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Background: We aimed to investigate the effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on blood pressure, blood glucose and blood lipid in diabetic patients with hypertension. Methods: A total of 300 diabetic patients and essential hypertension admitted to the Second Affiliated Hospital of Dalian Medical University, Dalian, China from January 2021 to December 2022 were selected. They were divided into an observation group and a control group using a random number table method. The control group was treated with conventional antihypertensive drugs, hypoglycemic drugs, and lipid-lowering drugs. The observation group was supplemented with liraglutide based on the control group. Blood pressure, blood glucose and blood lipid of the two groups were compared at the initial stage of medication and after 4 weeks and half a year, and the influencing factors of patients with persistent hypertension were further analyzed through Logistic regression. Results: After 4 weeks and 6 months of medication, inter group comparisons showed that systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG) and glycated hemoglobin (HbA1c), as well as total cholesterol (TC), triacylglycerol (TG), and plasma arteriosclerosis index (AIP) in the observation group were significantly lower than those in the control group (P<0.05). Multivariate Logistic regression model analysis showed that age, smoking history, drinking history, taking conventional antihypertensive drugs, taking hypoglycemic drugs, taking lipid-lowering drugs, BMI, FBG, HbA1c and LDL-C were independent influencing factors for persistent hypertension (P<0.05). Conclusion: GLP-1RAs could effectively improve the indexes including blood pressure, blood glucose and blood lipid in diabetic patients with hypertension.
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OBJECTIVE: To explore the relationship between rs1410996 polymorphism of CFH gene and essential hypertension (EH) in the Yunnan Han population. METHODS: rs1410996 of CFH gene was genotyped based on the collected clinical phenotypes of the EH patients (n = 520) and healthy people (n = 494). RESULTS: On the genotype model and dominance model, there was no relationship between rs1410996 of CFH gene and EH after adjustment (P > 0.05). On the dominance model of male EH patients, the pulse pressure (PP) level of CC genotype carriers was higher than that of (CT + TT) genotype carriers after adjustment (P < 0.05). CONCLUSION: rs1410996 of CFH gene has no correlation with the genetic susceptibility to EH in the Yunnan Han population, but it is related to the PP level in male patients.
Subject(s)
Asian People , Complement Factor H , Essential Hypertension , Genetic Predisposition to Disease , Genotype , Polymorphism, Single Nucleotide , Humans , Male , Essential Hypertension/genetics , Middle Aged , Female , China , Complement Factor H/genetics , Polymorphism, Single Nucleotide/genetics , Asian People/genetics , Gene Frequency/genetics , Aged , Case-Control Studies , Adult , Hypertension/genetics , Genetic Association Studies/methods , Alleles , Blood Pressure/geneticsABSTRACT
BACKGROUND: Elevated soluble stimulating factor 2 (sST2) level is observed in cardiovascular diseases, such as heart failure and acute coronary syndrome, which reflects myocardial fibrosis and hypertrophy, indicating adverse clinical outcomes. However, the association between sST2 and hypertensive heart disease are less understood. This study aimed to determine the relationship of sST2 with left ventricular hypertrophy (LVH) and geometric remodeling in essential hypertension (EH). METHODS: We enrolled 483 patients (aged 18-80 years; 51.35% female). sST2 measurements and echocardiographic analyses were performed. RESULTS: Stepwise multiple linear regression analysis showed significant associations between sST2, left ventricular (LV) mass, and LV mass index. The prevalence of LVH and concentric hypertrophy (CH) increased with higher sST2 grade levels (p for trend<0.05). Logistic regression analysis suggested that the highest tertile of sST2 was significantly associated with increased LVH risk, compared with the lowest tertile (multivariate-adjusted odds ratio [OR] of highest group: 6.61; p<0.001). Similar results were observed in the left ventricular geometric remodeling; the highest tertile of sST2 was significantly associated with increased CH risk (multivariate-adjusted OR of highest group: 5.80; p<0.001). The receiver operating characteristic analysis results revealed that sST2 had potential predictive value for LVH (area under the curve [AUC]: 0.752, 95% confidence interval [CI]: 0.704-0.800) and CH (AUC: 0.750, 95% CI: 0.699-0.802) in patients with EH. CONCLUSIONS: High sST2 level is strongly related to LVH and CH in patients with EH and can be used as a biomarker for the diagnosis and risk assessment of hypertensive heart disease.
