Cardiovascular
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Graphical abstract
Gender-affirming hormone therapy and cardiovascular disease risk in transgender individuals. CIMT, carotid intima–media thickness. CVD, cardiovascular disease. FMD, flow-mediated dilatation. PWV, pulse wave velocity. TGM, transgender men. Created using BioRender.com.
Abstract
Background
Gender-affirming hormone therapy (GAHT) is used in individuals with gender identity dysphoria to align their secondary sexual characteristics with their affirmed gender. We conducted a systematic review of the literature to explore the mechanisms regarding the effects of GAHT on the vasculature.
Methods
A literature search using PubMed, Embase, Scopus and LILACS was performed using search terms for GAHT, cardiovascular disease (CVD) risk and transgender. Studies were screened by two independent reviewers. Comparison to a cohort of transgender individuals naive or prior to GAHT or a cisgender population was required. Quality assessment was done using the relevant Critical Appraisal Skills Programme checklists.
Results
Out of 2,564 potentially eligible studies, 69 studies met the inclusion criteria. Studies provided evidence of beneficial changes in CVD risk profile, including reduced haemoglobin and pro-inflammatory markers, and atheroprotective changes in lipids in transgender women. In transgender men, there was evidence of negative changes in CVD risk profile, including atherogenic changes in lipids and increased haemoglobin, arterial stiffness and pro-inflammatory markers.
Conclusions
There is a paucity of research across non-traditional measures of CVD risk, which in combination with heterogeneous study design, loss of follow-up, low sample sizes and lack of diversity in age and ethnicity requires the results to be interpreted with caution. More evidence is required to elucidate the mechanisms behind the increased risk of CVD in the transgender population and determine whether GAHT is a contributing factor.
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Department of Clinical Medicine, University of Copenhagen,
International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital – Rigshospitalet,
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Department of Gynecology, Copenhagen University Hospital – Rigshospitalet, University of Copenhagen,
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Diabeter, Center for Pediatric and Adult Diabetes care and Research,
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Introduction
Cardiovascular disease is the most common cause of death in Turner syndrome (TS) for which arterial hypertension has a direct influence and is a key modifiable risk factor.
Objective
To investigate the prevalence and patterns of hypertension diagnosis and management in adult patients with TS who are registered in a large international multicentre database (TS-HTN study).
Methods
Retrospective multicentre observational study of patients aged ≥18 years included in the I-TS (International-TS) registry (2020–2022), using registry and participating centre-collected data.
Results
Twelve international centres participated, including 182 patients with a median age of 28 years (IQR 23–37.2). Arterial hypertension was recorded in 13.2% (n = 24). The median age at hypertension diagnosis was 27 years (range 10–56), with 92% aged less than 50 years at diagnosis. The majority (75%) were classified as primary hypertension (n = 18). In binomial regression analysis, higher body mass index was the only parameter significantly associated with the occurrence of hypertension (B = 1.487, P = 0.004). Among patients with aortic disease (n = 9), 50% had systolic BP ≥ 130 mmHg and 66.6% had diastolic BP ≥ 80 mmHg during the last clinic review. Angiotensin-converting enzyme inhibitors were the most common (n = 16) medication prescribed, followed by angiotensin receptor blockers (n = 6), beta-blockers (n = 6) and calcium channel blockers (n = 6).
Conclusions
Arterial hypertension is common in TS and occurs at a young age. Overweight/obesity was a notable risk factor for hypertension. The frequency of suboptimal BP control among high-risk patients highlights the importance of increased awareness and TS-specific consensus guidance on management.
Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Key Laboratory of Aging and Vascular Homeostasis at Chengdu Medical College of Sichuan Province,
Clinical Research Center for Geriatrics of Sichuan Province,
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Background
Primary aldosteronism (PA) is a prevalent cause of endocrine hypertension characterized by an excess of aldosterone that can induce proinflammatory, prooxidant and profibrotic effects on the heart. Emerging evidence indicates a heightened incidence of atrial fibrillation (AF) in patients with PA, suggesting a significant association between the two conditions. However, the underlying mechanisms remain unclear. The purpose of this study was to investigate the molecular networks associated with the development of both PA and AF.
