Elevated levels of asymmetric dimethylarginine (ADMA) as a marker of cardiovascular disease and mortality

2005 ◽  
Vol 43 (10) ◽  
Author(s):  
Rainer H. Böger ◽  
Renke Maas ◽  
Friedrich Schulze ◽  
Edzard Schwedhelm
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Vascular Function ◽  
Asymmetric Dimethylarginine ◽  
Metabolic Diseases ◽  
Serum Levels ◽  
Major Adverse Cardiovascular Events ◽  
Blood Levels ◽  
Increased Risk ◽  
Vasoactive Mediator

AbstractThe endothelium plays a crucial role in the maintenance of vascular tone and structure by releasing the endothelium-derived vasoactive mediator, nitric oxide (NO). NO is formed in healthy vascular endothelium from the amino acid precursor L-arginine. Endothelial dysfunction is caused by various cardiovascular risk factors, metabolic diseases, and systemic or local inflammation. One mechanism that explains the occurrence of endothelial dysfunction is the presence of elevated blood levels of asymmetric dimethylarginine (ADMA) – an L-arginine analogue that inhibits NO formation and thereby can impair vascular function. Accumulating evidence from prospective clinical studies suggests that elevated plasma or serum levels of ADMA are associated with an increased risk of major adverse cardiovascular events. This article gives an updated overview of the currently available literature on ADMA and cardiovascular disease from prospective clinical trials. Recently, advances have been made in the development of analytical methods that are reliable and fast enough to allow determination of ADMA in clinical routine.

scholarly journals Pathophysiological Role of Adiponectin, Leptin and Asymmetric Dimethylarginine in the Process of Atherosclerosis

Folia Medica ◽  
2016 ◽  
Vol 58 (4) ◽  
pp. 234-240 ◽  
Author(s):  
Daniela Iv. Koleva ◽  
Maria M. Orbetzova ◽  
Julia G. Nikolova ◽  
Tanya I. Deneva
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Endothelial Dysfunction ◽  
Proinflammatory Cytokines ◽  
Asymmetric Dimethylarginine ◽  
Serum Levels ◽  
Reactive Protein ◽  
Proinflammatory Mediators ◽  
Pathophysiological Role

Abstract Adipose tissue is recognized as a rich source of proinflammatory mediators that may directly contribute to vascular injury, insulin resistance, and atherogenesis. Many studies have shown that adiponectin has antiatherogenic and anti-inflammatory properties. Adiponectin acts not only as a factor increasing insulin sensitivity, and the protective effect may result from its ability to suppress production of proinflammatory cytokines. It negatively regulates the expression of TNF-alpha and C-reactive protein (CRP) in adipose tissue; reduces expression of vascular and intracellular adhesion molecules (VCAM-1, ICAM-1), E-selectin, interleukin-8 (IL-8). Hyperleptinemia has been linked with the development of hypertension and endothelial dysfunction/atherosclerosis, two main pathophysiological conditions associated with cardiovascular disease development. Leptin-mediated increases in sympathetic nervous system activity may be among the principal mechanisms evoking obesity related hypertension. Leptin stimulates the secretion of proinflammatory cytokines, and increases the release of endothelin-1 (ET-1), which may promote hypertension. Increased serum levels of asymmetric dimethylarginine (ADMA), a physiological regulator of the biosynthesis of nitric oxide (NO), promote the process of atherosclerosis, leading to the occurrence of endothelial dysfunction and cardiovascular disease.

scholarly journals Impaired Flow-Mediated Dilation Before, During, and After Preeclampsia

Hypertension ◽  
2016 ◽  
Vol 67 (2) ◽  
pp. 415-423 ◽  
Author(s):  
Tracey L. Weissgerber ◽  
Natasa M. Milic ◽  
Jelena S. Milin-Lazovic ◽  
Vesna D. Garovic
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Meta Analysis ◽  
Critical Role ◽  
Study Groups ◽  
Chronic Hypertension ◽  
Flow Mediated Dilation ◽  
Increased Risk

