Current Hypertension Reports最新文献

Purpose of review: In this review, we discuss the evidence that vitamin D affects cardiovascular disease through interventional and observational studies and their corresponding association mechanisms. We also highlight the need for further research to definitively conclude clinical recommendations based on preliminary data and determine the extent to which vitamin D levels may impact the incidence and prognosis of major cardiovascular diseases in the future.

Recent findings: Cardiovascular disease has long been recognized as the leading cause of morbidity and mortality worldwide, with many risk factors implicated in its pathogenesis. Vitamin D is a risk factor that, despite being known to be crucial for its role in maintaining bone health, also has several extra-skeletal effects due to vitamin D receptors in vascular smooth muscle and cardiomyocytes. Recent studies have documented a significant association between higher vitamin D levels and lower risk of each cardiovascular disease entity; 11 studies between serum vitamin D and heart failure, 7 studies between serum vitamin D and hypertension, 8 studies between serum vitamin D and coronary artery disease, and 5 studies between serum vitamin D and atrial fibrillation. More studies documenting a significant association between increased serum vitamin D and cardiovascular disease are in the context of heart failure compared to hypertension, coronary artery disease, and atrial fibrillation. Conversely, a significant association between increased serum vitamin D and a lower risk of atrial fibrillation is reported in fewer studies compared to the association of vitamin D with other cardiovascular disease entities. Although there is evidence documenting a clear significant association of vitamin D under each category, further research is still needed to definitively conclude the role of vitamin D in cardiovascular disease management.

Purpose of review: Metabolic-associated fatty liver disease (MAFLD) is a condition of fat accumulation in the liver that occurs in the majority of patients in combination with metabolic dysfunction in the form of overweight or obesity. In this review, we highlight the cardiovascular complications in MAFLD patients as well as some potential mechanisms linking MAFLD to the development of cardiovascular disease and highlight potential therapeutic approaches to treating cardiovascular diseases in patients with MAFLD.

Recent findings: MAFLD is associated with an increased risk of cardiovascular diseases (CVD), including hypertension, atherosclerosis, cardiomyopathies, and chronic kidney disease. While clinical data have demonstrated the link between MAFLD and the increased risk of CVD development, the mechanisms responsible for this increased risk remain unknown. MAFLD can contribute to CVD through several mechanisms including its association with obesity and diabetes, increased levels of inflammation, and oxidative stress, as well as alterations in hepatic metabolites and hepatokines. Therapies to potentially treat MAFLD-induced include statins and lipid-lowering drugs, glucose-lowering agents, antihypertensive drugs, and antioxidant therapy.

Purpose of review: The role and underlying mechanisms mediated by dietary salt in modulating the gut microbiota and contributing to heart failure (HF) are not clear. This review summarizes the mechanisms of dietary salt and the gut-heart axis in HF.

Recent findings: The gut microbiota has been implicated in several cardiovascular diseases (CVDs) including HF. Dietary factors including high consumption of salt play a role in influencing the gut microbiota, resulting in dysbiosis. An imbalance of microbial species due to a reduction in microbial diversity with accompanying immune cell activation has been implicated in the pathogenesis of HF via several mechanisms. The gut microbiota and gut-associated metabolites contribute to HF by reducing gut microbiota biodiversity and activating several signaling pathways. High dietary salt modulates the gut microbiota composition and exacerbate or induce HF by increasing the expression of the epithelial sodium/hydrogen exchanger isoform 3 in the gut, cardiac expression of beta myosin heavy chain, activation of the myocyte enhancer factor/nuclear factor of activated T cell, and salt-inducible kinase 1. These mechanisms explain the resulting structural and functional derangements in patients with HF.