Methods
Datasets were obtained from the Gene Expression Omnibus database. Hub genes were identified by enrichment and protein–protein interaction analysis. These hub genes were subsequently validated via two independent external datasets: GSE60042 (PA microarray dataset) and GSE41177 (AF microarray dataset). Following the identification of shared genes, quantitative real-time polymerase chain reaction (qPCR) was employed to verify the reliability of the dataset and to further confirm the presence of shared genes in clinical samples.
Results
The results of the common gene analysis revealed that immune and inflammatory responses may be shared features in the pathophysiology of PA and AF. One hub gene, specifically tumor necrosis factor superfamily member 10 (TNFSF10), was identified through various analyses and subsequently validated via qPCR. Compared with that in healthy controls, the expression level of TNFSF10 was lower in PA patients with AF.
Conclusion
Our findings indicate that TNFSF10 may play a role in the pathophysiology of AF complications associated with PA conditions, suggesting that it could serve as a potential target for the diagnosis or treatment of PA patients complicated with AF.
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Beijing Key Laboratory of Diabetes Research and Care,
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Beijing Key Laboratory of Diabetes Research and Care,
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Beijing Key Laboratory of Diabetes Research and Care,
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Objective
To evaluate the correlation between the serum prolactin (PRL) level and carotid intima-media thickness (CIMT) in patients with type 2 diabetes mellitus (T2DM).
Methods
In this study, 1,500 participants were divided into three groups based on the serum PRL level: hypoprolactinemia group (PRL ≤ 7 μg/L), normal PRL level group (7 μg/L < PRL ≤ 25 μg/L), and homeostatic functionally increased transient PRL (Ho-PRL) group (25 μg/L < PRL ≤ 100 μg/L). The independent-sample Kruskal–Wallis test was used to compare the CIMT among the three groups. The Spearman correlation test was used to examine the relationship between the CIMT, serum PRL level, and clinical data. Multivariate linear regression analysis was used to determine the independent factors that influence the CIMT.
Result
Individuals in the Ho-PRL group had a significantly lower CIMT compared to the hypoprolactinemia and normal PRL level groups (P < 0.001). The CIMT was positively correlated with age, systolic blood pressure (SBP), body mass index, duration of T2DM, and luteinizing hormone and follicle-stimulating hormone levels and negatively correlated with alanine transaminase and aspartate transaminase activities, estimated glomerular filtration rate, and PRL. Multivariate linear regression analysis revealed that only PRL was negatively associated with the CIMT, while age and SBP were positively associated with the CIMT.
Conclusion
In patients with T2DM, a PRL level within the mildly elevated range is negatively correlated with the CIMT. A mildly elevated serum PRL level may be a protective factor for preventing thickening of the carotid intima-media.
Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Objective
Cushing’s syndrome (CS) is associated with an 18-fold greater risk of venous thromboembolism (VTE). We aimed to identify factors which provoke VTE among patients with CS and VTE and to describe the anticoagulant regimen used in these cases.
Methods
In this retrospective observational study, patients included in the European Registry on CS (ERCUSYN) in Krakow center, Poland, were followed for the occurrence of VTE and anticoagulant treatment. We identified factors provoking VTE according to the International Society of Thrombosis and Hemostasis (ISTH), along with factors included in the Padua score and CS-VTE score.
Results
Of the 128 patients followed for a median of 4.3 years, there were nine patients who experienced ten VTE episodes (prevalence of 7.8% and incidence of 13.4 per 1000 patient-years). All VTEs were classified as provoked according to the ISTH guidance, predominantly due to the transient major and minor (50% and 20%, respectively) factors, while they were less commonly due to persistent (30%) factors. In 2/9 patients, we could not identify any risk factor for VTE according to the Padua score, while in 2/6 patients according to the CS-VTE score. Patients were mostly anticoagulated with vitamin K antagonists (4/8 patients), followed by direct oral anticoagulants (3/8) and low-molecular-weight heparin (1/8). The median duration of anticoagulation was 2.75 years and exceeded beyond the primary treatment in 28% of episodes provoked by transient factors.
Conclusion
Further, multicenter studies are required to create a validated thrombotic risk score and guidelines regarding VTE treatment in CS patients.