Endothelial dysfunction is believed to play a critical role in preeclampsia; however, it is unclear whether this dysfunction precedes the pregnancy or is caused by pathophysiological events in early pregnancy. It is also unclear for how long vascular dysfunction may persist postpartum and whether it represents a mechanism linking preeclampsia with future cardiovascular disease. Our objective was to determine whether women with preeclampsia had worse vascular function compared with women who did not have preeclampsia by performing a systematic review and meta-analysis of studies that examined endothelial dysfunction using flow-mediated dilation. We included studies published before May 29, 2015, that examined flow-mediated dilation before, during, or after preeclampsia. Differences in flow-mediated dilation between study groups were evaluated by standardized mean differences. Out of 610 abstracts identified through PubMED, EMBASE, and Web of Science, 37 studies were eligible for the meta-analysis. When compared with women who did not have preeclampsia, women who had preeclampsia had lower flow-mediated dilation before the development of preeclampsia (≈20–29 weeks gestation), at the time of preeclampsia, and for 3 years postpartum, with the estimated magnitude of the effect ranging between 0.5 and 3 standard deviations. Similar effects were observed when the analysis was limited to studies that excluded women with chronic hypertension, smokers, or both. Vascular dysfunction predates preeclampsia and may contribute to its pathogenesis. Future studies should address whether vascular changes that persist after preeclamptic pregnancies may represent a mechanistic link with increased risk for future cardiovascular disease.

scholarly journals AB0577 ENDOTHELIAL DYSFUNCTION AND ATHEROSCLEROSIS IN SYSTEMIC SCLEROSIS: A MULTIPARAMETRIC ANALYSIS USING IMAGING TECHNIQUE AND LABORATORY MARKERS OF INFLAMMATION AND VASCULAR FUNCTION: SCLERODERMA CV RISK STUDY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1585.2-1585
Author(s):  
N. Garg ◽  
A. Syngle ◽  
D. Gera ◽  
S. Kaur
Keyword(s):  
Cardiovascular Disease ◽  
Systemic Sclerosis ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Function ◽  
Disease Duration ◽  
Atherosclerotic Cardiovascular Disease ◽  
Accelerated Atherosclerosis ◽  
Markers Of Inflammation ◽  
Increased Risk

