Asymmetric dimethylarginine (ADMA) as a risk marker for stroke and TIA in a Swedish population

Wanby, Pär; Teerlink, Tom; Brudin, Lars; Brattström, Lars; Nilsson, Ingela; Palmqvist, Petter; Carlsson, Martin

doi:10.1016/j.atherosclerosis.2005.06.033

Cited by 95 publications

(77 citation statements)

References 27 publications

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“…A prospective study showed that ADMA elevation was a predictor of severe cardiovascular events and total mortality 9) . With regard to cerebrovascular disease, high ADMA levels have been identified in patients with ischemic stroke, transient ischemic attack, and cerebral small vessel disease 13,27) . To date, however, an association between ADMA and ischemic stroke has not been reported.…”

Section: Discussionmentioning

confidence: 99%

“…Among the convincing evidence, some studies have reported associations between elevated plasma ADMA and impaired NO synthesis in hypercholesterolemia, coronary heart disease 9,10) , and vascular risk factors 11) , while another found an independent association between a 1-mmol/L increase in plasma ADMA and 26% increase in the risk of all-cause mortality in patients with end-stage renal disease 12) . More recent studies indicated that ADMA is an independent marker for acute stroke and transient ischemic attack 13) . In our previous study, it was demonstrated that a higher ADMA concentration may be a useful marker of the future development of ischemic stroke 14) .…”

Section: Introductionmentioning

confidence: 99%

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Statin Treatment Decreased Serum Asymmetric Dimethylarginine (ADMA) Levels in Ischemic Stroke Patients

Nishiyama

Ueda

Otsuka

et al. 2011

JAT

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Aim: It remains unclear whether the decrease in the ADMA level associated with statin treatment results from the LDL-C-lowering effect or the pleiotropic effects of statins. A prospective, controlled study was conducted to examine whether statin treatment affects serum ADMA concentrations in ischemic stroke patients. Methods: Consecutive outpatients with non-cardiogenic ischemic stroke who had never been treated with statins and whose LDL-cholesterol level was higher than 140 mg/dL were enrolled and compared with control patients whose LDL-cholesterol level was lower than 140 mg/dL. Overall, 114 patients were enrolled in the study (56 and 58 in statin-treated and non-statin-treated groups, respectively). Patients in the statin group were treated with pravastatin 10 mg/day (n 15), fluvastatin 20 mg/day (n 14), pitavastatin 1 mg/day (n 14), or atorvastatin 10 mg/day (n 13).

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Statin Treatment Decreased Serum Asymmetric Dimethylarginine (ADMA) Levels in Ischemic Stroke Patients

Nishiyama

Ueda

Otsuka

et al. 2011

JAT

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“…Other studies on mortality and dimethylarginines in nonrenal patients (9) or patients with CKD 1 through 4 (34) failed to quantify SDMA. A recent study by Wanby et al (35), involving 363 patients, reported that there was a significant positive multivariate relationship between SDMA and cardioembolic infarction.…”

