Pathophysiology Of Hypertension Research Articles

Systemic Hormonal Unloading (SHU) in Secondary Hypertension: Addressing the Long-Term Adverse Cardiovascular Outcomes

Excess hormone production from adrenal tumors caused by primary hyperaldosteronism or pheochromocytoma are common etiologies for secondary hypertension. Studies have shown that sustained long-term circulating hormones in excess affect the blood vessels and cardiac structures. Inflammation of cardiomyocytes leads to fibrosis and eventual cardiomyopathy and is clinically presented as arrhythmia, nonfatal myocardial infarction, heart failure, or even death. The tissue changes and/or impaired cardiac function are reversible if early diagnosis and removal of the adrenal tumor by unilateral adrenalectomy is done. However, the condition becomes challenging if the adrenal lesions are bilateral. This article introduces the concept of systemic hormonal unloading and will discuss the philosophy of quality of life in managing bilateral adrenal disease. Keywords: systemic hormonal unloading, secondary hypertension, primary hyperaldosteronism, pheochromocytoma, bilateral adrenal venous sampling, cardiovascular adverse outcomes, quality of life

Immune mechanisms in the pathophysiology of hypertension.

Hypertension is a leading risk factor for morbidity and mortality worldwide. Despite current anti-hypertensive therapies, most individuals with hypertension fail to achieve adequate blood pressure control. Moreover, even with adequate control, a residual risk of cardiovascular events and associated organ damage remains. These findings suggest that current treatment modalities are not addressing a key element of the underlying pathology. Emerging evidence implicates immune cells as key mediators in the development and progression of hypertension. In this Review, we discuss our current understanding of the diverse roles of innate and adaptive immune cells in hypertension, highlighting key findings from human and rodent studies. We explore mechanisms by which these immune cells promote hypertensive pathophysiology, shedding light on their multifaceted involvement. In addition, we highlight advances in our understanding of autoimmunity, HIV and immune checkpoints that provide valuable insight into mechanisms of chronic and dysregulated inflammation in hypertension.

Hypoxic perfusion of pulmonary arterial vasa vasorum increases pulmonary arterial pressure.

The pathophysiology of pulmonary hypertension (PH) is not fully understood. Here, we tested the hypothesis that hypoxic perfusion of the vasa vasorum of the pulmonary arterial (PA) wall causes PH. Young adult pig lungs were explanted and placed into a modified ex vivo lung perfusion unit (organ care system, OCS) allowing the separate adjustment of parameters for mechanical ventilation, as well as PA perfusion and bronchial arterial (BA) perfusion. The PA vasa vasorum are branches of the BA. The lungs were used either as the control group (n = 3) or the intervention group (n = 8). The protocol for the intervention group was as follows: normoxic ventilation and perfusion (steady state), hypoxic BA perfusion, steady state, and hypoxic BA perfusion. During hypoxic BA perfusion, ventilation and PA perfusion maintained normal. Control lungs were kept under steady-state conditions for 105 min. During the experiments, PA pressure (PAP) and blood gas analysis were frequently monitored. Hypoxic perfusion of the BA resulted in an increase in systolic and mean PAP, a reaction that was reversible upon normoxic BA perfusion. The PAP increase was reproducible during the second hypoxic BA perfusion. Under control conditions, the PAP stayed constant until about 80 min of the experiment. In conclusion, the results of the current study prove that hypoxic perfusion of the vasa vasorum of the PA directly increases PAP in an ex situ lung perfusion setup, suggesting that PA vasa vasorum function and wall ischemia may contribute to the development of PH.NEW & NOTEWORTHY Hypoxic perfusion of the vasa vasorum of the pulmonary artery directly increased pulmonary arterial pressure in an ex vivo lung perfusion setup. This suggests that the function of pulmonary arterial vasa vasorum and wall ischemia may contribute to the development of pulmonary hypertension.

MFAP4-Deficiency Aggravates Age-Induced Changes in Resistance Artery Structure, While Ameliorating Hypertension.

