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The clinical significance of isolated systolic hypertension with normal central blood pressure known as spurious hypertension (sHT) in adolescents and its evolution over time is not known.

The aim of this study was to analyze changes in office, ambulatory blood pressure (ABPM), central systolic blood pressure (cSBP), hemodynamic parameters, and target organ damage (TOD) over a 1-year follow-up in a group of non-obese children with sHT.

Of 294 patients referred for primary hypertension, 138 patients (31 girls; 22%) had hypertension confirmed by ABPM. 48/138 (35%) patients (7 girls; 15%) were diagnosed with sHT (elevated office and ambulatory systolic BP, but normal cSBP); 43 of them (6 girls; 14%) were followed for 12 ± 3months during non-pharmacological therapy. At baseline 7 (16%) patients had borderline values of cIMT or LVMi indicating mild TOD. After 12months, 10/43 (3 girls; 23%) patients developed sustained HT (elevated office, ambulatory BP and cSBP), 11/43 (1 girl; 26%) maintained sHT, and 22/43 (2 girls; 51%) evolved to white coat hypertension or normotension. The cSBP values increased in 27 patients (4 girls; 63%), but the group average remained in the normal range. Prevalence of TOD did not change during observation. The multivariate regression analysis showed that the only predictor of cSBP change over time was a change in serum uric acid level.

In conclusion, after 1year of non-pharmacological treatment, 23% of adolescents with sHT developed sustained hypertension, with the main predictor of cSBP change being the change in serum uric acid.
In conclusion, after 1 year of non-pharmacological treatment, 23% of adolescents with sHT developed sustained hypertension, with the main predictor of cSBP change being the change in serum uric acid.Prematurity and perinatal stress, such as intrauterine growth restriction (IUGR) and chorioamnionitis, are pathological processes creating an impaired intrauterine environment. These intrauterine factors are associated with the development of proteinuria, hypertension, and chronic kidney disease (CKD) later in life. Initially, this was thought to be secondary to oligonephropathy, subsequent glomerular hypertrophy, and hyperfiltration, leading to glomerulosclerosis, a further decrease in nephron number, and finally CKD. Nowadays, there is increasing evidence that prematurity and perinatal stress affect not only nephron endowment but also the maturation of podocytes and vasculogenesis. IUGR is associated with podocyte damage and an aggravated course of nephrotic syndrome. Moreover, preterm birth and IUGR are known to cause upregulation of the postnatal renin-angiotensin system, resulting in hypertension. Chorioamnionitis causes damage to the glomeruli, thereby predisposing to the development of glomerulosclerosis. This review aims to summarize current knowledge on the influence of prematurity, IUGR, and chorioamnionitis on the development of different glomerular structures. After summarizing human and experimental data on low nephron number in general, a specific focus on the current understanding of podocyte and glomerular capillary formation in relation to prematurity and different causes of perinatal stress is presented.
Hypertension affects about half of all Americans, yet in the vast majority of cases, the factors causing the hypertension cannot be clearly delineated. Developing a more precise understanding of the molecular pathogenesis of HTN and its various phenotypes is therefore a pressing priority. Circulating and urinary extracellular vesicles (EVs) are potential novel candidates as biomarkers and bioactivators in HTN. EVs are a heterogeneous population of small membrane fragments shed from various cell types into various body fluids. As EVs carry protein, RNA, and lipids, they also play a role as effectors and novel cell-to-cell communicators. In this review, we discuss the diagnostic, functional, and regenerative role of EVs in essential HTN and focus on EV protein and RNA cargo as the most extensively studied EV cargo.

The field of EVs in HTN is still a young one and earlier studies have not used the novel EV detection tools currently available. More rigor and transparency in EV research are needed. Current datrs in HTN. EVs correlate with HTN severity and possibly end-organ damage. However, it has yet to be discerned which specific subtype(s) of EV reflects best HTN pathophysiology. Evolving studies are also showing that EVs might be novel regulators in vascular and renal tubular function and also be therapeutic. RNA in EVs has been studied in the context of hypertension, largely in the form of studies of miRNA, which are reviewed herein. read more Beyond miRNAs, mRNA in urinary EVs changed in response to sodium loading in humans. EVs represent promising novel biomarkers and bioactivators in essential HTN. Novel tools are being developed to apply more rigor in EV research including more in vivo models and translation to humans.
Patients with established cardiovascular disease are at high risk for recurrent myocardial infarction, stroke, and cardiovascular death. The term residual risk refers to this risk that persists, even after optimal treatment. Considerable progress has been made to understand the biological basis of residual risk and to devise therapies that can safely and effectively reduce risk. The presence of ongoing subclinical vascular inflammation is known to be a marker of elevated residual risk, and reductions in measures of vascular inflammation predict improved outcome in these patients.

