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(Circulation. 2002;106:173.)
© 2002 American Heart Association, Inc.

Editorial

Allopurinol and Endothelial Function in Heart Failure

Future or Fantasy?

Ulf Landmesser, MD; Helmut Drexler, MD

From Abteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Hannover, Germany.

Correspondence to Helmut Drexler, MD, Medizinische Hochschule Hannover, Abteilung Kardiologie und Angiologie, Carl Neuberg Str.1, 30625 Hannover, Germany. E-mail Drexler.Helmut@MH-Hannover.de

Key Words: Editorials • endothelium • heart failure • nitric oxide

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

The endothelium plays an important role in the control of vascular tone by releasing both vasodilating and vasoconstricting substances. These mechanisms are important for the regulation of both microvascular and larger conduit arteries.^1–3 Chronic heart failure (CHF) is characterized by increased vasoconstriction and a reduced vasodilator response during exercise.⁴ These abnormalities seem to be caused by a number of compensatory mechanisms, and some neurohumoral factors involved in this impaired vasodilator response have been studied extensively in the past. There is now growing evidence to suggest that the endothelium makes an important contribution to the abnormal vasodilator response in CHF. In particular, the role of endothelium-derived nitric oxide (NO^·) has received considerable attention.

See p 221

An impaired endothelium-dependent vasodilator response has been documented in the microcirculation of the myocardium,⁵ leg,⁶ and forearm^1,2 in patients with CHF. These data are compatible with the view that impairment of endothelium-dependent, NO^·-mediated vasodilator function is a generalized phenomenon in patients with CHF. Furthermore, flow-dependent, endothelium-mediated vasodilation of conduit arteries is impaired in patients with CHF, largely as a result of a reduced vascular bioavailability of nitric oxide.⁷

Pathophysiological Implications of Endothelial Dysfunction in CHF

Because endothelial vasodilator function is involved in control of tissue perfusion, impaired exercise-induced release of NO^· may contribute to reduced exercise capacity in CHF. Recent experimental studies have demonstrated that impaired endothelium-dependent vasodilation after NO^· synthase inhibition was associated with an early reduction of exercise capacity.⁸ Conversely, the improvement of endothelium-dependent vasodilation in patients with CHF after exercise training was closely correlated with the achieved . . . [Full Text of this Article]

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