Current Hypertension Reports最新文献

Purpose of review: Preeclampsia (PE) is a serious and distinct type of pregnancy-induced hypertension, with an incidence of 2-8% worldwide. PE is defined as pregnancy-related hypertension with proteinuria and peripheral edema after 20 weeks of gestation. Hypoxic placenta triggers the release of inflammatory and humoral substances into maternal circulation, leading to induction of oxidative stress, lipid peroxidation, endothelial dysfunction, and peripheral vasoconstriction. The objective of the present narrative review was to find the association between PE and hypoxia-inducible factor 1 (HIF-1) in pregnant women from a new perspective.

Recent findings: HIF-1 is the key transcription factor that regulates cellular responses to hypoxia and low oxygen tension. HIF-1α is involved in the differentiation and growth of the placenta mainly in the first and second trimesters. During normal gestation, HIF-1α responds to the alterations in oxygen tension, cytokine, and angiogenic factors release. HIF-1α is considered a key biomarker of placental function and vascularization during pregnancy. HIF-1α plays a crucial role in the pathogenesis of PE through activation of anti-angiogenic and inhibition of proangiogenic factors. As well, HIF-1α increases the expression of the p38MAPK and NLRP3 inflammasomes, which promote placental inflammation and dysfunction. HIF-1α acts as a potential link between inflammatory signaling pathways and the development of PE.

Purpose of review: To review the pathophysiology of hypertension in Alzheimer's disease and related dementias and explore the current landscape of clinical trials involving treatment of hypertension to improve cognition.

Recent findings: Hypertension is increasingly recognized as a contributor to cognitive impairment. Clinical trials that explore blood pressure reductions with cognitive outcomes have been promising. Various antihypertensives have been evaluated in clinical trials, with growing interest in those agents that impact the renin-angiotensin-aldosterone system due to its own association with cognitive impairment. No antihypertensive agent has been found to be superior to others in reducing cognitive impairment risk or conferring neuroprotective benefits. In this review, the pathophysiology of and clinical trial data involving hypertension and dementia will be explored. Hypertension is a significant risk factor for the development of neurodegenerative dementias, and clinical trials have been overall favorable in improving cognition by reductions in blood pressure using antihypertensive agents.

Purpose of review: The study aims to capture the history and lineage of hypertension researchers from the University of Toledo in Ohio and showcase their collective scientific contributions dating from their initial discoveries of the physiology of adrenal and renal systems and genetics regulating blood pressure (BP) to its more contemporary contributions including microbiota and metabolomic links to BP regulation.

Recent findings: The University of Toledo College of Medicine and Life Sciences (UTCOMLS), previously known as the Medical College of Ohio, has contributed significantly to our understanding of the etiology of hypertension. Two of the scientists, Patrick Mulrow and John Rapp from UTCOMLS, have been recognized with the highest honor, the Excellence in Hypertension award from the American Heart Association for their pioneering work on the physiology and genetics of hypertension, respectively. More recently, Bina Joe has continued their legacy in the basic sciences by uncovering previously unknown novel links between microbiota and metabolites to the etiology of hypertension, work that has been recognized by the American Heart Association with multiple awards. On the clinical research front, Christopher Cooper and colleagues lead the CORAL trials and contributed importantly to the investigations on renal artery stenosis treatment paradigms. Hypertension research at this institution has not only provided these pioneering insights, but also grown careers of scientists as leaders in academia as University Presidents and Deans of Medical Schools. Through the last decade, the university has expanded its commitment to Hypertension research as evident through the development of the Center for Hypertension and Precision Medicine led by Bina Joe as its founding Director. Hypertension being the top risk factor for cardiovascular diseases, which is the leading cause of human mortality, is an important area of research in multiple international universities. The UTCOMLS is one such university which, for the last 6 decades, has made significant contributions to our current understanding of hypertension. This review is a synthesis of this rich history. Additionally, it also serves as a collection of audio archives by more recent faculty who are also prominent leaders in the field of hypertension research, including John Rapp, Bina Joe, and Christopher Cooper, which are cataloged at Interviews .

Purpose of review: We reviewed the effects of hypertension and the means to prevent and treat it across the spectrum of a woman's lifespan and identified gaps in sex-specific mechanisms contributing to hypertension in women that need to be addressed.

Recent findings: Hypertension continues to be an important public health problem for women across all life stages from adolescence through pregnancy, menopause, and older age. There remain racial, ethnic, and socioeconomic differences in hypertension rates not only overall but also between the sexes. Blood pressure cutoffs during pregnancy have not been updated to reflect the 2017 ACC/AHA changes due to a lack of data. Additionally, the mechanisms behind hypertension development in menopause, including sex hormones and genetic factors, are not well understood. In the setting of increasing inactivity and obesity, along with an aging population, hypertension rates are increasing in women. Screening and management of hypertension throughout a women's lifespan are necessary to reduce the burden of cardiovascular disease, and further research to understand sex-specific hypertension mechanisms is needed.

Purpose of review: Anti-hypertensive and lipid lowering therapy addresses only half of the cardiovascular disease risk in patients with body mass index > 30 kg/m², i.e., obesity. We examine newer aspects of obesity pathobiology that underlie the partial effectiveness of anti-hypertensive lipid lowering therapy for the reduction of cardiovascular disease risk in obesity.

