Current Hypertension Reports最新文献

Purpose of the review: Τhe association between nocturnal blood pressure (BP) and alterations in the retinal microvasculature remains understudied, with few available studies to provide conflicting results. Therefore, we conducted a systematic review and meta-analysis to determine whether an association exists between retinal microvascular alterations and nocturnal BP patterns, determined by 24h ambulatory BP measurement.

Recent findings: Our search concluded to 1002 patients (6 studies). A total of 3 studies (411 patients) were enrolled in the meta-analysis. Central retinal arteriolar equivalent found to be not different between patients with and without dipping status (mean differences [MD]: -0.01; 95% CI: -0.23 to 0.20; I²=0%; P < 0.610). Regarding central retinal venular equivalent, dippers showed significantly lower values compared to non-dippers (MD: -0.25; 95% CI: -0.47 to -0.03; I²=0%; P < 0.024). For the comparison between nighttime and daytime BP regarding the damage in small retinal vessels, we identified only 5 studies. Due to different evaluated outcomes as well as due to the heterogeneity of outcomes and different grouping of patients based on different BP cut-off values, these results couldn't be analyzed quantitatively. In summary, this is the first effort to summarize evidence on the effects of day-to-night variation of BP on the retinal small vessels. According to the findings of the present systematic review and meta-analysis, non-dipping status may be associated with retinal venular dilatation, and elevated nighttime BP with retinal arteriolar narrowing. Further studies are warranted to elucidate the impact of nocturnal BP patterns in the retinal microvasculature.

Purpose of review: Hypertension remains a major chronic disease morbidity across the world, even in the twenty-first century, affecting ≈40% of the global population, adversely impacting the healthcare budgets in managing the high incidence of cardiovascular disease (CVD) complications and mortality because of elevated blood pressure (BP). However, evaluation and management of endocrine hypertension are not optimal in clinical practice. With three unique clinical case scenarios, we update the evidence base for diagnostic evaluation and management of endocrine hypertension in this review to inform appropriate day-to-day clinical practice decisions.

Recent findings: Although most individuals with high BP suffer from essential hypertension (≈85%), some patients may have a clear underlying etiology (termed secondary hypertension), and a significant proportion of these patients have endocrine hypertension (≈10%) consequent to hormone excess from dysfunction of one or more endocrine glands. Even if a relatively common disease in the general population, the correct diagnosis and appropriate treatment of endocrine hypertension is often delayed because of poor awareness among clinicians, including primary care providers and physicians in the secondary care settings. An accurate and timely diagnosis of endocrine hypertension is crucial to potentially cure or at least properly manage these patients because the consequences of delays in diagnosis can be catastrophic, with markedly higher end-organ complications such as CVD, chronic kidney disease, and even premature mortality among sufferers.

Purpose of review: The role of the lymphatic system in clearing extravasated fluids, lipid transport, and immune surveillance is well established, and lymphatic vasculature can provide a vital role in facilitating crosstalk among various organ systems. Lymphatic vessels rely on intrinsic and local factors to absorb and propel lymph from the interstitium back to the systemic circulation. The biological implications of local influences on lymphatic vessels are underscored by the exquisite sensitivity of these vessels to environmental stimuli. This review is intended to highlight the role of sodium within the local environment in mediating lymphatic and immune cell interactions that contribute to changes in function and disease progression.

Recent findings: We discuss evidence that accumulation of interstitial sodium modulates lymphatic growth, pumping dynamics, and permeability of renal lymphatics, which involves activation of sodium potassium chloride co-transporter (NKCC1) in lymphatic endothelial cells. These recent findings complement observations that sodium activates immune cells via the epithelial sodium channel (ENaC), leading to the formation and accumulation of lipid oxidation products, isolevuglandins (IsoLGs), in antigen presenting cells, which in turn promotes T cell activation and vasculopathy. In addition, we will underscore the physiologic relevance of altered interplay between immune cells and lymphatics in the sodium avid state that characterizes kidney diseases and consider how sodium accumulation in the interstitial compartment of the kidney modulates the lymphatic network and the interactions between renal lymphatics and activated immune cells. Finally, this article calls attention to persisting knowledge gaps and stresses the need for additional studies to identify salt-sensing mechanisms, including sodium-activated immune cells and lymphatic endothelial cell interactions, for targeted therapeutic interventions in the setting of renal disease.

