Copyright © 2003 by the European Society of Cardiology.
Editorial
Oxidative stress in heart failure
More than just damage
Department of Cardiology, Guy’s, King’s and St. Thomas’ School of Medicine, King’s College London,Bessemer Road, London SE5 9PJ, UK
* Corresponding author: Professor Ajay M Shah, Department of Cardiology, GKT School of Medicine, Bessemer Road, London SE5 9PJ. Tel.: + 44-20-7346-3865; Fax: +44-20-7346-4771
E-mail address: ajay.shah@kcl.ac.uk
Received 8 October 2003; accepted 16 October 2003
| The first 10% of the full text of this article appears below. |
See doi:10.1016/j.ehj.2003.09.022for the article to which this editorial refers
Chronic heart failure (CHF) continues to cause substantial morbidity and mortality despite major therapeutic advances, such as the use of angiotensin-converting enzyme (ACE) inhibitors and ß-blockers. The main causes of CHF today are ischaemic heart disease (IHD) and hypertension. Extensive experimental and clinical studies over the last 20 years have established that a fundamental process in the progression to CHF (especially in patients with prior myocardial infarction [MI]) is cardiac remodelling—a series of alterations in heart structure and function that involve significant changes in gene expression and protein function, both in the extracellular matrix and in cardiomyocytes. Although ventricular remodelling may initially be adaptive by normalizing wall stress and maintaining contractile function in the face of muscle loss or increased load, with time there is progressive
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