Abnormalities of resistance arteries may play essential roles in the pathophysiology of aging and hypertension. Deficiency of the vascular extracellular matrix protein MFAP4 (microfibrillar-associated protein 4) has previously been observed as protective against aberrant arterial remodeling. We hypothesized that MFAP4-deficiency would reduce age- and hypertension-dependent arterial changes in extracellular matrix composition and stiffening. Mesenteric arteries were isolated from old (20-23 months) littermate Mfap4+/+ and Mfap4-/- mice, and 2-photon excitation microscopy imaging was used to quantify elastin and collagen volumes and dimensions in the vascular wall. Ten-week-old littermate Mfap4+/+ and Mfap4-/- mice were subjected to 20 days of continuous Ang II (angiotensin II) infusion and hypertension was monitored using invasive blood pressure measurements. Arterial stiffness, responses to vascular constrictors, and myogenic tone were monitored using wire- or pressure-myography. Collagen contents were assessed by Western blotting. MFAP4-deficiency significantly increased collagen volume and elastin fragmentation in aged mesenteric arteries without affecting arterial stiffness. MFAP4-deficient mice exhibited reduced diastolic pressure in Ang II-induced hypertension. There was no significant effect of MFAP4-deficiency on mesenteric artery structural remodeling or myogenic tone, although collagen content in mesenteric arteries was tendentially increased in hypertensive Mfap4+/+ mice relative to Mfap4-/- mice. Increased efficacy of vasoconstrictors (phenylephrine, thromboxane) and reduced stiffness were observed in Ang II-treated Mfap4-/- mouse mesenteric arteries in ex vivo myography recordings. MFAP4-deficiency reduces the elastin/collagen ratio in the aging resistance artery without affecting arterial stiffness. In contrast, MFAP4-deficiency reduces the stiffness of resistance arteries and ameliorates Ang II-induced hypertension.

Foundations of the Diagnosis and Management of Idiopathic Intracranial Hypertension and Pulsatile Tinnitus

Venous sinus stenosis has garnered increasing academic attention as a potential etiology of idiopathic intracranial hypertension (IIH) and pulsatile tinnitus (PT). The complex anatomy of the cerebral venous sinuses and veins plays a crucial role in the pathophysiology of these conditions. Venous sinus stenosis, often found in the superior sagittal or transverse sinus, can lead to elevated intracranial pressure (ICP) and characteristic IIH symptoms. Stenosis, variations in dural venous anatomy, and flow dominance patterns contribute to aberrant flow and subsequent PT. Accurate imaging plays a vital role in diagnosis, and magnetic resonance (MR) venography is particularly useful for detecting stenosis. Management strategies for IIH and PT focus on treating the underlying disease, weight management, medical interventions, and, in severe cases, surgical or endovascular procedures. Recently, venous sinus stenting has gained interest as a minimally invasive treatment option for IIH and PT. Stenting addresses venous sinus stenosis, breaking the feedback loop between elevated ICP and stenosis, thus reducing ICP and promoting cerebrospinal fluid outflow. The correction and resolution of flow aberrances can also mitigate or resolve PT symptoms. While venous sinus stenting remains an emerging field, initial results are promising. Further research is needed to refine patient selection criteria and evaluate the long-term efficacy of stenting as compared to traditional treatments.

Fundus Bleeding

Abstract Fundus bleeding, commonly known as retinal haemorrhage, is a significant ocular manifestation associated with various systemic and ocular conditions. This abstract provides a comprehensive overview of the pathogenesis, diagnosis and management strategies of fundus bleeding. The abstract begins by discussing the underlying pathophysiology of fundus bleeding, which involves the rupture of retinal blood vessels leading to the extravasation of blood into the retinal layers. It highlights the diverse aetiologies of retinal haemorrhage, including trauma, vascular diseases, hypertension, diabetes, blood dyscrasias and ocular conditions such as retinal vein occlusion and macular degeneration. The manuscript further delves into the diagnostic modalities used to assess fundus bleeding, including fundus examination, optical coherence tomography (OCT), fluorescein angiography (FA) and fundus photography. It emphasizes the importance of accurate diagnosis to identify the underlying cause and guide appropriate management. The management strategies for fundus bleeding are discussed, considering both the underlying aetiology and severity of the haemorrhage. This includes conservative approaches, such as observation and control of systemic risk factors, as well as specific interventions like antivascular endothelial growth factor (anti-VEGF) therapy, laser photocoagulation and vitrectomy. In conclusion, this abstract provides a comprehensive overview of the pathogenesis, diagnosis and management of fundus bleeding or retinal haemorrhage. It serves as a valuable resource for clinicians and researchers involved in the care of patients with retinal haemorrhage, aiding in the understanding of its multifactorial aetiology and guiding evidence-based management strategies for improved visual outcomes.