Puberty is a complex process leading to physical, sexual, and psychosocial maturation. The changes in morphology and organ function during puberty also affect blood pressure (BP) regulation, and as a consequence (BP) values change noticeably, reaching values often higher than after reaching full maturity. In children entering puberty, BP, especially systolic, increases and then reaches adult values by the end of puberty. The mechanisms responsible for this process are complex and not fully understood. Sex hormones, growth hormone, insulin-like growth factor-1, and insulin, whose production increases during puberty, significantly regulate BP through complex and overlapping mechanisms. During puberty, the incidence of arterial hypertension also increases, especially in children with excess body weight. The present paper presents the current state of knowledge regarding the influence of processes occurring during puberty on blood pressure.

Purpose of review: The response to natural stressors involves both cardiac stimulation and vascular changes, primarily triggered by increases in sympathetic activity. These effects lead to immediate flow redistribution that provides metabolic support to priority target organs combined with other key physiological responses and cognitive strategies, against stressor challenges. This extremely well-orchestrated response that was developed over millions of years of evolution is presently being challenged, over a short period of time. In this short review, we discuss the neurogenic background for the origin of emotional stress-induced hypertension, focusing on sympathetic pathways from related findings in humans and animals.

Recent findings: The urban environment offers a variety of psychological stressors. Real or anticipatory, emotional stressors may increase baseline sympathetic activity. From routine day-to-day traffic stress to job-related anxiety, chronic or abnormal increases in sympathetic activity caused by emotional stressors can lead to cardiovascular events, including cardiac arrhythmias, increases in blood pressure and even sudden death. Among the various alterations proposed, chronic stress could modify neuroglial circuits or compromise antioxidant systems that may alter the responsiveness of neurons to stressful stimuli. These phenomena lead to increases in sympathetic activity, hypertension and consequent cardiovascular diseases. The link between anxiety, emotional stress, and hypertension may result from an altered neuronal firing rate in central pathways controlling sympathetic activity. The participation of neuroglial and oxidative mechanisms in altered neuronal function is primarily involved in enhanced sympathetic outflow. The significance of the insular cortex-dorsomedial hypothalamic pathway in the evolution of enhanced overall sympathetic outflow is discussed.

Purpose of review: Accumulating data on the consumption of plant-based diets and their impact on blood pressure indicate a consensus that plant-based diets are linked to reduced blood pressure. The suggested mechanisms of action are manifold, and, in this systematic review, we provide a summary of the most recent findings on plant-based diets and their impact on blood pressure, along with an analysis of the molecules accountable for the observed effects.

Recent findings: The overwhelming majority of intervention studies demonstrate that plant-based diets result in lower blood pressure readings when compared to diets that are based on animal products. The various mechanisms of action are being clarified. The data discussed in this systematic review allow us to conclude that plant-based diets are associated with lower blood pressure and overall better health outcomes (namely, on the cardiovascular system) when compared to animal-based diets. The mechanisms of action are being actively investigated and involve many macro- and micronutrients plentiful in plants and the dishes prepared with them.

Purpose of review: Preeclampsia (PE) is a leading global cause of maternal and fetal morbidity and mortality. The heterogeneity of this disorder contributes to its elusive etiology. Due to the ethical constraints surrounding human studies, animal models provide a suitable alternative for investigation into PE pathogenesis and novel therapeutic strategies. The purpose of this review is to compare and contrast the various rodent models used to study PE, in order to demonstrate their value in investigating and identifying different characteristics of this disorder.

Recent findings: Several approaches have been employed to create an appropriate animal model of PE, including surgical, genetic manipulation, and pharmacological methods in an attempt to mimic the maternal syndrome. Despite the absence of a model to completely model PE, these models have provided valuable information concerning various aspects of PE pathogenesis and novel therapeutic strategies and have led to the discovery of potential predictive markers of PE. Rodent and murine models have contributed significantly to the study of the pathology associated with specific aspects of the disorder. As a single fully encompassing animal model of PE remains absent, the use of a combination of models has potential value in understanding its etiology as well as in new treatment and management strategies.

Purpose of review: This is a pragmatic decision aid for initiating pharmacotherapy for stage 1 hypertension.