Background:Systemic sclerosis (SSc) patients have an increased risk for atherosclerotic cardiovascular disease (CVD), possibly mediated by inflammatory and fibrotic mechanisms1. However, pathogenesis of accelerated atherosclerosis in SSc remains to be elucidated. Endothelial dysfunction is the key initial event in atherosclerosis. Predictors for rapid evolution of cardiovascular complications would be highly desirable for CV risk stratification. This study aims to assess endothelial function and atherosclerosis in SSc, in context of markers of inflammation and vascular function in SSc patients.Objectives:To assess endothelial function and atherosclerosis in SSc in context of markers of inflammation and vascular function in SSc patients.Methods:A cross-sectional study was performed in 20 SSc patients meeting the 2013 European League Against Rheumatism (EULAR) and American College of Rheumatology (ACR) classification criteria and 18 healthy controls matched for age and sex. Flow-mediated dilatation (FMD) assessed by AngioDefender and CIMT measured ultrasonographically. Disease-specific measures included: Disease duration, Modified Rodnan Skin Score (mRSS), EUSTAR activity score in SSc. We also assayed markers of inflammation, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), proinflammatory cytokines (interleukin IL-1, IL-6, and IL-17), and endothelial dysfunction including lipids, serum nitrite and TBARS (marker of oxidative stress). Quality of life measured by Scleroderma Health Assessment Questionnaire (SHAQ).Results:FMD is significantly lower in SSc patients compared with controls (6.13±0.35% vs. 9.12±0.25%, p≤0.05). CIMT is significantly higher in SSc patients compared with controls (0.071±0.04cm vs. 0.035±0.02cm p≤0.05). Compared with controls, SSc patients had significantly (p≤0.05) elevated mRSS, EUSTAR score, ESR, CRP, IL-1, IL-6, IL-17, nitrite, TBARS and SHAQ whereas HDL levels are significantly reduced in SSc compared with controls (p≤0.05). In SSc, FMD inversely correlated with EUSTAR score, mRSS, IL-6 (Fig. 1A), serum nitrite (Fig. 1B), TBARS (Fig. 1C) and CIMT (Fig. 1D). CIMT positively correlated with age (Fig. 2A), disease duration, CRP (Fig. 2B) and IL-17 (Fig. 2C) and inversely correlated with HDL (Fig. 2D) (p< 0.05).Conclusion:In the present study, FMD and CIMT are impaired in SSc, indicating endothelial dysfunction and accelerated atherosclerosis, respectively. EUSTAR score, mRSS, IL-6, serum nitrite, CIMT and TBARS predicted endothelial dysfunction. Age, disease duration, CRP, IL-17, HDL and impaired FMD predicted accelerated atherosclerosis. SSc-related inflammatory mechanisms (IL-6, IL-17) and markers of vascular function (CRP, serum nitrite and TBARS) may all be involved in the development of vascular disease in SSc. Cytokine-triggered inflammation mediated by nitrite and TBARS is associated with endothelial dysfunction and accelerated atherosclerosis in SSc. These markers would possibly serve as predictors of endothelial dysfunction and atherosclerosis and more importantly therapeutic targets to prevent premature atherosclerosis and cardiovascular disease in SSc.References:[1]Pagkopoulou E, Poutakidou M, Garyfallos A, Kitas G, Dimitroulas T. Cardiovascular risk in systemic sclerosis: Micro- and Macro-vascular involvement. Indian Journal of Rheumatology 2017;12:S211-7.Acknowledgments:NoneDisclosure of Interests:None declared

scholarly journals The Role of Endothelial Dysfunction in the Pathogenesis of Vascular Complications of Diabetes Mellitus - A High Priority Area of Investigation

2015 ◽  
Vol 22 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Rodica Teodora Străchinariu
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Vascular Complications ◽  
Noninvasive Methods ◽  
Cardiovascular Damage ◽  
Vasoactive Substances ◽  
Organ Systems ◽  
Increased Risk

Abstract Endothelium, the inner layer of the vasculature, represents the interface between blood and organ systems and it is active in the process of contraction and relaxation of vascular smooth muscle and in functions like secretion of vasoactive substances. Endothelial dysfunction is an important cause of cardiovascular disease. The function of the endothelium can be assessed by invasive and noninvasive methods. Endothelial cells produce vasoactive substances like endothelium derived relaxing factor, prostacyclin, nitric oxide, and endothelium derived hyperpolarizing factor. Diabetes mellitus is associated with an increased risk of cardiovascular diseases. Hyperglycemia leads to cardiovascular damage through different pathways, including the polyol and hexosamine pathways, generation of advanced glycation end products, and activation of protein kinase C. Together with hyperglycemia induced mitochondrial dysfunction and endoplasmic reticulum stress, all these can promote the accumulation of reactive oxygen species. The oxidative stress induced by hyperglycemia promotes endothelial dysfunction with an important role in micro and macro vascular disease. Insulin-resistance could be independently predictive of cardiovascular disease. Life style modification and pharmacotherapy could possibly ameliorate the effect of insulin resistance

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives

2021 ◽  
Vol 320 (1) ◽  
pp. H29-H35
Author(s):  
Joshua M. Cherubini ◽  
Jem L. Cheng ◽  
Jennifer S. Williams ◽  
Maureen J. MacDonald
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Sleep Deprivation ◽  
Vascular Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Health Concern ◽  
Short Sleep ◽  
Inadequate Sleep

