Serum asymmetric dimethylarginine negatively correlates with intima-media thickness in early-onset atherosclerosis

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Abstract

Background: Asymmetric dimethylarginine (ADMA) assumes a significant role in atherosclerosis by inhibiting the endothelial nitric oxide synthase (eNOS). Moreover, ADMA inhibits the inducible NOS (iNOS), the isoform that triggers atherosclerosis via peroxynitrite formation. Therefore, we investigated whether ADMA is a risk or protective factor in the atherosclerotic process. Intima-media thickness (IMT) of the common carotid artery, a surrogate for vascular diseases, was chosen as the outcome variable of interest. Methods: Sixty patients younger than 55 years having at least 30% stenosis of the internal carotid artery and 30 age- and gender-matched controls were recruited at a community-based neurosonological laboratory. We investigated relatively young patients to circumvent the confounding effect age has in the development of atherosclerosis. Results: The IMT showed a negative correlation with ADMA upon analysis of the pooled data (Spearman correlation coefficient -0.300, p = 0.0041) and the atherosclerotic stratum (Spearman correlation coefficient -0.323, p = 0.012). A multiple linear regression model containing all determinant factors of IMT previously identified by simple regression was used to further quantify the relationship between IMT and ADMA. The negative association between IMT and ADMA remained statistically significant (β: -0.510, CI: -0.894, -0.127; p = 0.010), furthermore it was even stronger in the atherosclerotic stratum (β: -0.67, CI: -1.16, -0.18; p = 0.008). Conclusions: A minimal increase in ADMA concentration may be protective by inhibiting iNOS but not eNOS in states where iNOS is induced, e.g. inflammation accompanying atherosclerosis.

Original languageEnglish
Pages (from-to)388-394
Number of pages7
JournalCerebrovascular Diseases
Volume23
Issue number5-6
DOIs
Publication statusPublished - May 2007

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Atherosclerosis
Serum
Nitric Oxide Synthase Type III
Linear Models
Peroxynitrous Acid
Carotid Stenosis
Common Carotid Artery
N,N-dimethylarginine
Vascular Diseases
Protein Isoforms
Inflammation

Keywords

  • Atherosclerosis, inflammation
  • Carotid arteries
  • Nitric oxide synthase
  • Vascular risk factors

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

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title = "Serum asymmetric dimethylarginine negatively correlates with intima-media thickness in early-onset atherosclerosis",
abstract = "Background: Asymmetric dimethylarginine (ADMA) assumes a significant role in atherosclerosis by inhibiting the endothelial nitric oxide synthase (eNOS). Moreover, ADMA inhibits the inducible NOS (iNOS), the isoform that triggers atherosclerosis via peroxynitrite formation. Therefore, we investigated whether ADMA is a risk or protective factor in the atherosclerotic process. Intima-media thickness (IMT) of the common carotid artery, a surrogate for vascular diseases, was chosen as the outcome variable of interest. Methods: Sixty patients younger than 55 years having at least 30{\%} stenosis of the internal carotid artery and 30 age- and gender-matched controls were recruited at a community-based neurosonological laboratory. We investigated relatively young patients to circumvent the confounding effect age has in the development of atherosclerosis. Results: The IMT showed a negative correlation with ADMA upon analysis of the pooled data (Spearman correlation coefficient -0.300, p = 0.0041) and the atherosclerotic stratum (Spearman correlation coefficient -0.323, p = 0.012). A multiple linear regression model containing all determinant factors of IMT previously identified by simple regression was used to further quantify the relationship between IMT and ADMA. The negative association between IMT and ADMA remained statistically significant (β: -0.510, CI: -0.894, -0.127; p = 0.010), furthermore it was even stronger in the atherosclerotic stratum (β: -0.67, CI: -1.16, -0.18; p = 0.008). Conclusions: A minimal increase in ADMA concentration may be protective by inhibiting iNOS but not eNOS in states where iNOS is induced, e.g. inflammation accompanying atherosclerosis.",
keywords = "Atherosclerosis, inflammation, Carotid arteries, Nitric oxide synthase, Vascular risk factors",
author = "Judit Zsuga and Janos T{\"o}r{\"o}k and M. Magyar and A. Valikovics and R. Gesztelyi and S. K{\'e}ki and L. Csiba and M. Zsuga and D. Bereczki",
year = "2007",
month = "5",
doi = "10.1159/000101461",
language = "English",
volume = "23",
pages = "388--394",
journal = "Cerebrovascular Diseases",
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TY - JOUR

T1 - Serum asymmetric dimethylarginine negatively correlates with intima-media thickness in early-onset atherosclerosis

AU - Zsuga, Judit

AU - Török, Janos

AU - Magyar, M.

