Oxidative stress in heart failure: More than just damage

Extract

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 β-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 ventricular dilatation, increasing interstitial fibrosis and arrhythmia, and a decline in ejection fraction. At least part of the benefit of ACE inhibitors and β-blockers is believed to involve the amelioration of adverse cardiac remodelling.