During the last decade, considerable interest has been focused on the potential role of oxygen free radical generation in the pathophysiology of chronic congestive heart failure. Oxidative stress has been demonstrated in different animal models of congestive heart failure: volume overload, pressure overload, myocardial infarction, and adriamycin-induced cardiomyopathy. In contrast with animal studies, human studies are less convincing given that most of the traditional methods used to assess oxidative stress in the clinical setting are non-specific or inaccurate.1

A novel family of prostaglandin F₂ isomers, called F₂-isoprostanes, produced in vivo by a free radical peroxidation of arachidonic acid, has recently been described.2 Isoprostaglandin F_2α type III, formerly known as 8-iso-prostaglandin F_2α, is a biochemically stable F₂-isoprostane, formed by direct free radical peroxidation of arachidonic acid of cell membranes or circulating low density lipoprotein.2 Its quantification in tissues and biological fluids has been suggested to be a reliable measure of oxidant injury in vivo. Indeed, urinary excretion of this compound has been well characterised and is currently used as an index of lipid peroxidation in human diseases. A recent study has shown that concentrations of isoprostaglandin F_2α type III were increased in pericardial fluid of patients with symptomatic heart failure.3 However, urinary measurements may be of more clinical use for follow up studies. The purpose of the present study was to investigate urinary isoprostaglandin F_2α type III formation as an index of lipid peroxidation in patients suffering from severe heart failure.

Twenty five consecutive patients suffering from heart failure were included between April and July 1999. Patients were referred before heart transplantation or for a left ventricular failure episode. Patients were matched with 25 healthy volunteers (22 men, 3 women, median …