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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:e12.)
© 2004 American Heart Association, Inc.

Letters to the Editor

Promoter and Exon 7 Polymorphism of Endothelial Nitric Oxide Synthase: Impact on Endothelial Function and Its Correction by Exercise Training in Patients With Coronary Artery Disease

Sandra Erbs; Axel Linke; Gerhard Schuler; Rainer Hambrecht

Heart Center Department of Internal Medicine/Cardiology, University of Leipzig, Struempellstrasse, Leipzig, Germany

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

To the Editor:

In a recently published article in Arteriosclerosis, Thrombosis, and Vascular Biology, we assessed the impact of the promoter (T-786C) and exon 7 (G894T) polymorphism of the eNOS gene on endothelial function and endothelial response to physical exercise training in patients with coronary artery disease (CAD).¹ We were able to demonstrate, with a statistical power of 85%, that patients with CAD who were positive for the promoter (T-786C) or the exon 7 (G894T) polymorphism showed an impaired acetylcholine-mediated increase in blood flow average peak velocity compared with those with wild-type variants.¹

We point out that our study population consisted of carefully selected patients with CAD with a preserved left ventricular function who are suitable for a training program. The promoter polymorphism (T-786C) was shown to be associated with the occurrence of myocardial infarction and consequently reduced left ventricular function.² Because patients with an impairment of left ventricle function were excluded from study participation, this might explain why patients homozygous for the promoter polymorphism (T-786C) are underrepresented in our study population.¹ However, we did not exclude patients with myocardial infarction who had a global normal left ventricular function but local wall motion irregularities. Moreover, Nakayama et al clearly emphasized that the T-786C mutation is a feature of patients having an acute myocardial infraction caused by coronary vasospasm in the absence of a significant CAD.² In contrast, only 1 of 329 patients with stenosed coronary arteries was homozygous for the promoter polymorphism in their study,² which is in accordance . . . [Full Text of this Article]