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Patients with obstructive sleep apnea (OSA) experience insulin resistance and its clinical consequences, including hypertriglyceridemia, reduced high density lipoprotein-associated cholesterol (HDL-c), visceral adiposity, hepatic steatosis, increased epicardial fat thickness, essential hypertension, glucose intolerance, increased risk for type 2 diabetes, chronic kidney disease, subclinical vascular damage, and increased risk for cardiovascular events. Obesity is a major contributor to OSA. The prevalence of OSA is almost universal among patients with severe obesity undergoing bariatric surgery. However, insulin resistance and its clinical complications occur in OSA patients irrespective of general obesity (body mass index). In OSA patients, apnea episodes during sleep induce oxyhemoglobin desaturation and tissue hypoxia. Insulin resistance is an adaptive response to tissue hypoxia and develops in conditions with limited tissue oxygen supply, including healthy subjects exposed to hypobaric hypoxia (high altitude) and OSA patients. Indicators of oxyhemoglobin desaturation have been robustly and independently linked to insulin resistance and its clinical manifestations in patients with OSA. Insulin resistance mediates the elevated rate of type 2 diabetes, chronic kidney disease, and cardiovascular disease unexplained with traditional cardiovascular risk factors present in OSA patients. Pathophysiological processes underlying hypoxia-induced insulin resistance involve hypoxia inducible factor-1 upregulation and peroxisome proliferator-activated receptor-gamma (PPAR- γ ) downregulation. In human adipose tissue, PPAR- γ activity promotes glucose transport into adipocytes, lipid droplet biogenesis, and whole-body insulin sensitivity. Silencing of PPAR- γ in the adipose tissue reduces glucose uptake and fat accumulation into adipocytes and promotes insulin resistance. In conclusion, tissue hypoxia drives insulin resistance and its clinical consequences in patients with OSA, regardless of body mass index.
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Background: Continuity of care is one of the main principles of family medicine, described as a relationship with a single provider that extends beyond a single illness episode. This retrospective study, conducted at King Saud University Family Medicine Center in Riyadh, Saudi Arabia, aimed to investigate the impact of having a regular primary care provider on clinical outcomes and preventive service delivery for patients with diabetes and/or hypertension. Methods: The study, spanning 2017 to 2019, included 400 patients diagnosed with diabetes and/or hypertension for at least six months before the 6-month pre-attachment period to regular family medicine physicians in 2018. Data before and after attachment for at least six months were compared using electronic health records. Results: The mean age of the patients was 60.9, with a predominant female representation (66.8%) and 90.7% Saudis. Results indicated a significant improvement in glycated hemoglobin (HbA1c) levels (p = 0.005) and systolic blood pressure (p = 0.014) post-attachment. Preventive service delivery saw notable enhancements, with increased colon cancer screening (p = 0.03), breast cancer screening (p < 0.001), and retinal screening (p < 0.001) post-attachment. Conclusion: This study's findings underscore the importance of continuity of care in chronic disease management and provide valuable and promising insights into the Saudi healthcare context, aligning with the Saudi Ministry of Health's vision for universal access to regular primary care providers.