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/

scholarly journals The Effects of Nut Consumption on Vascular Function

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 116 ◽  
Author(s):  
Samantha Morgillo ◽  
Alison M. Hill ◽  
Alison M. Coates
Keyword(s):  
Cardiovascular Disease ◽  
Vascular Function ◽  
Wave Reflection ◽  
Epidemiological Studies ◽  
Cvd Risk ◽  
Future Studies ◽  
Tree Nut ◽  
Increased Risk ◽  
Flow Mediated Dilatation ◽  
Chronic Study

Vascular stiffness can be measured using numerous techniques including assessments of central haemodynamics, aortic arterial stiffness, and indices of aortic wave reflection and endothelial dilatation. Impaired vascular function is associated with increased risk of cardiovascular disease (CVD). Epidemiological studies indicate that regular nut consumption reduces CVD risk, with one of the proposed mechanisms being via improvements in vascular function. This narrative review summarizes the evidence from a systematic search of the literature of the effects of tree nut and peanut consumption on measures of vascular function excluding flow mediated dilatation. A total of 16 studies were identified, with a mix of acute controlled studies (n = 3), an uncontrolled pre/post chronic study (n = 1), chronic crossover (n = 7) and parallel studies (n = 5). Nut types tested included almonds, peanuts, pine nuts, pistachios and walnuts, with dose and length of supplementation varying greatly across studies. Most studies (n = 13) included individuals at risk for CVD, according to various criteria. Findings were inconsistent, with ten studies reporting no significant changes in vascular function and six studies (one acute and five chronic studies) reporting improvements in at least one measure of vascular function. In summary, nuts have the potential to improve vascular function and future studies should consider the population, dose and length of nut supplementation as well as suitability of the different vascular function techniques.

scholarly journals Serum Levels of Asprosin, a Novel Adipokine, Are Significantly Lowered in Patients with Acromegaly

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xiaoan Ke ◽  
Lian Duan ◽  
Fengying Gong ◽  
Yuelun Zhang ◽  
Kan Deng ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Metabolic Diseases ◽  
Influencing Factor ◽  
Clinical Information ◽  
Serum Levels ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Retrospective Case ◽  
Cell Adenoma ◽  
Increased Risk

Background. Asprosin is a novel identified adipokine secreted mainly by white adipose tissue, which is elevated in metabolic diseases such as diabetes and obesity. Acromegaly is a syndrome caused by pituitary growth hormone (GH) cell adenoma with excessive GH secretion. Serum adipocytokines levels may be involved in abnormal glycolipid metabolism in acromegaly patients. Objectives. To investigate serum asprosin levels in acromegaly patients and its correlation with high GH levels and glucolipid metabolic parameters. Methods. A retrospective case-control study was conducted and 68 acromegaly patients and 121 controls were included in this study. Clinical information and laboratory examinations were collected and serum asprosin levels were measured by commercial ELISA kits. Results. Serum asprosin levels in acromegaly patients were significantly lower than controls ( P < 0.001 ). Serum asprosin levels in patients with the course of acromegaly ≥5 years (compared with <5 years), high area under curve of growth hormone (GH-AUC) after 75 g oral glucose tolerance test (OGTT) (compared with low GH-AUC patients), and high IGF-1 SDS group (compared with low IGF-1 SDS group) were significantly reduced (all P < 0.05 ). Serum asprosin levels in acromegaly patients were negatively correlated with the course of acromegaly, IGF-1 SDS, nadir growth hormone value (GH-Nadir), and GH-AUC after OGTT. Multiple stepwise linear regression indicated that acromegaly was an independent influencing factor of serum asprosin levels. According to serum asprosin levels tertiles, the risk of acromegaly in the lowest group was 2.67 times higher than the highest group (OR ＝ 3.665, 95% CI 1.677 ∼ 8.007, P = 0.001 ), and the increased risk of the lowest group still existed after adjusting for gender, age, BMI, and TC (Model 2). Conclusions. Serum asprosin levels in acromegaly patients are lowered, which may be related to increased blood glucose and reduced body fat mass caused by long-term high GH levels exposure.