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Background
Hypertension-induced left ventricular hypertrophy (LVH) is intricately linked to insulin resistance (IR). This research aimed to elucidate the relationship of advanced indices, namely the triglyceride–glucose (TyG) index, the TyG adjusted for body mass index (TyG-BMI), the triglycerides-to-high-density lipoprotein cholesterol ratio (TG/HDL-c), and the metabolic score for IR (METS-IR), with LVH in hypertensive cohorts.
Methods
This analytical case–control investigation encompassed 800 individuals aged 18 or above from the Cardiology Department of the Second Affiliated Hospital of Baotou Medical College over a span from January 2021 to April 2022. Data extraction was conducted from inpatient records. The nexus between the four metrics and LVH susceptibility was ascertained via logistic regression models. Furthermore, the receiver operating characteristic (ROC) curve’s area (AUC) shed light on the discriminative capacities of the distinct IR indicators for LVH, considering other concomitant risk variables.
Results
Post multifaceted covariate adjustments, the fourth quartile figures for TyG-BMI emerged as the most starkly significant (OR: 5.211, 95% CI: 2.861–9.492), succeeded by METS-IR (OR: 4.877, 95% CI: 2.693–8.835). In juxtaposition with other IR-derived indices (TyG and TG/HDL-c), TyG-BMI manifested the paramount AUC (AUC: 0.657; 95% CI: 0.606–0.708). Concurrently, METS-IR exhibited commendable predictive efficacy for LVH (AUC: 0.646; 95% CI: 0.595–0.697).
Conclusion
TyG-BMI and METS-IR displayed superior discriminative capabilities for LVH, underscoring their potential as supplementary indicators in gauging LVH peril in clinical settings and prospective epidemiological research.
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Diabetic cardiomyopathy (DCM) is a serious complication of type 2 diabetes mellitus (T2DM) that contributes to cardiovascular morbidity and mortality. However, the metabolic alterations and specific biomarkers associated with DCM in T2DM remain unclear. In this study, we conducted a comprehensive metabolomic analysis using liquid chromatography–mass spectrometry (LC-MS) to investigate the plasma metabolite profiles of T2DM patients with and without DCM. We identified significant differences in metabolite levels between the groups, highlighting the dysregulation of various metabolic pathways, including starch and sucrose metabolism, steroid hormone biosynthesis, tryptophan metabolism, purine metabolism, and pyrimidine metabolism. Although several metabolites showed altered abundance in DCM, they also shared characteristics of DCM and T2DM rather than specific to DCM. Additionally, through biomarker analyses, we identified potential biomarkers for DCM, such as cytidine triphosphate, 11-ketoetiocholanolone, saccharopine, nervonic acid, and erucic acid. These biomarkers demonstrated distinct patterns and associations with metabolic pathways related to DCM. Our findings provide insights into the metabolic changes associated with DCM in T2DM patients and highlight potential biomarkers for further validation and clinical application. Further research is needed to elucidate the underlying mechanisms and validate the diagnostic and prognostic value of these biomarkers in larger cohorts.
Sahlgrenska Osteoporosis Centre, Center for Bone and Arthritis Research (CBAR), Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden
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Sahlgrenska Osteoporosis Centre, Center for Bone and Arthritis Research (CBAR), Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden
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Sahlgrenska Osteoporosis Centre, Center for Bone and Arthritis Research (CBAR), Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden
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Department of Endocrinology, Skaraborg Central Hospital, Skövde, Sweden
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Objective
Sex steroids exert important biological functions within the CNS, but the underlying mechanisms are poorly understood. The contribution of circulating sex steroids to the levels in CNS tissue and cerebrospinal fluid (CSF) has been sparsely investigated in human and with inconclusive results. This could partly be due to lack of sensitive validated assays. To address this, we validated a gas chromatography–tandem mass spectrometry (GC-MS/MS) assay for quantification of sex steroid hormones/precursors in CSF.
Methods
GC-MS/MS quantification of dihydrotestosterone (DHT, CSF lower limit of quantification, 1.5 pg/mL), testosterone (4.9), estrone (E1, 0.88), estradiol (E2, 0.25), dehydroepiandrosterone (DHEA, 38.4), androstenedione (4D, 22.3), and progesterone (P, 4.2) in CSF, and corresponding serum samples from 47 men.
