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(Hypertension. 2003;42:870.)
© 2003 American Heart Association, Inc.

Editorial Commentary

Is Very High Sympathetic Tone in Heart Failure a Result of Keeping Bad Company?

From Baker Heart Research Institute, Melbourne, Australia.

Correspondence to Prof Murray Esler, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia. E-mail murray.esler@baker.edu.au

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

The sympathetic nervous system is activated in patients with heart failure, with increase in the sympathetic outflows to the heart, kidneys, and the skeletal muscle vasculature having been clearly demonstrated through the use of isotope dilution-derived measures of norepinephrine spillover and the sympathetic nerve recording technique of clinical microneurography.^1–3 Prognosis in cardiac failure (congestive heart failure, CHF) is directly linked to the level of activation of the sympathetic nervous system present,⁴ most strongly with that in the sympathetic outflow to the heart.⁵ One of the major advances in cardiology of the past 10 years has been the successful therapeutic targeting with ß-adrenergic–blocking drugs of the defining neural pathophysiology of CHF, a pronounced and preferential stimulation of the cardiac sympathetic nerves,¹ which has materially improved the clinical outcome in patients with heart failure.^6,7

The regulatory processes underlying the sympathetic nervous activation of CHF remain uncertain. In both experimental⁸ and human^9,10 heart failure, there is evidence that rostral noradrenergic neuronal projections from the brain stem to hypothalamic nuclei, in particular the paraventricular nucleus of the hypothalamus, are important drivers of the increased sympathetic outflow. Whether the afferent mechanism for these CNS changes might perhaps involve hypoxia, arterial baroreflex impairment, or increased intracardiac pressure, or even combinations of all three, is disputed.^9,11

In the current issue of the Journal, Professor Grassi and colleagues from Milan, in an important paper provide intriguing results suggesting that another mechanism of sympathetic stimulation may also be operating, specifically that two conditions that importantly predispose to the development . . . [Full Text of this Article]

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