scholarly journals Antidepressant Use and the Risk of Major Adverse Cardiovascular Events in Patients Without Known Cardiovascular Disease: A Retrospective Cohort Study

2020 ◽  
Vol 11 ◽  
Author(s):  
Ha Young Jang ◽  
Jae Hyun Kim ◽  
Yun-Kyoung Song ◽  
Ju-Young Shin ◽  
Hae-Young Lee ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Risk Score ◽  
Cardiovascular Events ◽  
Major Adverse Cardiovascular Events ◽  
Cvd Risk ◽  
Hazard Ratios ◽  
Increased Risk ◽  
History Of ◽  
Antidepressant Use ◽  
Cox Proportional Hazard Regression

Aims: Conflicting data exist on whether an association exists between antidepressants and the risk of major adverse cardiovascular events (MACEs) in patients with depression. This may be due to the use of various study designs and residual or unmeasured confounding. We aimed to assess the association between antidepressant use and the risk of MACEs while considering various covariates, including severity of depression and the cardiovascular disease (CVD) risk score.Methods: Patients newly diagnosed with depression with no history of ischemic heart disease and stroke were followed-up from 2009 to 2015. We conducted Cox proportional hazard regression analysis to estimate hazard ratios (HRs) for each antidepressant for MACE risk.Result: We followed-up (median, 4.4 years) 31,830 matched patients with depression (15,915 antidepressant users and 15,915 non-users). In most patients (98.7%), low-dose tricyclic antidepressants (TCAs) were related with a significantly increased risk of MACEs [adjusted HR = 1.20, 95% confidence interval (CI) = 1.03–1.40]. Duration response relationship showed a gradually increasing HR from 1.15 (95% CI = 0.98–1.33; &lt;30 days of use) to 1.84 (95% CI = 1.35–2.51; ≥365 days of use) (p for trend &lt;0.01). High Korean atherosclerotic CVD risk score (≥7.5%) or unfavorable lifestyle factors (smoking, alcohol intake, and exercise) were significantly associated with MACEs.Conclusion: Even at low doses, TCA use was associated with MACEs during primary prevention. Longer duration of TCA use correlated with higher HR. Careful monitoring is needed with TCA use in patients with no known CVD history.

scholarly journals Risk of cardiovascular disease, end-stage renal disease, and stroke in postpartum women and their fetuses after a hypertensive pregnancy

2018 ◽  
Vol 315 (3) ◽  
pp. R521-R528 ◽  
Author(s):  
Mark W. Cunningham ◽  
Babbette LaMarca
Keyword(s):  
Cardiovascular Disease ◽  
Renal Disease ◽  
Pregnancy Complications ◽  
End Stage Renal Disease ◽  
Metabolic Diseases ◽  
Cerebral Disease ◽  
Hypertensive Pregnancy ◽  
Increased Risk ◽  
Stage Renal Disease ◽  
End Stage

Women with hypertensive pregnancy complications are at greater risk of developing cardiovascular disease (CVD), metabolic diseases, stroke, and end-stage renal disease (ESRD) later in life. Pregnancy complications affect not only the mother’s long-term health but also the health of the fetus immediately after delivery and into adulthood. The health of the fetus until adulthood can be influenced by developmental programming, in which the fetus is exposed to insults that will ultimately affect the growth of the offspring and increase the offspring’s risk of developing hypertension, coronary heart disease, metabolic disease, and chronic kidney disease in adulthood. Preeclampsia, the onset of hypertension during pregnancy, is one of the major risk factors for the development of renal disease, cerebral disease, and CVD in the mother. Women with preeclampsia are at a 5–12-fold increased risk of developing ESRD, 2-fold increased risk of stroke, and 2-fold increased risk of developing CVD later in life. In this review article, we discuss 1) preeclampsia, 2) the risk of developing CVD, renal disease, or stroke later in life for women with hypertensive pregnancies, and 3) the effects of a hypertensive pregnancy on the offspring.

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