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Background: While aldosterone plays an important role in blood pressure regulation, its role in essential hypertension (EHT) remains unclear. Here, we systematically investigated the secretion of biologically-active free aldosterone in saliva in response to awakening (AldAR) and during the day (AldDay) in EHT compared to normotensive controls (NT). Methods: In 30 men with EHT and 30 age-matched NT, AldAR saliva samples were collected immediately after awakening and 15, 30, 45, and 60â min thereafter and AldDay samples were collected from 08:30-22:00â h on two consecutive days. Results: Over the course of the day, men with EHT had higher repeated AldDay levels compared to NT (p = .002) with higher concentrations in the morning hours (p's ≤ .047), a steeper decline over the course of the day (p's ≤ .018), and similar concentrations in the evening (p's ≥ .21). Regarding AldAR, we observed higher concentrations in EHT at awakening (p = .017) and borderline higher concentrations at 15â min (p = .086). No differences were found 30-60â min after awakening (p's ≥ .34). Analyses with repeated and aggregated AldAR levels resulted in borderline significantly higher free aldosterone in EHT (p's ≤ .077). Complementary analyses confirmed linear associations between higher blood pressure and higher AldAR and AldDay levels. Conclusions: Our data point to elevated salivary free aldosterone secretion in EHT over the course of the day, particularly in the morning hours. As the free aldosterone fraction is considered biologically active, our data may point to a biological mechanism underlying EHT.
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The EXCITE-HT study aimed to evaluate the efficacy and safety of esaxerenone versus thiazide diuretics (trichlormethiazide) as second-line treatment for Japanese patients with uncontrolled essential hypertension. This was a 12-week, multicenter, randomized, open-label, parallel-group study. The non-inferiority of esaxerenone to trichlormethiazide was confirmed if the upper limit of the two-sided 95% confidence interval (CI) for the difference in systolic blood pressure (SBP)/diastolic blood pressure (DBP) change between groups was below 3.9/2.1 mmHg. A total of 295 and 290 patients were included in the esaxerenone and trichlormethiazide groups, respectively. The non-inferiority of esaxerenone to trichlormethiazide was demonstrated: least squares mean change differences in morning home SBP/DBP at end of treatment (EOT) were -2.2 (95% CI, -3.6, -0.8) mmHg for SBP/-0.6 (-1.4, 0.2) mmHg for DBP. Morning home, bedtime home, and office BP significantly decreased (all p < 0.001) from baseline to EOT in both groups. The urinary albumin-to-creatinine ratio and N-terminal pro-brain natriuretic peptide level decreased from baseline to Week 12 in both groups, with no notable intergroup difference. Serum potassium elevations occurred more frequently with esaxerenone, while serum potassium reductions occurred more with trichlormethiazide. Uric acid elevations were observed in both groups, but more frequently with trichlormethiazide than esaxerenone. No cases of gout occurred in this study. Reductions in estimated glomerular filtration rate were similarly observed in both groups. EXCITE-HT is the first randomized controlled study to demonstrate evidence that esaxerenone is non-inferior to trichlormethiazide as second-line treatment for Japanese patients with uncontrolled essential hypertension, with no new safety concerns. The EXCITE-HT study demonstrated the non-inferiority of esaxerenone to trichlormethiazide in its morning home blood pressure lowering effect and safety profile in Japanese patients with uncontrolled essential hypertension who were previously treated with an angiotensin II receptor blocker or calcium channel blocker.
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Endothelial dysfunction is acknowledged as a marker for subclinical target organ damage (STOD) in hypertension, though its therapeutic potential has not yet been clarified. This study assessed whether early endothelial function improvement (EEFI) reduced STOD in patients with essential hypertension (EH). We conducted a retrospective cohort analysis of 456 EH patients initially free from STOD. Endothelial function was assessed using brachial artery flow-mediated dilation (FMD), with values ≤ 7.1% indicating dysfunction. Patients were initially categorized by endothelial status (dysfunction: n = 180, normal: n = 276), and further divided into improved or unimproved groups based on changes within three months post-enrollment. During a median follow-up of 25 months, 177 patients developed STOD. The incidence of STOD was significantly higher in patients with initial dysfunction compared to those with normal function. Kaplan-Meier analysis indicated that the improved group had a lower cumulative incidence of STOD compared to the unimproved group (p < 0.05). Multivariable Cox regression confirmed EEFI as an independent protective factor against STOD in EH patients (p < 0.05), regardless of their baseline endothelial status, especially in those under 65 years old, non-smokers, and with low-density lipoprotein cholesterol levels ≤ 3.4 mmol/L. In conclusion, EEFI significantly reduces STOD incidence in EH patients, particularly in specific subgroups, emphasizing the need for early intervention in endothelial function to prevent STOD.