AU - Valikovics, A.

AU - Gesztelyi, R.

AU - Kéki, S.

AU - Csiba, L.

AU - Zsuga, M.

AU - Bereczki, D.

PY - 2007/5

Y1 - 2007/5

N2 - Background: Asymmetric dimethylarginine (ADMA) assumes a significant role in atherosclerosis by inhibiting the endothelial nitric oxide synthase (eNOS). Moreover, ADMA inhibits the inducible NOS (iNOS), the isoform that triggers atherosclerosis via peroxynitrite formation. Therefore, we investigated whether ADMA is a risk or protective factor in the atherosclerotic process. Intima-media thickness (IMT) of the common carotid artery, a surrogate for vascular diseases, was chosen as the outcome variable of interest. Methods: Sixty patients younger than 55 years having at least 30% stenosis of the internal carotid artery and 30 age- and gender-matched controls were recruited at a community-based neurosonological laboratory. We investigated relatively young patients to circumvent the confounding effect age has in the development of atherosclerosis. Results: The IMT showed a negative correlation with ADMA upon analysis of the pooled data (Spearman correlation coefficient -0.300, p = 0.0041) and the atherosclerotic stratum (Spearman correlation coefficient -0.323, p = 0.012). A multiple linear regression model containing all determinant factors of IMT previously identified by simple regression was used to further quantify the relationship between IMT and ADMA. The negative association between IMT and ADMA remained statistically significant (β: -0.510, CI: -0.894, -0.127; p = 0.010), furthermore it was even stronger in the atherosclerotic stratum (β: -0.67, CI: -1.16, -0.18; p = 0.008). Conclusions: A minimal increase in ADMA concentration may be protective by inhibiting iNOS but not eNOS in states where iNOS is induced, e.g. inflammation accompanying atherosclerosis.

AB - Background: Asymmetric dimethylarginine (ADMA) assumes a significant role in atherosclerosis by inhibiting the endothelial nitric oxide synthase (eNOS). Moreover, ADMA inhibits the inducible NOS (iNOS), the isoform that triggers atherosclerosis via peroxynitrite formation. Therefore, we investigated whether ADMA is a risk or protective factor in the atherosclerotic process. Intima-media thickness (IMT) of the common carotid artery, a surrogate for vascular diseases, was chosen as the outcome variable of interest. Methods: Sixty patients younger than 55 years having at least 30% stenosis of the internal carotid artery and 30 age- and gender-matched controls were recruited at a community-based neurosonological laboratory. We investigated relatively young patients to circumvent the confounding effect age has in the development of atherosclerosis. Results: The IMT showed a negative correlation with ADMA upon analysis of the pooled data (Spearman correlation coefficient -0.300, p = 0.0041) and the atherosclerotic stratum (Spearman correlation coefficient -0.323, p = 0.012). A multiple linear regression model containing all determinant factors of IMT previously identified by simple regression was used to further quantify the relationship between IMT and ADMA. The negative association between IMT and ADMA remained statistically significant (β: -0.510, CI: -0.894, -0.127; p = 0.010), furthermore it was even stronger in the atherosclerotic stratum (β: -0.67, CI: -1.16, -0.18; p = 0.008). Conclusions: A minimal increase in ADMA concentration may be protective by inhibiting iNOS but not eNOS in states where iNOS is induced, e.g. inflammation accompanying atherosclerosis.

KW - Atherosclerosis, inflammation

KW - Carotid arteries

KW - Nitric oxide synthase

KW - Vascular risk factors

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