From Sugar Spikes to Pressure Peaks: Navigating the World of Diabetes, Hypertension, Obesity, and Kidney Health.

Diabetes, hypertension, obesity, and chronic kidney disease (CKD) are major public health challenges globally, contributing significantly to morbidity and mortality. The co-occurrence and interplay among these conditions exacerbate health outcomes, highlighting the need for an integrated understanding and approach to management. This narrative review aims to explore the complex relationships between diabetes, hypertension, obesity, and CKD, elucidating their collective impact on health. It discusses the epidemiological trends, underlying pathophysiological mechanisms, genetic predispositions, current treatment strategies, and the future direction of research and therapy. An extensive review of current literature was conducted, focusing on the epidemiology, pathophysiology, risk factors, diagnosis, and treatment of diabetes, hypertension, obesity, and CKD. Additionally, the review delves into the genetic and molecular biology underlying these conditions, the potential for personalized medicine, and the importance of a multidisciplinary approach to care. The review identifies key areas where these conditions intersect, enhancing disease progression and complicating management. It highlights the role of genetic and environmental factors in disease etiology, the critical need for personalized treatment strategies, and the gaps in current management approaches. Innovations in pharmacotherapy, monitoring technologies, and the potential of pharmacogenomics are discussed as avenues for advancing patient care. Diabetes, hypertension, obesity, and CKD are intricately linked, necessitating an integrated, patient-centered approach to care that goes beyond traditional treatment modalities. Future research should focus on collaborative models and interdisciplinary strategies to address the multifaceted challenges posed by these conditions. Emphasizing personalized medicine and leveraging technological advancements offer promising pathways to improve outcomes and reduce the global health burden of these metabolic disorders.

Management of hypertension in heart transplant recipients: an ongoing conundrum.

Hypertension remains one of the most common clinical problems leading to significant posttransplant complications. This study reviews the pathophysiology of hypertension in the postcardiac transplant phase and provides an update on currently available antihypertensive therapies for heart transplant patients. The true prevalence of hypertension in the heart transplant population remains unknown. Effective blood pressure (BP) control is key to prevent left ventricular remodeling, diastolic dysfunction and stroke. Calcium channel blockers (CCBs) are the most commonly and preferred agents in the early posttransplant phase and may have renal protective effects. Angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs) can all be used as second line antihypertensive agents and may have a role in preventing other long-term complications such as calcineurin-inhibitor induced nephropathy. Although more data are needed, sodium-glucose co-transporter 2 inhibitors (SGLT2i) appeared to be well tolerated and could be considered especially in the presence of type diabetes and chronic kidney disease. Conversely, angiotensin receptor-neprilysin inhibition (ARNI) have not been studied in the heart transplant population therefore cannot be recommended at this time. Hypertension is very common after heart transplant. Early steroid wean and traditional risk factor modification play an important part in the management of post-heart transplant hypertension. CCB, ACEI, ARB are the preferred antihypertensive agents to improve postcardiac transplant complications. Novel therapies such as SGLT2i appear well tolerated and may have benefits in both BP and glycemic control in heart transplant; however, larger trials are needed.

Association between skin lymphangiogenesis parameters and arterial hypertension status in patients: An observational study.

Recent studies have indicated that the skin lymphatic system and interstitium may play a role in the pathophysiology of arterial hypertension (AH). We aimed to determine whether the set of pathway parameters described previously in rodents would allow for the distinction between hypertensive and normotensive patients. Molecular and histopathological parameters from the skin and blood of patients with AH (AH group, n = 53), resistant AH (RAH group, n = 32) and control (C group, n = 45) were used, and a statistical multivariate bootstrap methodology combining partial least squares-discriminant analysis (PLS-DA) and selectivity ratio (SR) were applied. The C vs RAH model presented the best prediction performance (AUC test = 0.90) and had a sensitivity and specificity of 73.68% and 83.33%, respectively. However, the parameters selected for the C vs AH group model were the most important for the pathway described in the rodent model, i.e., greater density of the skin lymphatic vessels (D2-40 expression) and greater number of macrophages (CD68 expression), higher expression of the messenger ribonucleic acid (mRNA) of nuclear factor of activated T cells 5 (NFAT5), vascular endothelial growth factor C (VEGFC) and podoplanin (PDPN) in the skin, greater concentration of hyaluronic acid (HA) in the skin, and lower serum concentration of VEGF-C. Our study suggests that the NFAT5/VEGF-C/lymphangiogenesis pathway, previously described in rodent studies, may also be present in human HA. Further experiments are needed to confirm our findings.

