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Cardiovascular Research Advance Access first published online on May 16, 2008
This version [Corrected Proof] published online on May 20, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn109
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Heart-rate reduction and beta blockade in early post-infarction cardiac remodelling

Robert E. Goldstein* and Mark C.P. Haigney

Cardiology Division, Department of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, USA

* Corresponding author. Tel: +1 301 295 3601; fax: +1 301 295 3557. E-mail address: rgoldstein@usuhs.mil

This editorial refers to ‘Effect of metoprolol and ivabradine on left ventricular remodelling and Ca2+ handling in the post-infarction rat heart’ by Maczewski M and Mackiewitz U, doi:10.1093/cvr/cvn057

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

Soon after acute myocardial infarction, the heart may experience extensive changes in function, structure, tissue architecture, and biochemical properties collectively known as cardiac remodelling. Many of the deleterious changes can be attenuated by treatment with beta-adrenergic blocking agents1–3 or with alternative drugs that reduce post-infarction heart rate without interrupting beta-adrenergic signalling.4,5 In a study appearing in this issue of Cardiovascular Research,6 Maczewski and Mackiewitz employed a rat model to elucidate the benefits of post-infarction beta blockade by comparing effects of heart-rate reduction without beta blockade (using ivabradine) and effects observed when the same reduction in heart rate was . . . [Full Text of this Article]


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Effect of metoprolol and ivabradine on left ventricular remodelling and Ca2+ handling in the post-infarction rat heart
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Cardiovasc Res 2008 79: 42-51. [Abstract] [FREE Full Text]  

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Effect of metoprolol and ivabradine on left ventricular remodelling and Ca2+ handling in the post-infarction rat heart
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