Subject(s)
Endothelium, Vascular , Hypertension , Humans , Male , Female , Middle Aged , Endothelium, Vascular/physiopathology , Aged , Retrospective Studies , Hypertension/physiopathology , Incidence , Brachial Artery/physiopathology , Essential Hypertension/physiopathology , Risk Factors , VasodilationABSTRACT
It remained debates on metabolic-related disorders in patients with primary aldosteronism (PA) and essential hypertension (EH). A systematic review and meta-analysis was conducted to explore the prevalence of metabolic syndrome (MS) and the related indicators in PA and EH. PubMed, Embase, Web of Science and the Cochrane Central Register of Controlled Trials from their commencement to December 2023 were searched for eligible studies. The meta-analysis was performed by Review Manager 5.3 and STATA 15.1 software. A total of 12 studies were included, revealing that there was no significant difference between PA and EH in the prevalence of MS (1.27[0.92, 1.76], p = 0.14) with higher heterogeneity (I2 = 68%, p = 0.0002), while it became significant different (1.45[1.17, 1.81], p = 0.0008) and lower heterogeneity (I2 = 26%, p = 0.19) in patients who were overweight or obese by subgroup analysis. Higher systolic blood pressure (2.99[0.67, 5.31], p = 0.01; I2 = 43%, p = 0.06) and diastolic blood pressure (2.10[0.82, 3.38], p = 0.001; I2 = 36%, p = 0.11) with lower heterogeneity, and lower triglyceride in PA group with higher heterogeneity (-0.23[-0.37, -0.09], p = 0.001; I2 = 76%, p < 0.0001) were observed. No significant difference was found in other indicators. This study showed a higher prevalence of MS in patients who were overweight or obese with PA. However, it was not the same in these patients who were in normal weight. More researches were needed to explore the relationship between PA and metabolism of glucose and lipid.
Subject(s)
Essential Hypertension , Hyperaldosteronism , Metabolic Syndrome , Metabolic Syndrome/epidemiology , Hyperaldosteronism/epidemiology , Hyperaldosteronism/complications , Humans , Prevalence , Essential Hypertension/epidemiology , Essential Hypertension/physiopathology , Blood Pressure/physiology , Female , Middle Aged , Male , Obesity/epidemiology , Obesity/complications , Adult , Overweight/epidemiology , Overweight/complicationsABSTRACT
Introduction To enhance the diagnosis of anatomic left ventricular hypertrophy (LVH) using electrocardiography (ECG), we aimed to identify common ECG amplitude and non-amplitude abnormalities in Nigerian patients with hypertensive echocardiographic LVH. Method The study included 1,765 patients with essential hypertension aged 18 years and older from the Federal Medical Centre Abuja Hypertension Registry (FMCAHR). Participants underwent echocardiography and ECG following the American College of Cardiology and the American Society of Echocardiography guidelines. Results The prevalence of overall ECG LVH amplitude criteria (43.8%) and individual criteria of Cornell voltage (27.1%), Sokolow-Lyon voltage (23.2%), and Gubner-Ungerleider (13.9%) were higher than non-amplitude ECG abnormalities among patients with echocardiographic LVH. The sensitivity and specificity of LVH criteria were 43.8% and 79.5% for overall ECG LVH, 23.2% and 87.2% for Sokolow-Lyon voltage, 27.1% and 93.3% for Cornell voltage, and 13.9% and 95.4% for Gubner-Ungerleider criteria, respectively. After multivariable adjustment, non-amplitude ECG changes, including prolonged corrected QT (QTc) (odds ratio (OR): 1.68, 95% confidence interval (CI): 1.06-2.66), left ventricular (LV) strain pattern (OR: 1.83, CI: 1.23-2.72), left axis deviation (OR: 1.56, CI: 1.09-2.24), poor R wave progression (OR: 2.36, CI: 1.40-3.97), premature ventricular contractions (OR: 1.80, CI: 1.10-2.91), premature atrial contractions (OR: 2.06, CI: 1.10-3.87), atrial fibrillation (OR: 2.40, CI: 1.20-4.82), and left atrial abnormality (OR: 8.43, CI: 2.95-24.05), were associated with echocardiographic LVH (p < 0.05). Conclusion In our cohort of hypertensive patients, ECG LVH amplitude criteria were the most frequently observed abnormalities associated with echocardiographic LVH. Our findings suggest that despite the low sensitivity, ECG LVH amplitude criteria may remain valuable in diagnosing echocardiographic LVH.