Targeting Hypertension: A Review on Pathophysiological Factors and Treatment Strategies.

Hypertension is one of the primary causes of cardiovascular diseases and death, with a higher prevalence in low- and middle-income countries. The pathophysiology of hypertension remains complex, with 2% to 5% of patients having underlying renal or adrenal disorders. The rest are referred to as essential hypertension, with derangements in various physiological mechanisms potentially contributing to the development of essential hypertension. Hypertension elevates the risk of cardiovascular disease (CVD) events (coronary heart disease, heart failure, and stroke) and mortality. First-line therapy for hypertension is lifestyle change, which includes weight loss, a balanced diet that includes low salt and high potassium intake, physical exercise, and limitation or elimination of alcohol use. Blood pressure-lowering effects of individual lifestyle components are partially additive, enhancing the efficacy of pharmaceutical treatment. The choice to begin antihypertensive medication should be based on the level of blood pressure and the existence of a high atherosclerotic CVD risk. First-line hypertension treatment includes a thiazide or thiazide-like diuretic, an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, and a calcium channel blocker. Addressing hypertension will require continued efforts to improve access to diagnosis, treatment, and lifestyle interventions.

Pathophysiology, Diagnosis, and Management of Portal Hypertension in the Pediatric Population

AbstractPortal hypertension is caused by resistance to the portal blood flow, which most commonly occurs in the setting of cirrhosis. Complications of portal hypertension can cause significant morbidity and mortality in the pediatric population. Portal hypertension is diagnosed when the hepatic venous pressure gradient (HVPG) is more than 5 mm Hg, and potential bleeding complications from esophageal and gastric varices are more likely when the HVPG is more than 10 mm Hg. Diagnosis can be made clinically; however, liver biopsy with measurement of the HVPG is ultimately required. The management of portal hypertension in pediatric patients is typically aimed at treatment of the complications. Despite the multiple pharmacologic, endoscopic, surgical, and interventional radiologic management techniques that are available, some pediatric patients will ultimately require liver transplant. Prompt referral is needed in such cases.

Evaluation of Patients Diagnosed with Essential Hypertension in Terms of Mental and Personality Disorders.

Recent studies have suggested a link between hypertension and psychiatric disorders. However, the relationship between hypertension and mental health conditions remains unclear. So in this study, it was aimed to compare the prevalence of psychiatric diseases seen in hypertension patients with the healthy group. Psychiatric interviews were conducted with 104 patients in the hypertension group and 102 participants in the control group. The Sociodemographic and Clinical Data Form, Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scale (HAM-A), Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) Disorders, Structured Clinical Interview for DSM-5-Clinician Version, and DSM-5 Structured Clinical Interview for Personality Disorders were implemented for participants. Patients with hypertension were found to have a significantly higher number of psychiatric disorders compared to the control group (χ 2 = 29.389; P = .001). Statistically significant difference in the diagnosis of severe depression, chronic depression disorder, and specific phobia was discovered between the 2 groups (P < .05). The HAM-A and HAM-D scores were also significantly higher in the hypertension group (P < .001). No statistically significant difference was found between the patient and control groups in terms of the frequency of personality disorders. (χ 2 = 0.045; P = .833). The fact that depression and anxiety symptoms are more common in hypertension patients stands out as a subject that needs further investigation in terms of both the pathophysiology of hypertension. In this regard, since essential hypertension is a serious risky disease for mortality and morbidity on its own, it is critical to conduct psychiatric screening and develop new additional treatments to provide patients with supportive care.

