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(Circulation. 2003;107:2766.)
© 2003 American Heart Association, Inc.

Editorials

Heads and Hearts

The Endothelial Connection

Robert A. Vogel, MD

From the Division of Cardiology, Department of Medicine, University of Maryland School of Medicine, Baltimore.

Reprint requests to Robert A. Vogel, MD, University of Maryland Hospital, 22 S Greene St, Room S3B06, Baltimore, MD 21201. E-mail rvogel@heart.umaryland.edu

Key Words: Editorials • endothelium • cerebrovascular disorders • atherosclerosis

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

Atherosclerosis is an inflammatory, proliferative, thrombotic arterial disease initiated by risk factor injury to the endothelium. Although obstructive plaques develop locally, the disease is always diffuse if examined by intravascular ultrasound or histology. Assessing and treating the initiating risk factors and the resulting obstructive disease has been the traditional approach to managing atherosclerosis. Our recent understanding of how the related pathophysiological processes of endothelial dysfunction and inflammation connect risk factors and disease expression has led to an interest in using these pathways to assess patient risk and determine therapies.^1,2 In the future, we will also directly assess our genetic predisposition for developing and clinically manifesting atherosclerosis.

See p 2805

In response to physical and chemical stimuli, the endothelium regulates vascular physiology through control of vasoactivity, inflammation, vessel growth and remodeling, monocyte adhesion, platelet activation, thrombosis, and thrombolysis.³ Normal endothelium is associated with a vasodilatory, antiatherogenic state, whereas dysfunctional endothelium is associated with a proatherogenic state and plaque instability. The predominant endothelium-derived vasodilator, nitric oxide, has several antiatherogenic properties, including inhibition of platelet aggregation and smooth muscle cell proliferation. In experimental animals, nitric oxide availability is inversely related to disease progression. Endothelial function is impaired by all traditional risk factors. Endothelial function is thought to be a gauge of cumulative risk factor burden modified by genetic susceptibility. Conversely, improvements in endothelial function have been demonstrated with risk factor modification, such as with cholesterol and blood pressure reduction. Risk factors and risk factor modification change endothelial function very rapidly, and endothelial dysfunction . . . [Full Text of this Article]

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