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Hypertension is a very prevalent condition associated with high mortality and morbidity, secondary to changes resulting in blood vessels and resultant end-organ damage. Haemodynamic changes, including an initial rise in cardiac output followed by an increase in total peripheral resistance, denote the early changes associated with borderline or stage 1 hypertension, especially in young men. Increased sodium reabsorption leading to kidney damage is another mechanism proposed as one of the initial triggers for essential hypertension. The underlying pathophysiological mechanisms include catecholamine-induced α1- and ß1-adrenoceptor stimulation, and renin-angiotensin-aldosterone system activation leading to endothelial dysfunction which is believed to lead to persistent blood pressure elevation.α1 blockers, α2 agonists, and ß blockers were among the first oral anti-hypertensives. They are no longer first-line therapy after outcome trials did not demonstrate any benefits over and above other agents, despite similar blood pressure reductions. Angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers), calcium channel blockers, and thiazide-like diuretics are now considered the first line of therapy, although adrenoceptor agents still have a role as second- or third-line therapy. The chapter also highlights hypertension in specific medical conditions such as pregnancy, phaeochromocytoma, hyperthyroidism, portal hypertension, pulmonary arterial hypertension, and ocular hypertension, to provide an overview for clinicians and researchers interested in the role of adrenoceptors in the pathophysiology and management of hypertension.
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Background: Previous studies have indicated a strong link between blood metabolites and hypertension, however the causality of metabolites and hypertension is unknown. Methods: Two-sample Mendelian randomization (MR) analysis was performed to assess the causal relationship between 486 blood metabolites and essential hypertension (EHT). Blood metabolite GWAS data was utilized as the exposure, with EHT GWAS data as the outcome. To further verify the results, another different source of EHT GWAS data was repeatedly analyzed. The major MR analytic approach used to determine causality was inverse variance weighted (IVW), with MR-Egger, Weighted Median, and MR-PRESSO models serving as supplements. We used the Cochran Q test to examine heterogeneity. Horizontal pleiotropy was examined using MR-Egger intercept and MR-PRESSO global test. The MR Steiger test confirmed the causal relationship between blood metabolites and EHT. Results: In this study, nine blood metabolites associated with EHT were preliminarily identified by MR analysis, including four known metabolites (N-acetylornithine, X-12510-2-aminooctanoic acid, creatine, hexadecanedioate) and five unknown metabolites. Then another source of EHT GWAS data was repeatedly analyzed for further verification, and two overlapped metabolites (N-acetylornithine, X-12510-2-aminooctanoic acid) were found. There was a negative correlation between N-acetylornithine and EHT (OR = 0.987, 95% CI = 0.980-0.993, P = 1.01 × 10-4), Cochran's Q test suggested there was no heterogeneity (Q = 31.7586, P = 0.1331), MR-Egger intercept and MR-PRESSO global test suggested there was no horizontal pleiotropy (P > 0.05), Leave-one-out analysis indicated that no single single-nucleotide polymorphism (SNP) had a significant effect on the results, and MR Steiger test confirmed that the direction of causality was correct (P < 0.001). There was a negative correlation between X-12510-2-aminooctanoic acid and EHT (OR = 0.982, 95% CI = 0.972-0.993, P = 0.0017), and there was no evidence of heterogeneity or pleiotropy in multiple sensitivity analyses. Conclusion: The study discovered some blood metabolites causally linked to EHT, which might lead to new understandings of the pathophysiology of hypertension.