Recent findings: If a stage 1 patient presents with clinical signs of fluid retention, then a diuretic should be the primary agent. However, if the patient is normovolemic, then a vasodilator should be the primary agent. If targeted blood pressure is not achieved with the primary agent, then the choices are dose escalation or the addition of a second drug. For stage 1, the addition of secondary agents is preferred. This approach includes the polypill (a single pill with multiple low-dose antihypertensive agents). The positives are the polypill lessens the need to make decisions associated with up-titration and the low doses mitigate adverse side effects. The polypill targets several concurrent mechanisms to counteract hypertension. For stage 1, the goal should be to lower blood pressure with a simple regiment which minimizes adverse side affects.

Purpose of review: To address the mechanistic pathways focusing on mitochondria dysfunction, oxidative stress, sirtuins imbalance, and other contributors in patient with metabolic syndrome and cardiovascular disease. Sodium glucose co-transporter type 2 (SGLT-2) inhibitors deeply influence these mechanisms. Recent randomized clinical trials have shown impressive results in improving cardiac function and reducing cardiovascular and renal events. These unexpected results generate the need to deepen our understanding of the molecular mechanisms able to generate these effects to help explain such significant clinical outcomes.

Recent findings: Cardiovascular disease is highly prevalent among individuals with metabolic syndrome and diabetes. Furthermore, mitochondrial dysfunction is a principal player in its development and persistence, including the consequent cardiac remodeling and events. Another central protagonist is the renin-angiotensin system; the high angiotensin II (Ang II) activity fuel oxidative stress and local inflammatory responses. Additionally, sirtuins decline plays a pivotal role in the process; they enhance oxidative stress by regulating adaptive responses to the cellular environment and interacting with Ang II in many circumstances, including cardiac and vascular remodeling, inflammation, and fibrosis. Fasting and lower mitochondrial energy generation are conditions that substantially reduce most of the mentioned cardiometabolic syndrome disarrangements. In addition, it increases sirtuins levels, and adenosine monophosphate-activated protein kinase (AMPK) signaling stimulates hypoxia-inducible factor-1β (HIF-1 beta) and favors ketosis. All these effects favor autophagy and mitophagy, clean the cardiac cells with damaged organelles, and reduce oxidative stress and inflammatory response, giving cardiac tissue protection. In this sense, SGLT-2 inhibitors enhance the level of at least four sirtuins, some located in the mitochondria. Moreover, late evidence shows that SLGT-2 inhibitors mimic this protective process, improving mitochondria function, oxidative stress, and inflammation. Considering the previously described protection at the cardiovascular level is necessary to go deeper in the knowledge of the effects of SGLT-2 inhibitors on the mitochondria function. Various of the protective effects these drugs clearly had shown in the trials, and we briefly describe it could depend on sirtuins enhance activity, oxidative stress reduction, inflammatory process attenuation, less interstitial fibrosis, and a consequent better cardiac function. This information could encourage investigating new therapeutic strategies for metabolic syndrome, diabetes, heart and renal failure, and other diseases.

Purpose of review: To describe the physiological aspects of blood pressure and arterial stiffness, as well as explain how these processes are related. To review the available evidence on the effect of treatment with different classes of antihypertensive drugs on improving arterial stiffness.

Recent findings: Specific classes of antihypertensive drugs may have effects directly on improving arterial stiffness independent of lowering blood pressure. The maintenance of normal blood pressure levels is essential for the homeostasis of the whole organism; the increase in blood pressure is directly related to the increased risk of cardiovascular diseases. Hypertension is characterized by structural and functional changes in blood vessels and is associated with a more accelerated progression of arterial stiffness. Randomized clinical trials have shown that some specific classes of antihypertensive drugs can improve arterial stiffness independently of their effect on lowering brachial blood pressure. These studies show that calcium channel blockers (CCBs), angiotensin II receptor blockers (ARBs), and angiotensin-converting enzyme (ACE) inhibitors have been shown to have a better effect on arterial stiffness compared to diuretics and beta-blockers in individuals with arterial hypertension and other cardiovascular risk factors. More real-world studies are needed to assess whether this effect on arterial stiffness can improve the prognosis of patients with hypertension.