Section: Why Did Sdma Not Predict Cardiovascular Events and Mortalitymentioning

confidence: 94%

Symmetrical Dimethylarginine

Bode‐Böger

Scalera

Kielstein

et al. 2006

Journal of the American Society of Nephrology

255

204

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Symmetrical dimethylarginine (SDMA) is the structural isomer of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine. Whereas the major route of asymmetric dimethylarginine elimination is the hydrolytic degradation by dimethylarginine dimethylaminohydrolase, SDMA is eliminated by renal excretion. SDMA does not directly inhibit NOS but is a competitor of arginine transport. This study showed for the first time that measurement of SDMA can be a marker of estimated GFR and extent of coronary artery disease (CAD). In 97 patients with CAD, SDMA was a marker of estimated GFR. On multiple regression analysis of the CAD parameter stenosis score, SDMA was the only parameter retained. In addition, endothelial cells from the third passage were cultured in medium that contained 70 mol/L arginine and was incubated for 24 h in the presence of various concentration of SDMA (0, 2, 5, 10, and 100 mol/L). The levels of nitrate and nitrite in conditioned media, the protein expression of NOS, and the content of reactive oxygen species in endothelial cells were determined. SDMA inhibited dose dependently the NO synthesis in intact endothelial cells, whereas it had no effect on protein expression of NOS. This effect was associated with an increase in reactive oxygen species. Co-incubation with S ymmetrical dimethylarginine (SDMA) is the structural isomer of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA). ADMA has been shown to correlate with risk factors for coronary artery disease (CAD) such as hypertension (1,2), hypercholesterolemia (3), hyperhomocysteinemia (4 -6), insulin resistance (7), age (1), and mean arterial pressure (1). Moreover, ADMA correlates with the extent and the severity of coronary atherosclerosis (8) and is a strong and independent marker of cardiovascular events and mortality in selected patient populations (9 -11). Although there is mounting evidence that chronically elevated ADMA may contribute to progression of vascular disease via endothelial damage, little attention has been paid to the role of SDMA. Both ADMA and SDMA derive from intranuclear methylation of l-arginine residuals and are released into the cytoplasm after proteolysis (12). SDMA is produced by protein-arginine methyltransferase 5 (PRMT 5) and PRMT 7 (both type II methyltransferases) (13,14). Only ADMA but not SDMA is metabolized by dimethylarginine dimethylaminohydrolase to citrulline and dimethylamine (15). SDMA seems to be strictly eliminated by renal excretion (16,17). A recent study by Fliser et al. (18) showed a very close correlation among serum creatinine, GFR (measured by iodothalamate clearance technique), and SDMA. The authors speculated that SDMA, equal to serum creatinine, can serve as a marker of renal function, but SDMA seems to be more than a simple indicator of renal function. In animals, a high-fat, high-cholesterol diet increases SDMA serum levels (19,20) without affecting renal function (20), indicating that cardiovascular risk factors other than impaired...

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“…Chronic renal failure associated with hypertension [1,3,14,15] Stroke [16,17] Pulmonary hypertension [18][19][20] Left ventricular hypertrophy [21,22] Type II diabetes [23][24][25] Pre-eclampsia [26,27] Heart failure [28] Ischaemia [29,30] Hypercholesterolemia [31,32] Atherosclerosis [33,34] Alzheimers* [35,36] …”

Section: Cardiovascular Disorder Change In Adma Referencementioning

confidence: 99%

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

Smith¹

2007

CPD

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This is an electronic version of an article published in Current Pharmaceutical Design, 13 (16). pp. [1619][1620][1621][1622][1623][1624][1625][1626][1627][1628][1629] 2007. The definitive version is available online at:http://www.bentham.org/cpd/index.htmThe WestminsterResearch online digital archive at the University of Westminster aims to make the research output of the University available to a wider audience. Copyright and Moral Rights remain with the authors and/or copyright owners. Users are permitted to download and/or print one copy for non-commercial private study or research. Further distribution and any use of material from within this archive for profit-making enterprises or for commercial gain is strictly forbidden.Whilst further distribution of specific materials from within this archive is forbidden, you may freely distribute the URL of WestminsterResearch.(http://www.wmin.ac.uk/westminsterresearch).In case of abuse or copyright appearing without permission e-mail wattsn@wmin.ac.uk. Abstract: C-reactive protein (CRP) has received much attention as a cardiovascular risk factor and has been recommended to be used in screening to assist in predicting the occurrence of cardiovascular disorders. There are numerous association studies documenting changes in circulating CRP concentrations, there are, however, fewer studies providing evidence that CRP mediates the progression of cardiovascular pathologies. Elucidating the potential mechanisms for CRP has been confounded by recent reports that contaminants of CRP are partially responsible for observed effects.In this review the use of CRP as a tool to predict cardiovascular disorders will be discussed alongside a more recently described cardiovascular risk factor asymmetric dimethylarginine (ADMA). An endogenously occurring nitric oxide synthase inhibitor, ADMA, is formed by the action of protein arginine methyltransferases and subsequent proteolysis and it is metabolised in vivo by the dimethylarginine dimethylaminohydrolases (DDAH). The evidence available documenting the effects of CRP and ADMA, the regulatory mechanisms and the genetic influences, will be discussed in order to determine whether CRP and ADMA are mediators in the progression of cardiovascular disorders or merely useful biomarkers.

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Asymmetric dimethylarginine (ADMA) as a risk marker for stroke and TIA in a Swedish population

Cited by 95 publications

References 27 publications

Statin Treatment Decreased Serum Asymmetric Dimethylarginine (ADMA) Levels in Ischemic Stroke Patients

Statin Treatment Decreased Serum Asymmetric Dimethylarginine (ADMA) Levels in Ischemic Stroke Patients

Symmetrical Dimethylarginine

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

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