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Tao Gao Department of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

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Rui Liu Department of Oncology. The Second Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

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Chunli Li Institute of Life Sciences, Chongqing Medical University, Chongqing, China

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Xinglin Chu Department of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

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Qiao Guo Department of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

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Dazhi Ke Department of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

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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.

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Shuang Wan Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China
Department of Endocrinology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China

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Chengcheng Zheng Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China

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Tao Chen Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China

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Lu Tan Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China

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Jia Tang Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China

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Haoming Tian Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China

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Yan Ren Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, 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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Mette Faurholdt Gude Medical/Steno Aarhus Research Laboratory, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

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Rikke Hjortebjerg Department of Molecular Endocrinology, University of Southern Denmark, Odense, Denmark
Steno Diabetes Centre Odense, Odense University Hospital, Odense, Denmark

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Mette Bjerre Medical/Steno Aarhus Research Laboratory, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

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Morten Haaning Charles Department of Public Health, Aarhus University, Aarhus, Denmark
Steno Diabetes Centre Aarhus, Aarhus University Hospital, Aarhus, Denmark

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Daniel R Witte Department of Public Health, Aarhus University, Aarhus, Denmark
Steno Diabetes Centre Aarhus, Aarhus University Hospital, Aarhus, Denmark

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Annelli Sandbæk Department of Public Health, Aarhus University, Aarhus, Denmark
Steno Diabetes Centre Aarhus, Aarhus University Hospital, Aarhus, Denmark

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Jan Frystyk Endocrine Research Unit, Department of Endocrinology, Odense University Hospital & Department of Clinical Research, Faculty of Health, University of Southern Denmark, Odense, Denmark

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Objective

Physiologically, pregnancy-associated plasma protein-A (PAPP-A) serves to liberate bound IGF1 by enzymatic cleavage of IGF-binding proteins (IGFBPs), IGFBP4 in particular. Clinically, PAPP-A has been linked to cardiovascular disease (CVD). Stanniocalcin-2 (STC2) is a natural inhibitor of PAPP-A enzymatic activity, but its association with CVD is unsettled. Therefore, we examined associations between the STC2–PAPP-A–IGFBP4–IGF1 axis and all-cause mortality and CVD in patients with type 2 diabetes (T2D).

Design

We followed 1284 participants with T2D from the ADDITION trial for 5 years.

Methods

Circulating concentrations of STC2, PAPP-A, total and intact IGFBP4 and IGF1 and -2 were measured at inclusion. End-points were all-cause mortality and a composite CVD event: death from CVD, myocardial infarction, stroke, revascularisation or amputation. Survival analysis was performed by Cox proportional hazards model.

Results

During follow-up, 179 subjects presented with an event. After multivariable adjustment, higher levels of STC2, PAPP-A, as well as intact and total IGFBP4, were associated with all-cause mortality; STC2: hazard ratio (HR) = 1.84 (1.09–3.12) (95% CI); P = 0.023, PAPP-A: HR = 2.81 (1.98–3.98); P < 0.001, intact IGFBP4: HR = 1.43 (1.11–1.85); P = 0.006 and total IGFBP4: HR = 3.06 (1.91–4.91); P < 0.001. Higher PAPP-A levels were also associated with CVD events: HR = 1.74 (1.16–2.62); P = 0.008, whereas lower IGF1 levels were associated with all-cause mortality: HR = 0.51 (0.34–0.76); P = 0.001.

Conclusions

This study supports that PAPP-A promotes CVD and increases mortality. However, STC2 is also associated with mortality. Given that STC2 inhibits the enzymatic effects of PAPP-A, we speculate that STC2 either serves to counteract harmful PAPP-A actions or possesses effects independently of the PAPP-A–IGF1 axis.

Significance statement

PAPP-A has pro-atherosclerotic effects and exerts these most likely through IGF1. IGF1 is regulated by the STC2–PAPP-A–IGFBP4–IGF1 axis, where STC2, an irreversible inhibitor of PAPP-A, has been shown to reduce the development of atherosclerotic lesions in mice. We examined the association of this axis to mortality and CVD in T2D. We demonstrated an association between PAPP-A and CVD. All components of the STC2–PAPP-A–IGFBP4–IGF1 axis were associated with mortality and it is novel that STC2 was associated with mortality in T2D. Our study supports that inhibition of PAPP-A may be a new approach to reducing mortality and CVD. Whether modification of STC2 could serve as potential intervention warrants further investigation.