Results
Analyses of CSF revealed that DHEA was the major sex steroid (73.5 ± 31.7 pg/mL) followed by 4D (61.4 ± 29.6 pg/mL) and testosterone (49.5 ± 18.9 pg/mL). The CSF levels of DHT, E2, and E1 were substantially lower, and P was in general not detectable in CSF. For all sex steroids except E2, strong associations between corresponding CSF and serum levels were observed. We propose that testosteronein CSF is derived from circulating testosterone, DHT in CSF is from local conversion from testosterone, while E2 in CSF is from local conversion from 4D in CNS.
Conclusions
We describe the first thoroughly validated highly sensitive mass spectrometric assay for a broad sex steroid hormone panel suitable for human CSF. This assay constitutes a new tool for investigation of the role of sex steroid hormones in the human CNS.
Significance statement
In this study, a fully validated highly sensitive mass spectrometric assay for sex steroids was applied to human CSF. The results were used to describe the relative contribution of peripheral circulating sex steroids together with locally transformation of sex steroids to the levels in CSF. The results are of importance to understand the biological processes of the human brain.
Department of Endocrinology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China
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We applied 24-h Holter monitoring to analyze the characteristics of arrhythmias and heart rate variability in Chinese patients with primary aldosteronism (PA) and compared them with age-, sex-, and blood pressure-matched primary hypertension (PH) patients. A total of 216 PA patients and 261 PH patients were enrolled. The nonstudy data were balanced using propensity score matching (PSM), and the risk variables for developing arrhythmias were then analyzed using logistic regression analysis. Before PSM, the proportion of PA patients with combined atrial premature beats and prolonged QT interval was higher than the corresponding proportion in the PH group. After PSM, the PA group had a larger percentage of transient atrial tachycardia and frequent atrial premature beats, and it had higher heart rate variability metrics. The proportion of unilateral PA combined with multiple ventricular premature beats was higher than that of bilateral PA. Older age, grade 3 hypertension, and hypokalemia were independent risk factors for the emergence of arrhythmias in PA patients. PA patients suffer from a greater prevalence of arrhythmias than well-matched PH patients.
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Background
Fetuin-B, a cytokine that regulates lipid metabolism, has recently been linked to cardiovascular diseases such as coronary heart disease. In this study, we discussed the relationship between fetuin-B and essential hypertension.
Method
A bioinformatics analysis of fetuin-B was performed. A total of 206 with essential hypertension and 180 age- and-sex-matched healthy subjects were enrolled. Plasma fetuin-B, endothelin 1 (ET-1), nitric oxide (NO), and adiponectin (ADI) levels were measured using ELISA kits.
Results
Bioinformatics analysis has revealed that fetuin-B plays an important role in pathways such as lipid metabolism. Compared with healthy subjects, serum fetuin-B levels in patients with essential hypertension were significantly increased. Correlation analysis showed that the serum fetuin-B level was positively correlated with systolic blood pressure (SBP), diastolic blood pressure, body mass index, fat percentage in vivo, waist–hip ratio, intima–media thickness, low-density lipoprotein cholesterol (LDL-C), glutamyltranspeptidase, alanine transaminase, albumin, fasting blood glucose (FBG), glycated hemoglobin, and ET-1 in the overall study subjects (all P < 0.05) and negatively correlated with HDL-C, ADI, and NO (all P < 0.05). Multivariate linear regression analysis showed that SBP, FBG, LDL-C, ADI, and ET-1 were independent factors affecting serum fetuin-B. A binary logistic regression analysis showed that fetuin-B was an independent risk factor for primary hypertension (odds ratio: 1.060, 95% CI: 1.034–1.086, P < 0.001). Receiver operating characteristic curve analysis was used to evaluate the predictive value of fetuin-B for primary hypertension, and the optimal cutoff point was 83.14 μg/mL (sensitivity 77.4%, specificity 63.3%) (area under the curve) = 0.7738, 95% CI 0.7276–0.8200, P < 0.001).
Conclusion
Elevated fetuin-B levels are associated with an increased risk of essential hypertension.