Clinical Correlates of a Nonplexiform Vasculopathy in Patients With a Diagnosis of Idiopathic Pulmonary Arterial Hypertension

The clinical phenotype of idiopathic pulmonary arterial hypertension (IPAH) patients has changed. . Whether or not subgroups of IPAH patients have different vascular phenotypes is a subject of debate. What are the histological patterns and their clinical correlates in patients diagnosed with IPAH or hereditary PAH? In this this cross-sectional registry study lung histology of 50 IPAH patients was qualitatively assessed by two experienced pathologists. In addition, quantitative analysis by means of histopathological morphometry using immunohistochemistry was performed. Histopathological characteristics were correlated with clinical and hemodynamic parameters. In this cohort of 50 IPAH patients, a plexiform vasculopathy was observed in 26/50 (52%) of patients, while 24/50 (48%) patients had a non-plexiform vasculopathy. The non-plexiform vasculopathy was characterized by prominent pulmonary microvascular (arterioles and venules) remodeling and vascular rarefaction. While hemodynamic parameters were comparable in plexiform versus non-plexiform vasculopathy, patients with non-plexiform vasculopathy were older, more often male, had a stronger history of cigarette smoking and lower diffusing capacity for carbon monoxide (DLCO) at diagnosis No mutations in established PAH genes were found in the non-plexiform group. This study reveals different vascular phenotypes within the current spectrum of patients diagnosed with IPAH, separated by clinical characteristics (age, sex, , history of cigarette smoking, and DLCO at diagnosis). Potential differences in underlying pathobiological mechanisms between patients with plexiform and non-plexiform / microvascular disease should be taken into account in future research strategies unravelling the pathophysiology of pulmonary hypertension and developing biology-targeted treatment approaches.

The pharmaco-epigenetics of hypertension: a focus on microRNA.

Hypertension is a major harbinger of cardiovascular morbidity and mortality. It predisposes to higher rates of myocardial infarction, chronic kidney failure, stroke, and heart failure than most other risk factors. By 2025, the prevalence of hypertension is projected to reach 1.5 billion people. The pathophysiology of this disease is multifaceted, as it involves nitric oxide and endothelin dysregulation, reactive oxygen species, vascular smooth muscle proliferation, and vessel wall calcification, among others. With the advent of new biomolecular techniques, various studies have elucidated a gaping hole in the etiology and mechanisms of hypertension. Indeed, epigenetics, DNA methylation, histone modification, and microRNA-mediated translational silencing appear to play crucial roles in altering the molecular phenotype into a hypertensive profile. Here, we critically review the experimentally determined associations between microRNA (miRNA) molecules and hypertension pharmacotherapy. Particular attention is given to the epigenetic mechanisms underlying the physiological responses to antihypertensive drugs like candesartan, and other relevant drugs like clopidogrel, aspirin, and statins among others. Furthermore, how miRNA affects the pharmaco-epigenetics of hypertension is especially highlighted.

Mesenteric artery smooth muscle cells from hypertensive rats have increased microtubule acetylation.

The dynamic nature of the microtubule network is dependent in part by post-translational modifications (PTMs) - particularly through acetylation, which stabilizes the microtubule network. Whether PTMs of the microtubule network in vascular smooth muscle cells (VSMCs) contribute to the pathophysiology of hypertension is unknown. The aim of this study was to determine the acetylated state of the microtubule network in the mesenteric arteries of spontaneously hypertensive rats (SHR). Experiments were performed on male normotensive rats and SHR mesenteric arteries. Western blotting and mass spectrometry determined changes in tubulin acetylation. Wire myography was used to investigate the effect of tubacin on isoprenaline-mediated vasorelaxations. Isolated cells from normotensive rats were used for scanning ion conductance microscopy (SICM). Mass spectrometry and Western blotting showed that tubulin acetylation is increased in the mesenteric arteries of the SHR compared with normotensive rats. Tubacin enhanced the β-adrenoceptor-mediated vasodilatation by isoprenaline when the endothelium was intact, but attenuated relaxations when the endothelium was denuded or nitric oxide production was inhibited. By pre-treating vessels with colchicine to disrupt the microtubule network, we were able to confirm that the effects of tubacin were microtubule-dependent. Using SICM, we examined the cell surface Young's modulus of VSMCs, but found no difference in control, tubacin-treated, or taxol-treated cells. Acetylation of tubulin at Lys40 is elevated in mesenteric arteries from the SHR. Furthermore, this study shows that tubacin has an endothelial-dependent bimodal effect on isoprenaline-mediated vasorelaxation.