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Shenghe Luo College of Pharmacy, Yanbian University, Yanji, China

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Yunhui Zuo Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, China
Department of Cardiology, Yanbian University Hospital, Yanji, China

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Xiaotian Cui Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, China

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Meiping Zhang Department of Cardiology, Yanbian University Hospital, Yanji, China

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Honghua Jin Department of Pharmacy, Yanbian University Hospital, Yanji, China

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Lan Hong Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, China

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To observe the effects of liraglutide (analog of glucagon-like peptide 1 (GLP-1)) on atrial natriuretic peptide (ANP) secretion and atrial dynamics, an ex vivo isolated rat atrial perfusion model was used to determine atrial ANP secretion and pulse pressure. DPP-4−/− mice were also established in vivo. ANP levels were determined by radioimmunoassay; GLP-1 content was determined by Elisa. The expression levels of GLP-1 receptor (GLP-1R), PI3K/AKT/mTOR, piezo 1, and cathepsin K were analyzed by Western blot. In the clinical study, patients with acute coronary syndrome (ACS) had low levels of plasma GLP-1 but relatively high levels of plasma ANP. In ex vivo (3.2 nmol/L) and in vivo (30 μg/kg) models, liraglutide significantly decreased ANP levels and atrial pulse pressure. Exendin9–39 alone (GLP-1R antagonist) reversibly significantly increased ANP secretion, and the reduction effect of liraglutide on the secretion of ANP was significantly alleviated by Exendin9–39. Exendin9–39 demonstrated slightly decreased atrial pulse pressure; however, combined liraglutide and Exendin9–39 significantly decreased atrial pulse pressure. Ly294002 (PI3K/AKT inhibitor) inhibited the increase of ANP secretion by liraglutide for a short time, while Ly294002 didn't counteract the decrease in pulse pressure by liraglutide in atrial dynamics studies. Liraglutide increased the expression of GLP-1R and PI3K/AKT/mTOR in isolated rat atria and the hearts of mice in vivo, whereas Exendin9–39 reversibly reduced the expression of GLP-1R and PI3K/AKT/mTOR. Piezo 1 was significantly decreased in wild type and DPP-4−/− mouse heart or isolated rat atria after being treated with liraglutide. Cathepsin K expression was only decreased in in vivo model hearts. Liraglutide can inhibit ANP secretion while decreasing atrial pulse pressure mediated by GLP-1R. Liraglutide probably plays a role in the reduction of ANP secretion via the PI3K/AKT/mTOR signaling pathway. Piezo 1 and cathepsin K may be involved in the liraglutide mechanism of reduction.

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Paweł Komarnicki Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Paweł Gut Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Jan Musiałkiewicz Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Maja Cieślewicz Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Adam Maciejewski Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Prachi Patel Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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George Mastorakos Unit of Endocrinology, Diabetes Mellitus and Metabolism, Aretaieion University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Marek Ruchała Department of Endocrinology, Metabolism and Internal Diseases, Poznan University of Medical Sciences, Poznań, Poland

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Introduction

Neuroendocrine tumors (NETs) are rare neoplasms that occur in various locations throughout the body. Despite their usually benign character, they might manifest with distant metastases. N-terminal prohormone of brain natriuretic peptide (NT-proBNP) has previously been described as a useful biomarker in diagnosing carcinoid heart disease (CHD), a common advanced NETs manifestation. We observed plasma concentrations of NT-proBNP in metastatic midgut NETs over a 4-year period.

Objectives

We aimed to explore NT-proBNP concentrations in states of varying levels of cell proliferation and disease status. Our goal was to investigate NT-proBNP’s role in predicting disease progression in relation to previous research and up-to-date scientific guidelines.

Patients and methods

We performed a retrospective multivariate analysis of NT-proBNP concentrations in 41 midgut NETs patients treated with somatostatin analogs, all with liver metastases. NT-proBNP concentrations were measured in every patient across 16 evenly distanced time points over a 48-month period and were compared to variables such as sex, age, grading, Ki-67, primary tumor location, and CT findings.

Results

NT-proBNP concentrations correlated positively with higher liver tumor burden, higher grading, high Ki-67 levels, and with progressive disease in CT. There were no differences in NT-proBNP levels with regard to primary location (ileum vs jejunum), sex, and age.