Recent trials of anti-inflammatory agents have specifically tested the hypothesis that inflammation reduction reduces residual cardiovascular risk. Most prominent among these are the CANTOS, COLCOT, and CIRT trials. CANTOS enrolled patients with prior myocardial infarction (MI) and a high-sensitivity C-reactive protein ≥ 2 mg/L and reported a 15% reduction in major adverse cardiovascular events (MACE; HR 0.85, 95% CI 0.74-0.98) w5% reduction in major adverse cardiovascular events (MACE; HR 0.85, 95% CI 0.74-0.98) with the interleukin-1β inhibitor canakinumab. In COLCOT, colchicine 0.5 mg daily led to a 23% relative risk reduction (HR 0.77, 95% CI 0.61-0.96) in major vascular events in patients with recent acute coronary syndrome. By contrast, CIRT was stopped early for lack of benefit of low-dose methotrexate in preventing MACE in patients with coronary artery disease and either type 2 diabetes or the metabolic syndrome. Ongoing subclinical inflammation is an important marker of risk in patients with established cardiovascular disease, and novel therapies targeted at specific inflammatory pathways now demonstrate efficacy for the prevention of major adverse cardiovascular events.
To explore the prevalence, treatment particularities, and research agenda in the management of resistant hypertension among patients with chronic kidney disease (CKD).

The prevalence of resistant hypertension is reported to be 2-3 times higher in patients with CKD than in the general hypertensive population. Based in part on the results of the PATHWAY-2 trial showing add-on spironolactone to be superior to placebo or active treatment with an α- or β-blocker in reducing BP, international guidelines recommend the use of spironolactone as fourth-line agent in pharmacotherapy of resistant hypertension. Despite the several-fold higher burden of resistant hypertension among patients with stage 3b-4 CKD, the use of spironolactone in this population has been restricted, mainly due to the risk of hyperkalemia. The recently reported AMBER trial showed that among patients with uncontrolled resistant hypertension and an estimated glomerular filtration rate of 25-45ml/min/1.73m
, the newer potassium-binder patiromer hich is an effective add-on therapy to control BP in patients with resistant hypertension and advanced CKD. Future trials are now warranted to explore whether this strategy confers benefits on "hard" clinical outcomes in this high-risk population.
Hypertension heralds the diagnosis of heart failure (HF) with preserved ejection fraction (HFpEF) in 75-85% of cases and shares many of its adverse outcomes as well as its acute and chronic symptoms. This review provides important new data about the pathophysiology and mechanisms that connect hypertension and HFpEF as well as therapy used in both conditions.

The traditional model of HFpEF pathophysiology emphasizes the role of hypertension causing increased afterload on the left ventricle (LV), leading to LV hypertrophy (LVH) and subsequent LV diastolic dysfunction. Recent work has provided valuable insights into the mechanisms underlying the transition from hypertension to HFpEF, showing that the pathophysiology extends beyond LVH and diastolic dysfunction. An evolving paradigm suggests that HFpEF is inflammatory in nature with multifactorial pathophysiology, affected by age-related changes and comorbidities. Hypertension shares many of the proinflammatory mechanisms of HFpEF. Furthermore, hypertension p, obesity, and sleep apnea could be used. Due to its heterogeneity, delineation of standardized therapies for HFpEF has been challenging. Focusing on the tremendous overlap of hypertensive heart disease with HFpEF, it is proposed that approaches currently used to guide therapies for hypertension be applied to the treatment of HFpEF.
This review sought to evaluate the role of exercise in patients with obesity and comorbid hypertension, with a focus on contemporary literature (since January 2015).

No reviews have included patients classified with both obesity and hypertension and there is a paucity of randomised controlled trials examining the benefits of exercise in this population. Moreover, just one of 19 reviews examining the role of exercise on blood pressure included studies that met pre-defined inclusion criterion for hypertension, although seven conducted subgroup analyses stratified by mean baseline blood pressure. These demonstrated significantly larger reductions in blood pressure in hypertensive than pre-hypertensive and normotensive samples. There is a significant research-practice gap for understanding and influencing the role of exercise for patients with obesity and hypertension. This review provides recommendations for future research and consensus-based recommendations that promote exercise as a principle therapy for patients with obesity and hypertension.
No reviews have included patients classified with both obesity and hypertension and there is a paucity of randomised controlled trials examining the benefits of exercise in this population. Moreover, just one of 19 reviews examining the role of exercise on blood pressure included studies that met pre-defined inclusion criterion for hypertension, although seven conducted subgroup analyses stratified by mean baseline blood pressure. These demonstrated significantly larger reductions in blood pressure in hypertensive than pre-hypertensive and normotensive samples. There is a significant research-practice gap for understanding and influencing the role of exercise for patients with obesity and hypertension. This review provides recommendations for future research and consensus-based recommendations that promote exercise as a principle therapy for patients with obesity and hypertension.
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