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Primary hypertension is a significant risk factor for cardiovascular diseases. However, the pathogenesis of primary hypertension involves multiple biological processes, including the nervous system, circulatory system, endocrine system, and more. Despite extensive research, there is no clear understanding of the regulatory mechanism underlying its pathogenesis. In recent years, miRNAs have gained attention as a regulatory factor capable of modulating the expression of related molecules through gene silencing. Therefore, exploring differentially expressed miRNAs in patients with essential hypertension (EH) may offer a novel approach for future diagnosis and treatment of EH. This study included a total of twenty Han Chinese population samples from Hefei, China. The samples consisted of 10 healthy individuals and 10 patients with EH. Statistical analysis was conducted to analyze the general information of the two-sample groups. High-throughput sequencing and base identification were performed to obtain the original sequencing sequences. These sequences were then annotated using various databases including Rfam, cDNA sequences, species repetitive sequences library, and miRBase database. The number of miRNA species contained in the samples was measured. Next, TPM values were calculated to determine the expression level of each miRNA. The bioinformatics of the differentiated miRNAs were analyzed using the OECloud tool, and RPM values were calculated. Furthermore, the reliability of the expression was analyzed by calculating the area under the Roc curve using the OECloud tools. Statistical analysis revealed no significant differences between the two samples in terms of age distribution, gender composition, smoking history, and alcohol consumption history (P > 0.05). However, there was a notable presence of family genetic history and high BMI in the EH population (P < 0.05). The sequencing results identified a total of 245 miRNAs, out of which 16 miRNAs exhibited differential expression. Among the highly expressed miRNAs were let-7d-5p, miR-101-3p, miR-122-5p, miR-122b-3p, miR-192-5p, and miR-6722-3p. On the other hand, the lowly expressed miRNAs included miR-103a-3p, miR-16-5p, miR-181a-2-3p, miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-221-3p, miR-30d-5p, miR-342-5p, and miR-543. This study initially identified 16 miRNAs that are aberrantly expressed and function in various processes associated with the onset and progression of essential hypertension. These miRNAs have the potential to be targeted for future diagnosis and treatment of EH. However, further samples are required to provide additional support for this study.
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Wnt/ß-catenin signaling dysregulation is associated with the pathogenesis of many human diseases, including hypertension and heart disease. The aim of this study was to immunohistochemically evaluate and compare the expression of the Fzd8, WNT1, GSK-3ß, and ß-catenin genes in the hearts of rats with spontaneous hypertension (SHRs) and deoxycorticosterone acetate (DOCA)-salt-induced hypertension. The myocardial expression of Fzd8, WNT1, GSK-3ß, and ß-catenin was detected by immunohistochemistry, and the gene expression was assessed with a real-time PCR method. In SHRs, the immunoreactivity of Fzd8, WNT1, GSK-3ß, and ß-catenin was attenuated in comparison to that in normotensive animals. In DOCA-salt-induced hypertension, the immunoreactivity of Fzd8, WNT1, GSK-3ß, and ß-catenin was enhanced. In SHRs, decreases in the expression of the genes encoding Fzd8, WNT1, GSK-3ß, and ß-catenin were observed compared to the control group. Increased expression of the genes encoding Fzd8, WNT1, GSK-3ß, and ß-catenin was demonstrated in the hearts of rats with DOCA-salt-induced hypertension. Wnt signaling may play an essential role in the pathogenesis of arterial hypertension and the accompanying heart damage. The obtained results may constitute the basis for further research aimed at better understanding the role of the Wnt/ß-catenin pathway in the functioning of the heart.