Purpose of review: To review the most current recommendations regarding assessment and treatment of asymptomatic hypertension treatment in the emergency department (ED) and to provide guidance for prescribing oral antihypertensive therapy for ED providers.

Recent findings: There are varying management strategies for the treatment of asymptomatic hypertension in the ED likely due to a lack of direct guidelines for treatment. There is an increasing body of evidence for the safety of initiating therapy to treat chronic asymptomatic hypertension in the ED. Initiation and optimization of oral antihypertensive therapy in indicated patients can be done by ED providers to enhance and expediate transition of care for patients and can ultimately aid in prevention of cardiovascular disease (CVD). This review provides guidance of when oral antihypertensive therapy can be initiated, medication options depending on the patient's blood pressure and other concurrent medications (if applicable), as well as other factors that may influence choice of therapy are described. Oral antihypertensive therapies can be initiated and optimized in the ED for patients with asymptomatic chronic hypertension.

Purpose of review: To review currently existing knowledge on a new type of antihypertensive treatment, small interfering RNA (siRNA) targeting hepatic angiotensinogen.

Recent findings: Targeting angiotensinogen synthesis in the liver with siRNA allows reaching a suppression of renin-angiotensin system (RAS) activity for up to 6 months after 1 injection. This might revolutionize antihypertensive treatment, as it could overcome non-adherence, the major reason for inadequate blood pressure control. Animal data support that its effects on blood pressure and end-organ damage are fully comparable to those of classical RAS blockers, and phase I and II clinical trials confirm its antihypertensive effectiveness and long-term action. Although its side effect profile is placebo-like, its long-term effects also pose a threat in patients who require immediate restoration of RAS activity, like in shock. Here tools are being developed, called REVERSIR, that allow immediate annihilation of the siRNA effect in the liver. One subcutaneous injection of angiotensinogen siRNA lowers blood pressure for 6 months without severe side effects. The decrease in angiotensinogen and blood pressure can be reversed with a drug called REVERSIR if needed.

Purpose of review: One of the challenges in the diagnosis and management of primary aldosteronism (PA), the most common type of secondary hypertension with curative potential, is the modification of antihypertensive medications. We seek to explore whether these medications can be continued during the diagnostic process of PA to minimize the duration and risks associated with medication adjustments.

Recent findings: We searched PubMed for eligible original literature between 1990 and 2024 using the following keywords: (screening) AND (primary aldosteronism); (confirmatory) AND (primary aldosteronism); (adrenal vein sampling) AND primary aldosteronism). Some recent studies support the feasibility of PA-related tests and even adrenal vein sampling (AVS) without the need to discontinue antihypertensive medications in certain cases. In this review, we propose a management approach that considers the specific effects of antihypertensive medications on the RAAS axis and the patient's disease phenotype. Based on this, we suggest a strategy that enables the diagnosis of PA in certain patients without discontinuing their antihypertensive medications.

Purpose of review: Extremes of blood pressure (BP) are common among patients that visit emergency departments. In this review article, we discuss the specific indications for invasive blood pressure monitoring in the ED, particularly in the context of undifferentiated shock and hypertensive emergencies.

Recent findings: In most cases, non-invasive techniques suffice for blood pressure monitoring, however, in certain patient presentations intermittent automated oscillometry bears significant drawbacks. The most evident drawback is the extended intervals between measurements. Invasive BP (IBP) monitoring offers a pivotal tool for patients with critical illness who require accurate, timely, blood pressure monitoring and indirectly monitors for complications involving vital organ systems. In the management of patients with critical illness or at risk for end organ injury, invasive methods that directly measure BP via arterial cannulation continues to be an established standard. Overall, evaluating patients on an individual basis, with the understanding that patients who present with extreme blood pressure values need closer monitoring, should prompt consideration of invasive methods of blood pressure monitoring.

