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(Circulation Research. 2007;101:221.)
© 2007 American Heart Association, Inc.

Editorials

Brain Mechanisms Contributing to Sympathetic Hyperactivity and Heart Failure

Frans H.H. Leenen

From the University of Ottawa Heart Institute, Ontario, Canada.

Correspondence to Frans H.H. Leenen, MD, PhD, FRCPC, FAHA, Hypertension Unit, University of Ottawa Heart Institute, H360, 40 Ruskin Street, Ottawa, Ontario, Canada K1Y 4W7. E-mail fleenen@ottawaheart.ca

See related article, pages 304–312

Key Words: proinflammatory cytokines • aldosterone • angiotensin II • hypothalamus • sympathetic activity • cardiac function

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

It is well recognized that the initial myocardial injury and associated decrease in left ventricular (LV) function activate progressively a variety of systems, which in the long-term contribute to progressive cardiac dysfunction and clinical heart failure. Studies on the pathophysiology of the CHF syndrome have extensively focused on the activity of systems such as the sympathetic nervous system (SNS) or the renin-angiotensin-aldosterone system (RAAS) and their effects on the heart. From a therapeutic perspective, activation of the different mechanisms is generally considered to occur independent of each other, resulting in the current polypharmacy approach to CHF. Current interventional approaches counter only the peripheral effects of increased sympathetic drive by ß-blockers. The latter approach does not inhibit the sympathetic hyperactivity per se and effects mediated via eg, -receptors in the heart, kidneys and blood vessels. Much less is known about the determinants of the activation of the SNS or the RAAS, to prevent their activation and thereby their contribution to progressive cardiac remodeling and dysfunction. In this regard, it is essential to know whether the contributing mechanisms are activated in a coordinated fashion. In this case strategies can focus on maintaining normal activity in this coordinating center, and one may envision that 1 (or 2) interventions may be sufficient. In recent years it is becoming apparent that the CNS may act as the conductor integrating input from a variety of sources in the body which leads to activation of CNS mechanisms whose peripheral output plays a major role in progressive cardiac . . . [Full Text of this Article]

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