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Cardiovascular Research 2005 65(2):299-301; doi:10.1016/j.cardiores.2004.11.024
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Copyright © 2004, European Society of Cardiology

Pathophysiology of heart failure: more bricks in the "crumbling sarcolemmal scaffolding" paradigm?

Stéphane Baudet*

Intervet Pharma R&D, BP 67131, F-49071 Beaucouzé Cédex, France

* Tel.: +33 2 41 22 8269; fax: +33 2 41 8228. Email address: stephane.baudet@intervet.com

Received 16 November 2004; accepted 17 November 2004

The first 10% of the full text of this article appears below.

See article by Takahashi et al. (pages 356–365) in this issue.

Despite major progress in the pharmacological management of congestive heart failure (CHF), life expectancy of patients suffering from CHF remains low [1]. Progress in the treatment of CHF (currently based on diuretics, angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II (Ang II) type 1 receptor (AT1R) blockers (ARB), and β-blockers [1]) has relied on the recognition of the primary role of the adrenergic and renin–angiotensin–aldosterone (RAA) systems, which are initially activated to compensate for the decreased cardiac output, but which, in the long run, aggravate myocardial performance, therefore perpetuating the vicious circle of the CHF process [2].

The myocardium is one final target of the deleterious effects of catecholamines and . . . [Full Text of this Article]


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