Purpose of review: Chronic kidney disease and end-stage kidney disease (ESKD) are well-established risk factors for cardiovascular disease (CVD), the leading cause of mortality in the dialysis population. Conventional therapies, such as statins, blood pressure control, and renin-angiotensin-aldosterone system blockade, have inadequately addressed this cardiovascular risk, highlighting the unmet need for effective treatment strategies. Sodium-glucose transporter 2 (SGLT2) inhibitors have demonstrated significant renal and cardiovascular benefits among patients with type 2 diabetes, heart failure, or CKD at risk of progression. Unfortunately, efficacy data in dialysis patients is lacking as ESKD was an exclusion criterion for all major clinical trials of SGLT2 inhibitors. This review explores the potential of SGLT2 inhibitors in improving cardiovascular outcomes among patients with ESKD, focusing on their direct cardiac effects.

Recent findings: Recent clinical and preclinical studies have shown promising data for the application of SGLT2 inhibitors to the dialysis population. SGLT2 inhibitors may provide cardiovascular benefits to dialysis patients, not only indirectly by preserving the remaining kidney function and improving anemia but also directly by lowering intracellular sodium and calcium levels, reducing inflammation, regulating autophagy, and alleviating oxidative stress and endoplasmic reticulum stress within cardiomyocytes and endothelial cells. This review examines the current clinical evidence and experimental data supporting the use of SGLT2 inhibitors, discusses its potential safety concerns, and outlines ongoing clinical trials in the dialysis population. Further research is needed to evaluate the safety and effectiveness of SGLT2 inhibitor use among patients with ESKD.

Purpose of review: Resistant Hypertension (RH) poses a significant public health challenge, contributing to increased mortality, cardiovascular events and organ damage. Both clinical and experimental research are striving for higher standards in a translational manner to integrate new findings and confirm hypotheses. Considering that many are the aspects of RH that are still under investigation, this review aims to shed light on the advances made in experimental research concerning RH. It seeks to underscore the pivotal role of experimental studies in shaping clinical practices and also explore future perspectives.

Recent findings: It is important to emphasize the significance of experimental models, primarily for advancing our understanding: experimental models have greatly contributed to our comprehension of the underlying mechanisms in RH, including factors like sympathetic activation, endothelial dysfunction and structural vessel abnormalities. Secondly, for assessing treatment approaches: animal models have also played a crucial role in evaluating the potential effectiveness of diverse treatment approaches for RH. These encompass both pharmacological options, involving combinations of established drugs or novel pharmaceuticals, and non-pharmacological alternatives, which include surgical procedures like renal denervation, medical devices like baroreceptor stimulators, and lifestyle modifications. The most lacking component in translational research is the fact that there is no well-established animal model that perfectly replicates RH. Consequently, alternative strategies, including the combination of models, must be considered. What remains clear is that the development of animal models closely mimicking RH holds the promise of providing valuable insights into the essential mechanisms and responses necessary to combat or slow the global progression of RH.

Purpose of review: For a healthy pregnancy to occur, a controlled interplay between the maternal circulating renin-angiotensin-aldosterone system (RAAS), placental renin-angiotensin system (RAS) and intrarenal renin-angiotensin system (iRAS) is necessary. Functionally, both the RAAS and iRAS interact to maintain blood pressure and cardiac output, as well as fluid and electrolyte balance. The placental RAS is important for placental development while also influencing the maternal circulating RAAS and iRAS. This narrative review concentrates on the (pro)renin receptor ((P)RR) and its soluble form (s(P)RR) in the context of the hypertensive pregnancy pathology, preeclampsia.

Recent findings: The (P)RR and the s(P)RR have become of particular interest as not only can they activate prorenin and renin, thus influencing levels of angiotensin II (Ang II), but s(P)RR has now been shown to directly interact with and stimulate the Angiotensin II type 1 receptor (AT₁R). Levels of both placental (P)RR and maternal circulating s(P)RR are elevated in patients with preeclampsia. Furthermore, s(P)RR has been shown to increase blood pressure in non-pregnant and pregnant rats and mice. In preeclamptic pregnancies, which are characterised by maternal hypertension and impaired placental development and function, we propose that there is enhanced secretion of s(P)RR from the placenta into the maternal circulation. Due to its ability to both activate prorenin and act as an AT₁R agonist, excess maternal circulating s(P)RR can act on both the maternal vasculature, and the kidney, leading to RAS over-activation. This results in dysregulation of the maternal circulating RAAS and overactivation of the iRAS, contributing to maternal hypertension, renal damage, and secondary changes to neurohumoral regulation of fluid and electrolyte balance, ultimately contributing to the pathophysiology of preeclampsia.