Recent findings: Obesity-related insulin resistance, vascular endothelium dysfunction, increased sympathetic nervous system/renin-angiotensin-aldosterone system activity, and glomerulopathy lead to type 2 diabetes, coronary atherosclerosis, and chronic disease kidney disease that besides hypertension and dyslipidemia increase cardiovascular disease risk. Obesity increases cardiovascular disease risk through multiple pathways. Optimal reduction of cardiovascular disease risk in patients with obesity is likely to require therapy targeted at both obesity and obesity-associated conditions.

Purpose of review: Arterial stiffness (AS) was mainly associated with cardiovascular morbidity and mortality in a hypertensive patient. Some risk factors contribute to the development of AS, such as aging, high blood pressure, vascular calcification, inflammation, and diabetes mellitus. The WNT/β-catenin pathway is implicated in numerous signaling and regulating pathways, including embryogenesis, cell proliferation, migration and polarity, apoptosis, and organogenesis. The activation of the WNT/β-catenin pathway is associated with the development of these risk factors.

Recent findings: Aortic pulse wave velocity (PWV) is measured to determine AS, and in peripheral artery disease patients, PWV is higher than controls. An augmentation in PWV by 1 m/s has been shown to increase the risk of cardiovascular events by 14%. AS measured by PWV is characterized by the deregulation of the WNT/β-catenin pathway by the inactivation of its two inhibitors, i.e., DKK1 and sclerostin. Thus, this review focuses on the role of the WNT/β-catenin pathway which contributes to the development of arterial stiffness.

Purpose of review: The purpose of this review is to provide an overview of existing and emerging lifestyle treatments in the clinical management of primary elevated blood pressure and hypertension in pediatric patients. The authors hope to expand the knowledge base surrounding pediatric hypertension and update clinicians on best practices to improve outcomes.

Recent findings: Elevated blood pressure is traditionally addressed with broad lifestyle recommendations such as limiting salt consumption and losing weight. This approach is not well adapted for pediatric patients. Novel and often underutilized approaches to the treatment of hypertension in pediatrics include psychological counseling for behavior modification, circadian nutrition, consistent use of interdisciplinary teams, manipulation of macronutrients, stress management, technology-infused interventions, and systemic changes to the food environment. Elevated blood pressure is a pervasive condition affecting cardiovascular disease and mortality risk. Increasingly, pediatric patients are presenting with elevated blood pressure with etiologies known to be affected by lifestyle behaviors. Weight management, dietary modifications, and daily physical activity are well-researched methods for improving individual blood pressure measurements. These strategies can sometimes be as effective as pharmacological interventions at lowering blood pressure. However, compliance with these individual recommendations is not consistent and has led to unsatisfactory results. There are emerging treatment trends that may provide non-traditional and more effective non-pharmacologic routes to blood pressure management in pediatric patients.

Purpose of review: To discuss the interplay behind how a high-fibre diet leads to lower blood pressure (BP) via the gut microbiome.

Recent findings: Compelling evidence from meta-analyses support dietary fibre prevents the development of cardiovascular disease and reduces BP. This relation is due to gut microbial metabolites, called short-chain fatty acids (SCFAs), derived from fibre fermentation. The SCFAs acetate, propionate and butyrate lower BP in independent hypertensive models. Mechanisms are diverse but still not fully understood-for example, they include G protein-coupled receptors, epigenetics, immune cells, the renin-angiotensin system and vasculature changes. Lack of dietary fibre leads to changes to the gut microbiota that drive an increase in BP. The mechanisms involved are unknown. The intricate interplay between fibre, the gut microbiota and SCFAs may represent novel therapeutic approaches for high BP. Other gut microbiota-derived metabolites, produced when fibre intake is low, may hold potential therapeutic applications. Further translational evidence is needed.

Purpose of review: This review summarizes the involvement of inflammaging in vascular damage with focus on the epigenetic mechanisms by which inflammaging-induced hypertension is triggered.

Recent findings: Inflammaging in hypertension is a complex condition associated with the production of inflammatory mediators by the immune cells, enhancement of oxidative stress, and tissue remodeling in vascular smooth muscle cells and endothelial cells. Cellular processes are numerous, including inflammasome assembly and cell senescence which may involve mitochondrial dysfunction, autophagy, DNA damage response, dysbiosis, and many others. More recently, a series of noncoding RNAs, mainly microRNAs, have been described as possessing epigenetic actions on the regulation of inflammasome-related hypertension, emerging as a promising therapeutic strategy. Although there are a variety of pharmacological agents that effectively regulate inflammaging-related hypertension, a deeper understanding of the epigenetic events behind the control of vessel deterioration is needed for the treatment or even to prevent the disease onset.

Purpose of review: To summarise evidence on both appropriate and inappropriate antihypertensive drug withdrawal.

Recent findings: Deprescribing should be attempted in the following steps: (1) identify patients with several comorbidities and significant functional decline, i.e. people at higher risk for negative outcomes related to polypharmacy and lower blood pressure; (2) check blood pressure; (3) identify candidate drugs for deprescribing; (4) withdraw medications at 4-week intervals; (5) monitor blood pressure and check for adverse events. Although evidence is accumulating regarding short-term outcomes of antihypertensive deprescribing, long-term effects remain unclear. The limited evidence for antihypertensive deprescribing means that it should not be routinely attempted, unless in response to specific adverse events or following discussions between physicians and patients about the uncertain benefits and harms of the treatment.

Perspectives: Clinical controlled trials are needed to examine the long-term effects of deprescribing in older subjects, especially in those with comorbidities, and significant functional decline.