Conclusion

We conclude that NT-proBNP is a useful analyte for monitoring NETs progression, due to its increased concentration in scenarios implying increased cellular proliferation. These long-term follow-up results align with previous findings and suggest an additional role for NT-proBNP in diagnostic algorithms, beyond a CHD biomarker.

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Eng-Loon Tng Department of Medicine, Level 8, Tower A, Ng Teng Fong General Hospital, Singapore

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Yee Sian Tiong Department of Medicine, Level 8, Tower A, Ng Teng Fong General Hospital, Singapore

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Aye Thida Aung Department of Medicine, Level 8, Tower A, Ng Teng Fong General Hospital, Singapore

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Nicole Ya Yuan Chong Department of Medicine, National University Hospital, Singapore

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Zhemin Wang Department of Medicine, National University Hospital, Singapore

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Background

Evidence on the efficacy and safety of anticoagulation in preventing stroke and thromboembolic events in people with thyrotoxic atrial fibrillation is scarce.

Objective

We evaluated the efficacy and safety of anticoagulation in people with thyrotoxic atrial fibrillation.

Methods

Our study protocol was published in the International Prospective Register of Systematic Reviews (registration no. CRD42020222782). Four databases and two systematic review registers were searched through 25 November 2020 for interventional and observational studies comparing anticoagulation therapy with active comparators, placebo, or no treatment in people with thyrotoxic atrial fibrillation. Random-effects meta-analysis and sensitivity analysis were performed. Quality of evidence was described using the GRADE framework.

Results

In the study, 23,145 records were retrieved. One randomized controlled trial and eight cohort studies were ultimately included. Effect estimates on the efficacy and safety of anticoagulation were extracted. Meta-analysis using the inverse variance and random-effects methods was conducted on four cohort studies with 3443 participants and 277 events. Anticoagulation in people with thyrotoxic atrial fibrillation reduced the risk of ischemic stroke and systemic thromboembolism by 3% (95% CI: 1–6%). Warfarin may prevent ischemic stroke in people with thyrotoxic atrial fibrillation if the CHA2DS2-VASc score exceeds 1 and when atrial fibrillation persists beyond 7 days. Direct oral anticoagulants may be associated with fewer bleeding events than warfarin.

Conclusions

Anticoagulation prevents ischemic stroke and systemic thromboembolism in people with thyrotoxic atrial fibrillation. Direct oral anticoagulants may be associated with fewer bleeding events.

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Yumei Zhai The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia Autonomous Region, P.R. China

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Haiming Fu Department of Clinical Laboratory, Baotou Maternal and Child Health Center, Baotou, Inner Mongolia Autonomous Region, P.R. China

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Yu Li The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia Autonomous Region, P.R. China

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Siyuan Li The First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia Autonomous Region, P.R. China

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Wenchen Zhang The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia Autonomous Region, P.R. China

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Jianwei Yue The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia Autonomous Region, P.R. China

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Zichao Wang The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia Autonomous Region, P.R. China

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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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Run-Qing Xiong Department of Ultrasonic Imaging, Xiamen Medical College Affiliated Second Hospital, Fujian, China

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Yan-Ping Li Key Laboratory of Functional and Clinical Translational Medicine, Fujian Province University, Xiamen Medical College, Fujian, China

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Lu-Ping Lin Department of Endocrinology, Xiamen Medical College Affiliated Second Hospital, Fujian, China

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Jeng-Yuan Yao Key Laboratory of Functional and Clinical Translational Medicine, Fujian Province University, Xiamen Medical College, Fujian, China

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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.

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Alicia Romano Department of Pediatrics, New York Medical College, Valhalla, New York, USA

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Juan Pablo Kaski Centre for Inherited Cardiovascular Diseases, Great Ormond Street Hospital & UCL Institute of Cardiovascular Science, London, UK

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Jovanna Dahlgren Department of Paediatrics, Region Västra Götaland, Sahlgrenska University Hospital, Gothenburg, Sweden

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Nicky Kelepouris US Medical Affairs, Novo Nordisk Inc., Plainsboro, New Jersey, USA

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Alberto Pietropoli Global Medical Affairs, Novo Nordisk Health Care AG, Zurich, Switzerland

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Tilman R Rohrer Department of Pediatric Endocrinology, University Children’s Hospital, Saarland University Medical Center, Homburg, Germany

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Michel Polak Paediatric Endocrinology, Diabetology and Gynaecology Department, Hôpital Universitaire Necker Enfants-Malades, AP-HP, Université de Paris, Imagine Institute, Paris, France

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Objective

The study aims to assess the cardiovascular safety of growth hormone (GH) treatment in patients with Noonan syndrome (NS) in clinical practice.