Chronic intermittent hypoxia-induced hypertension: the impact of sex hormones.

Obstructive sleep apnea, a common form of sleep-disordered breathing, is characterized by intermittent cessations of breathing that reduce blood oxygen levels and contribute to the development of hypertension. Hypertension is a major complication of obstructive sleep apnea that elevates the risk of end-organ damage. Premenopausal women have a lower prevalence of obstructive sleep apnea and cardiovascular disease than men and postmenopausal women, suggesting that sex hormones play a role in the pathophysiology of sleep apnea-related hypertension. The lack of protection in men and postmenopausal women implicates estrogen and progesterone as protective agents but testosterone as a permissive agent in sleep apnea-induced hypertension. A better understanding of how sex hormones contribute to the pathophysiology of sleep apnea-induced hypertension is important for future research and possible hormone-based interventions. The effect of sex on the pathophysiology of sleep apnea and associated intermittent hypoxia-induced hypertension is of important consideration in the screening, diagnosis, and treatment of the disease and its cardiovascular complications. This review summarizes our current understanding of the impact of sex hormones on blood pressure regulation in sleep apnea with a focus on sex differences.

Lipid Horizons: Recent Advances and Future Prospects in LBDDS for Oral Administration of Antihypertensive Agents.

The lipid-based drug delivery system (LBDDS) is a well-established technique that is anticipated to bring about comprehensive transformations in the pharmaceutical field, impacting the management and administration of drugs, as well as treatment and diagnosis. Various LBDDSs verified to be an efficacious mechanism for monitoring hypertension systems are SEDDS (self-nano emulsifying drug delivery), nanoemulsion, microemulsions, vesicular systems (transferosomes and liposomes), and solid lipid nanoparticles. LBDDSs overcome the shortcomings that are associated with antihypertensive agents because around fifty percent of the antihypertensive agents experience a few drawbacks including short half-life because of hepatic first-pass metabolism, poor aqueous solubility, low permeation rate, and undesirable side effects. This review emphasizes antihypertensive agents that were encapsulated into the lipid carrier to improve their poor oral bioavailability. Incorporating cutting-edge technologies such as nanotechnology and targeted drug delivery, LBDDS holds promise in addressing the multifactorial nature of hypertension. By fine-tuning drug release profiles and enhancing drug uptake at specific sites, LBDDS can potentially target renin-angiotensin-aldosterone system components, sympathetic nervous system pathways, and endothelial dysfunction, all of which play crucial roles in hypertension pathophysiology. The future of hypertension management using LBDDS is promising, with ongoing reviews focusing on precision medicine approaches, improved biocompatibility, and reduced toxicity. As we delve deeper into understanding the intricate mechanisms underlying hypertension, LBDDS offers a pathway to develop next-generation antihypertensive therapies that are safer, more effective, and tailored to individual patient needs.

Clinical Characteristics and Outcomes of Patients with Heart Failure of Hypertensive Etiology: Analysis of Colombian Heart Failure Registry (RECOLFACA)

Introduction: Arterial hypertension represents one of the main comorbidities observed in patients with heart failure (HF) and one of the main risk factors for its development. Despite this, studies assessing this hypertensive etiology are scarce in Latin America. Our objective was to analyze the prevalence of HF of hypertensive etiology and evaluate its prognosis in patients enrolled in the Colombian Heart Failure Registry (RECOLFACA by its Spanish acronym). Methods: RECOLFACA recruited adult patients diagnosed with HF in 60 centers in Colombia between 2017 and 2019. The primary outcome was all-cause mortality. A Cox proportional hazards regression model was used to assess factors associated with primary outcomes in patients with hypertensive HF. A p value <0.05 was considered significant. All statistical tests were two-tailed. Results: Out of the total number of patients evaluated in RECOLFACA (n = 2,514), 804 had a diagnosis of HF with hypertensive etiology (31.9%). These patients were less frequently males and had a significantly older age and lower prevalence of comorbidities than those with HF of other etiologies. Additionally, patients with hypertensive HF had a higher prevalence of HF with preserved ejection fraction (HFpEF) (34.1% vs. 28.3%; p = 0.004). Finally, type 2 diabetes mellitus, chronic obstructive pulmonary disease diagnosis, and NYHA class IV were classified as independent mortality risk factors. Conclusions: Hypertensive HF represents about one-third of the total number of patients with HF in RECOLFACA. Compared with HF of other etiologies, it presents a differential clinical profile – older age and a higher prevalence of HFpEF. RECOLFACA has become a useful tool to characterize patients with HF in Colombia, with which it has been possible to carry out a more specific search and reach the diagnosis of this pathology in our population, and it has served as an example to stimulate registries of patients with HF in other countries in the region.

