depending on the composite patient profiles. When found in other trials as well, a priori knowledge about response rates of various patient-profile treatment regimens may help choose the best treatment in individual patients and improve overall blood pressure control rates.

Objectives: To investigate the associations of plasma aldosterone concentration (PAC), plasma renin activity (PRA), and aldosterone-to-renin ratio (ARR) with Gompertz law-based biological age difference (GOLD BioAgeDiff) in patients with primary aldosteronism versus essential hypertension (EHT), and to determine whether GOLD BioAgeDiff relates to cardiac mass.

Methods: We conducted a retrospective cross-sectional study of 1201 hypertensive adults (785 with primary aldosteronism and 416 with EHT). GOLD BioAgeDiff was defined as the calculated biological age minus chronological age. Multivariable linear regression was used to evaluate the associations of PAC, PRA, and ARR with GOLD BioAgeDiff. Furthermore, we assessed the relationship between GOLD BioAgeDiff and echocardiographic indices, including left ventricular mass index (LVMI) and excessive LVMI (eLVMI).

Results: Primary aldosteronism patients demonstrated significantly higher GOLD BioAgeDiff than EHT patients. In fully adjusted models, ARR was positively associated with GOLD BioAgeDiff in the primary aldosteronism group (β = 0.292, P = 0.008) but not in the EHT group (P for interaction = 0.032). PAC and postcaptopril PAC were also positively associated with GOLD BioAgeDiff in primary aldosteronism. Furthermore, higher GOLD BioAgeDiff was associated with greater eLVMI (β = 0.591, P < 0.001) and LVMI (β = 0.640, P = 0.001) in primary aldosteronism patients, suggesting a potential mediating role in the relationship between ARR and cardiac remodeling.

Conclusion: Among patients with primary aldosteronism, elevated ARR and PAC were independently associated with GOLD BioAgeDiff, and GOLD BioAgeDiff was correlated with LVMI/eLVMI and may be involved in the association between ARR and eLVMI. Prospective studies are required to confirm causality and evaluate the clinical utility of this biological aging marker.

Obesity is a key contributor to heart failure, driving increased morbidity, mortality, and healthcare costs. This association is supported by multiple pathophysiological mechanisms and consistent epidemiological evidence, particularly not only in heart failure with preserved ejection fraction (HFpEF), but also in heart failure with reduced ejection fraction (HFrEF). Given the rising prevalence of both diseases, integrated management strategies are essential. This review outlines current management options in patients with heart failure and obesity, from lifestyle modification to pharmacological and surgical treatment, and explores emerging treatments aimed at mitigating this growing burden.

Background and aim: Arterial hypertension is a major epidemiological risk factor for left ventricular hypertrophy (LVH) and heart failure (HF). Within this framework, the theory of hypertensive heart disease (HHD) has historically been proposed as the conceptual substrate for HF with preserved ejection fraction (HFpEF). The aim of this state-of-the-art review is to re-examine whether secondary hypertrophic remodelling due to chronic pressure overload represents an intrinsically dysfunctional myocardial state prone to HF, beyond the well recognized role of severe excess afterload as a haemodynamic precipitant of decompensation.

Content and range of evidence: This state-of-the-art review critically examines historical, experimental, imaging, histopathological, and clinical trial evidence addressing the relationship between arterial hypertension, afterload, myocardial remodelling, and HF.

Summary and main points: Across these domains, available evidence does not demonstrate arterial hypertension as a sufficient condition to cause HF, nor does it establish hypertensive myocardial remodelling as an intrinsic cardiomyopathy predisposed to decompensation. Clarifying this distinction has important implications for phenotyping, diagnosis, and interpretation of HF in hypertensive populations.