Subject(s)
Glycogen Synthase Kinase 3 beta , Hypertension , Myocardium , Wnt Signaling Pathway , beta Catenin , Animals , Hypertension/metabolism , Hypertension/etiology , Hypertension/chemically induced , Hypertension/pathology , Rats , Glycogen Synthase Kinase 3 beta/metabolism , Male , Myocardium/metabolism , Myocardium/pathology , beta Catenin/metabolism , beta Catenin/genetics , Wnt1 Protein/metabolism , Wnt1 Protein/genetics , Rats, Inbred SHR , Frizzled Receptors/metabolism , Frizzled Receptors/genetics , Desoxycorticosterone AcetateABSTRACT
Objective: 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. Methods: 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. Results: 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). Conclusion: 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.
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BACKGROUND: This study aimed to investigate the association between abdominal aortic calcification (AAC) and coronary heart disease (CHD) in essential hypertension (EH). METHODS: This study included patients diagnosed with EH during the 2013-2014 NHANES survey cycle. The study cohort was categorized into the following four groups based on their AAC-24 score: no AAC (0); mild AAC (1-4); moderate AAC (5-15); and severe AAC (16-24). Logistic regression models were used to assess the association between AAC and CHD. Restricted cubic spline curves (RCS) were used to explore possible nonlinear relationships between AAC and CHD. RESULTS: The prevalence of CHD was found to be higher in the moderate AAC and severe AAC groups than in the group without AAC (40.1% versus 30.9%, 47.7% versus 30.9%). On a continuous scale, the fully adjusted model showed a 7% increase in the risk of CHD prevalence per score increase in AAC [OR (95% CI) = 1.07 (1.03-1.11)]. On a categorical scale, the fully adjusted model showed the risk of CHD prevalence in EH patients with moderate AAC and severe AAC was 2.06 (95%CI, 1.23-3.45) and 2.18 (1.09-5.25) times higher than that in patients without AAC, respectively. The RCS curve suggested a dose-response linear relationship between AAC and CHD. CONCLUSION: These findings highlight that in patients with EH, a higher severity of AAC is associated with a higher risk of CHD prevalence.
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BACKGROUND: This study aimed to investigate the potential association between the circadian rhythm of blood pressure and deceleration capacity (DC)/acceleration capacity (AC) in patients with essential hypertension. METHODS: This study included 318 patients with essential hypertension, whether or not they were being treated with anti-hypertensive drugs, who underwent 24-hour ambulatory blood pressure monitoring (ABPM). Patients were categorized into three groups based on the percentage of nocturnal systolic blood pressure (SBP) dipping: the dipper, non-dipper and reverse dipper groups. Baseline demographic characteristics, ambulatory blood pressure monitoring parameters, Holter recordings (including DC and AC), and echocardiographic parameters were collected. RESULTS: In this study, the lowest DC values were observed in the reverse dipper group, followed by the non-dipper and dipper groups (6.46 ± 2.06 vs. 6.65 ± 1.95 vs. 8.07 ± 1.79 ms, P < .001). Additionally, the AC gradually decreased (-6.32 ± 2.02 vs. -6.55 ± 1.95 vs. -7.80 ± 1.73 ms, P < .001). There was a significant association between DC (r = .307, P < .001), AC (r=-.303, P < .001) and nocturnal SBP decline. Furthermore, DC (ß = 0.785, P = .001) was positively associated with nocturnal SBP decline, whereas AC was negatively associated with nocturnal SBP (ß = -0.753, P = .002). By multivariate logistic regression analysis, deceleration capacity [OR (95% CI): 0.705 (0.594-0.836), p < .001], and acceleration capacity [OR (95% CI): 1.357 (1.141-1.614), p = .001] were identified as independent risk factors for blood pressure nondipper status. The analysis of ROC curves revealed that the area under the curve for DC/AC in predicting the circadian rhythm of blood pressure was 0.711/0.697, with a sensitivity of 73.4%/65.1% and specificity of 66.7%/71.2%. CONCLUSIONS: Abnormal DC and AC density were correlated with a blunted decline in nighttime SBP, suggesting a potential association between the circadian rhythm of blood pressure in essential hypertension patients and autonomic nervous dysfunction.