Design

The study design involves two observational, multicentre studies (NordiNet® IOS and the ANSWER Program) evaluating the long-term effectiveness and safety of GH in >38,000 paediatric patients, of which 421 had NS.

Methods

Serious adverse events, serious adverse reactions (SARs) and non-serious adverse reactions (NSARs) were reported by the treating physicians. Cardiovascular comorbidities at baseline and throughout the studies were also recorded.

Results

The safety analysis set comprised 412 children with NS (29.1% females), with a mean (s.d.) baseline age of 9.29 (3.88) years, treated with an average GH dose of 0.047 (0.014) mg/kg/day during childhood. Cardiovascular comorbidities at baseline were reported in 48 (11.7%), most commonly pulmonary valve stenosis (PVS) and atrial septal defects. Overall, 22 (5.3%) patients experienced 34 safety events. The most common were the NSARs: headache (eight events in seven patients) and arthralgia (five events in three patients). Two SARs occurred in one patient (brain neoplasm and metastases to spine). No cardiovascular safety events were recorded in patients with NS. Five cardiovascular comorbidities in five patients were reported after initiation of GH treatment: three cases of unspecified cardiovascular disease, one ruptured abdominal aortic aneurysm and one PVS.

Conclusions

GH treatment had a favourable safety profile in patients with NS, including those with cardiovascular comorbidities. Prospective studies are warranted to systematically assess the safety of GH treatment in patients with NS and cardiovascular disease.

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Charlotte Höybye Department of Endocrinology and Department of Molecular Medicine and Surgery, Karolinska University Hospital and Karolinska Institute, Stockholm, Sweden

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Beverly M K Biller Neuroendocrine Unit, Massachusetts General Hospital, Massachusetts General Hospital, Boston, Massachusetts, USA

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Jean-Marc Ferran Qualiance ApS, Copenhagen, Denmark

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Murray B Gordon Allegheny Neuroendocrinology Center, Division of Endocrinology, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA

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Nicky Kelepouris US Medical Affairs-Rare Endocrine Disorders, Novo Nordisk, Inc, Plainsboro, New Jersey, USA

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Navid Nedjatian Global Medical Affairs – Rare Endocrine Disorders, Novo Nordisk Health Care AG, Zurich, Switzerland

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Anne H Olsen Epidemiology, Novo Nordisk A/S, Soborg, Denmark

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Matthias M Weber Unit of Endocrinology, 1, Medical Department, University Hospital, Universitätsmedizin Mainz, der Johannes Gutenberg-Universität, Mainz, Germany

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Adult growth hormone deficiency (AGHD) is associated with an increased risk of cardiovascular (CV) disease. Long-term growth hormone (GH) treatment could improve CV outcomes. The objective of this study was to evaluate CV disease risk in patients with AGHD who received GH replacement therapy for up to 10 years as part of NordiNet® IOS (NCT00960128) and the ANSWER Program (NCT01009905). The studies were observational, non-interventional and multicentre, monitoring long-term effectiveness and safety of GH treatment. NordiNet® IOS involved 23 countries (469 sites) across Europe and the Middle East. The ANSWER Program was conducted in the USA (207 sites). This analysis included patients aged 18–75 years who were GH naïve at study entry, who had ≤10 years of GH treatment data and who could be assessed for CV risk for at least 1 follow-up year. The main outcome measure was risk of CV disease by age 75 years, as calculated with the Multinational Cardiovascular Risk Consortium model (Brunner score) using non-high-density lipoprotein cholesterol adjusted for age, sex and CV risk factors. The results of this analysis showed that CV risk decreased gradually over the 10-year period for GH-treated patients. The risk was lower for patients treated for 2 and 7 years vs age- and sex-matched control groups (not yet started treatment) (14.51% vs 16.15%; P = 0.0105 and 13.53% vs 16.81%; P = 0.0001, respectively). This suggests that GH treatment in people with AGHD may reduce the risk of CV disease by age 75 years compared with matched controls.

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