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Circulation Research. 2005;97:e84

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(Circulation Research. 2005;97:e84.)
© 2005 American Heart Association, Inc.


Letters to the Editor

ADMA, Endothelial Progenitor Cells, and Cardiovascular Risk

T. Thum, J. Bauersachs

Internal Medicine I, Cardiology, Julius-Maximilians University, Würzburg, Germany


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

We read with interest the article by Schnabel and colleagues1 exploring the prognostic value of asymmetric dimethylarginine (ADMA) with regard to cardiovascular risk. Baseline serum ADMA levels in patients with coronary artery disease were associated with the primary end point of death from cardiovascular cause or nonfatal myocardial infarction, whereas no relationship was observed with death from other causes. Thus ADMA was identified as an independent risk factor beyond traditional risk factors and novel biomarkers.

Because of its role as an endogenous inhibitor of the endothelial nitric oxide synthase (eNOS), increased ADMA levels likely contribute to the development of endothelial dysfunction and coronary artery disease.2 eNOS is also critically involved in the regulation of endothelial progenitor cells (EPC) and repair of vascular lesions.3 Interestingly, Schmidt-Lucke et al identified an association between reduced levels of circulating EPC and incidence of subsequent cardiovascular events.4 By multivariate analysis, reduced EPC levels were a significant independent predictor of poor prognosis, even after adjustment for traditional cardiovascular risk factors. Unfortunately, neither Schmidt-Lucke et al4 measured ADMA levels in the investigated study cohort, nor did Schnabel et al1 determine circulating EPC. However, the study of Schnabel et al implicates that ADMA may impair endogenous regeneration of diseased blood vessels resulting in progressive development of vascular lesions. Recently, we have shown an inverse correlation between ADMA plasma concentration and circulating EPC levels in patients with coronary artery disease.5 Adjusting for all patient characteristics, these findings were confirmed in multivariate regression analyses. In vitro studies . . . [Full Text of this Article]




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A. M. Wilson, R. Harada, N. Nair, N. Balasubramanian, and J. P. Cooke
L-Arginine Supplementation in Peripheral Arterial Disease: No Benefit and Possible Harm
Circulation, July 10, 2007; 116(2): 188 - 195.
[Abstract] [Full Text] [PDF]