Free radicals may be involved in the genesis of certain types of acute myocardial dysfunction ("reperfusion injury" and "stunning").1,2 Free radicals could also be implicated in the development and progression of chronic myocardial impairment. Underlying coronary artery disease may predispose to stunning. Repeated episodes of stunning may lead to permanent myocardial dysfunction.3 Additional factors could also favor free radical generation in congestive heart failure (CHF). Many other organ beds such as the kidneys and skeletal muscle undergo hypoperfusion/reperfusion cycles in patients with CHF, especially during exercise. Lactic acidosis may enhance hyperoxia in these tissues.4 Adrenergic activity is increased in CHF.5 Catecholamines may augment free radical generation by increasing mitochondrial respiration and undergoing autooxidation.6,7 In support of these possibilities antioxidant therapy has been shown to protect against catecholamine cardiomyopathies in animals.8,9 We have therefore measured malondialdehyde-like material in patients with CHF. This may give some indication of lipid peroxidation, an injurious process to membranes mediated by free radicals.10 We have also measured plasma thiol concentration. Thiols are thought to act as free radical scavengers and reduction in plasma thiol levels may reflect oxidative stress.11.