The mediating effect of sleep disturbance on the association between hypertension and depression: a national data analysis

BackgroundSleep disturbance is a common among people with hypertension. However, the mediating role of sleep disturbance in the association between hypertension and depression remains unclear. This study aims to investigate the mediating role of sleep disturbance in the association between hypertension and depression.Materials and methodsThis was cross-sectional study. The data were derived from the Indonesian Family Life Survey Fifth Wave (2014–2015). We include a total of 19,138 adults’ participants with age range from 18 to 65 years old who completed response on the variable of hypertension, sleep disturbance, and depression. The mediating model analysis was processed using the PROCESS macro ins SPSS from Hayes model.ResultsDepression was reported by 22% of total respondents. The group with hypertension showed a substantially higher prevalence of depression than non-hypertension group (P < 0.001). Hypertension had a significant overall effect on depression (β = 0.682; 95%CI 0.489 to 0.875, P < 0.001). The direct effect of hypertension on depression was significant (β = 0.418; 95%CI 0.244 to 0.592, P < 0.001) and the indirect effect that mediated by sleep disturbance was also significant (β = 0.264, 95%CI 0.174 to 0.356, P < 0.001). It is worth noting that sleep disturbance partially mediated the association between hypertension and depression.ConclusionThe findings of this study indicated that sleep disturbance contributed to the etiology of depression and hypertension in adult populations. Nurses should be involved in managing sleep disturbances, such as using behavioral therapy, as it may serve as both a treatment and primary prevention measure for depression and hypertension.Graphical

Jagged 2 inhibition attenuates hypoxia-induced mitochondrial damage and pulmonary hypertension through Sirtuin 1 signaling.

Notch pathway has played a significant role in the pathophysiology of pulmonary hypertension (PH). However, the role of Jagged 2 (Jag2), one ligand of Notch, remains to be elucidated.Therefore, determining the contribution of Jag2 to PH and its impact on pulmonary artery smooth muscle cells (PASMCs) was the aim of this investigation. Adeno-associated virus-mediated Jag2 inhibition was used to explore the role of Jag2 in peripheral pulmonary vascular remodeling assessed in a rat model of chronic hypoxia (10% O2, 4 weeks) induced pulmonary hypertension. In vitro, the effect of Jag2 silencing on hypoxia (1% O2, 24h) induced rat PASMCs was determined. Group differences were assessed using a 2-sided unpaired Student's t-test for two groups and one-way ANOVA for multiple groups. Jag2 upregulation was first confirmed in rats with sustained hypoxia-induced PH using publicly available gene expression data, experimental PH rat models and hypoxia induced rat PASMCs. Jag2 deficiency decreased oxidative stress injury, peripheral pulmonary vascular remodeling (0.276±0.020 vs. 0.451±0.033 μm, P<0.001, <50μm), and right ventricular systolic pressure (36.8±3.033 vs. 51.8±4.245 mmHg, P<0.001) in the chronic hypoxia-induced rat model of PH. Moreover, Jag2 knockdown decreased proliferation (1.227±0.051 vs. 1.45±0.07, P = 0.012), increased apoptosis (16.733%±0.724% vs. 6.56%±0.668%, P<0.001), and suppressed mitochondrial injury in hypoxia-treated rat PASMCs. Jag2 inhibition restored the activity of the Nrf2/HO-1 pathway, which was abolished by Sirtuin 1 deficiency. These findings show that Jag2 is essential for modulating pulmonary vascular dysfunction and accelerating PH, and that inhibition of Jag2 expression suppresses the progression and development of PH.