Subject(s)
Antihypertensive Agents , Blood Pressure Monitoring, Ambulatory , Blood Pressure , Circadian Rhythm , Essential Hypertension , Heart Rate , Humans , Male , Female , Middle Aged , Essential Hypertension/physiopathology , Essential Hypertension/diagnosis , Essential Hypertension/drug therapy , Time Factors , Antihypertensive Agents/therapeutic use , Aged , Predictive Value of Tests , Adult , Risk Factors , Electrocardiography, Ambulatory , Acceleration , DecelerationABSTRACT
PURPOSE: This study aimed to evaluate the efficacy and tolerability of irbesartan (IRB) and amlodipine (AML) combination therapy in patients with essential hypertension whose blood pressure (BP) was not controlled by IRB monotherapy. METHODS: Two multicenter, randomized, double-blind, placebo-controlled, phase III studies were conducted in Korea (the I-DUO 301 study and the I-DUO 302 study). After a 4-week run-in period with either 150 mg IRB (I-DUO 301 study) or 300 mg IRB (I-DUO 302 study), patients with uncontrolled BP (ie, mean sitting systolic BP [MSSBP] ≥140 mmHg to <180 mmHg and mean sitting diastolic BP <110 mmHg) were randomized to the placebo, AML 5 mg, or AML 10 mg group. A total of 428 participants were enrolled in the 2 I-DUO studies. In the I-DUO 301 study, 271 participants were randomized in a 1:1:1 ratio to receive either IRB/AML 150/5 mg, IRB/AML 150/10 mg, or IRB 150 mg/placebo. In the I-DUO 302 study, 157 participants were randomized in a 1:1 ratio to receive IRB/AML 300/5 mg or IRB 300 mg/placebo. The primary endpoint was the change in MSSBP from baseline to week 8. Tolerability was assessed according to the development of treatment-emergent adverse events (TEAEs) and clinically significant changes in physical examination, laboratory tests, pulse, and 12-lead electrocardiography. FINDINGS: In I-DUO 301, the mean (SD) changes of MSSBP at week 8 from baseline were -14.78 (12.35) mmHg, -21.47 (12.78) mmHg, and -8.61 (12.19) mmHg in the IRB/AML 150/5 mg, IRB/AML 150/10 mg, and IRB 150 mg/placebo groups, respectively. In I-DUO 302, the mean (SD) changes of MSSBP at week 8 from baseline were -13.30 (12.47) mmHg and -7.19 (15.37) mmHg in the IRB/AML 300/5 mg and IRB 300 mg/placebo groups, respectively. In both studies, all combination groups showed a significantly higher reduction in MSSBP than the IRB monotherapy groups (P < 0.001 for both). TEAEs occurred in 10.00%, 10.99%, and 12.22% of participants in the IRB/AML 150/5 mg, IRB/AML 150/10 mg, and IRB 150 mg/placebo groups, respectively, in I-DUO 301 and in 6.33% and 10.67% of participants in the IRB/AML 300/5 mg and IRB 300 mg/placebo groups, respectively, in I-DUO 302, with no significant between-group differences. Overall, there was one serious adverse event throughout I-DUO study. IMPLICATIONS: The combination of IRB and AML has superior antihypertensive effects compared with IRB alone over an 8-week treatment period, with placebo-like tolerability. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT05476354 (I-DUO 301), NCT05475665 (I-DUO 302).