Asymmetric dimethylarginine (ADMA) as a possible risk marker for ischemic stroke

Nishiyama, Yasuhiro; Ueda, Masayuki; Katsura, Ken‐ichiro; Otsuka, Toshiaki; Abe, Arata; Nagayama, Hiroshi; Katayama, Yasuo

doi:10.1016/j.jns.2009.12.020

Cited by 41 publications

(30 citation statements)

References 14 publications

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“…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) . Elevated ADMA concentrations are highly prevalent in patients with hypercholesterolemia, and a positive correlation between plasma LDL-C and ADMA concentration has been reported 8) .…”

Section: Introductionmentioning

confidence: 98%

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: Introductionmentioning

confidence: 98%

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

Nishiyama

Ueda

Otsuka

et al. 2011

JAT

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“…A massive systemic inflammatory response is triggered by SAH and induces an increase in inflammatory markers such as C-Reactive Protein (CRP) [12]. High ADMA concentrations after ischemic stroke has been associated to un-favourable outcome, and elevated concentrations of ADMA can be lowered by anti-inflammatory treatment with statins [13,14]. However, the timing of ADMA and CRP as markers for inflammatory response after SAH remains to be elucidated [15].…”

Section: Introductionmentioning

confidence: 99%

Subarachnoid haemorrhage induces an inflammatory response followed by a delayed persisting increase in asymmetric dimethylarginine

Rodling-Wahlström

Olivecrona

Koskinen

et al. 2012

Scandinavian Journal of Clinical and Laboratory Investigation

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This is an accepted version of a paper published in Scandinavian Journal of Clinical and Laboratory Investigation. This paper has been peer-reviewed but does not include the final publisher proof-corrections or journal pagination.Citation for the published paper: Rodling Wahlström, M., Olivecrona, M., Koskinen, L., Naredi, S., Hultin, M. (2012) "Subarachnoid haemorrhage induces an inflammatory response followed by a delayed persisting increase in asymmetric dimethylarginine" Scandinavian Journal of Clinical and Laboratory Investigation, Access to the published version may require subscription. AbstractObject: Subarachnoid haemorrhage (SAH) is associated with an inflammatory systemic response and cardiovascular complications. Asymmetric dimethyl arginine (ADMA), an endogenous inhibitor of nitric oxide synthase, mediates vasoconstriction and might contribute to cerebral vasoconstriction and cardiovascular complications after SAH. ADMA is also involved in inflammation and induces endothelial dysfunction. The aim of this study was to evaluate whether and how CRP (marker for systemic inflammation) and ADMA increased in patients during the acute phase (first week) after SAH. The ADMA level was also assessed in the patients in a non-acute phase (three months), and in healthy controls. Methods: Prospective study of 20 patients with aneurysmal SAH. ADMA and CRP were followed daily during the first week after SAH and a follow up sample for ADMA was obtained three months later. A single blood sample for ADMA was collected from age and sex matched healthy controls (n=40, 2 for each case). Conclusion:After SAH, CRP and ADMA in serum increased significantly during the first week and ADMA remained elevated three months later.

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“…(ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), are associated with the atherosclerotic burden and increase progressively with the number of stroke risk factors 1) . Increased plasma levels have been observed in patients with hypertension 1,2) , hyperlipidemia 1,3) , hyperhomocysteinemia 4) , diabetes 5) and in subjects with a history of stroke 8) .…”

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confidence: 99%

“…Increased plasma levels have been observed in patients with hypertension 1,2) , hyperlipidemia 1,3) , hyperhomocysteinemia 4) , diabetes 5) and in subjects with a history of stroke 8) . Currently, ADMA is considered to be not only a marker but also a mediator of oxidative stress via the inhibition and uncoupling of NOS 9) .…”

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High Plasma Dimethylarginine Levels are Associated with Adverse Clinical Outcome After Stroke

Worthmann

Chen

Martens‐Lobenhoffer

et al. 2011

JAT

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Aim: Increased levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, have been observed in patients with cardiovascular risk factors and atherosclerosis and in patients with a history of stroke. The role of ADMA and its analogue symmetric dimethylarginine (SDMA) in acute ischemic stroke is yet unclear. We hypothesized that plasma dimethylarginine levels increase in the hyper-acute phase after ischemic stroke and that their time course is related to stroke outcome. Methods: Plasma dimethylarginines ADMA and SDMA and L-arginine levels were measured in 67 patients at 6, 12, 24 hours, as well as 3 and 7 days after stroke onset using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS-MS). Data were compared to control data from 32 age-adjusted healthy volunteers. Clinical outcome was assessed using the modified Rankin Scale (mRS) at 90 days after stroke. Results: At baseline, plasma ADMA levels were higher in stroke patients than in controls, whereas plasma SDMA and L-arginine levels did not differ from control subjects. The time courses of ADMA and SDMA were related to the clinical outcome. Binary logistic regression analysis showed that ADMA levels of ≥ 0.566 mol/L at day 3, ≥ 0.530 mol/L at day 7 and SDMA levels of ≥ 0.59 mol/L at 24 hours predicted an unfavorable clinical outcome. Conclusions: An increase of both ADMA and SDMA plasma levels within the first 72 hours after the onset of ischemic stroke predicts a poor outcome. J Atheroscler Thromb, 2011; 18:753-761.

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Asymmetric dimethylarginine (ADMA) as a possible risk marker for ischemic stroke

Cited by 41 publications

References 14 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

Subarachnoid haemorrhage induces an inflammatory response followed by a delayed persisting increase in asymmetric dimethylarginine

High Plasma Dimethylarginine Levels are Associated with Adverse Clinical Outcome After Stroke

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