Oxidative stress in pericardial fluid and plasma and its association with ventricular function Jose Luis Vukasovic a, * , Francisco Moraga b , Guillermo Dı ´az-Araya b , Eduardo Turner c , Mario Chiong b , Polentzi Uriarte c , Fernando Florenzano a , Sergio Lavandero b, * a Department of Cardiovascular Diseases, Faculty of Medicine, University of Chile. Av. Salvador 364 Santiago, Chile b Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Olivos 1007, Santiago 6640750 Chile c National Thorax Institute, Jose ´ Miguel Infante 717, Santiago, Chile Received 25 August 2003; received in revised form 13 February 2004; accepted 1 March 2004 Available online 18 May 2004 Abstract There are no studies evaluating oxidative stress markers both in pericardial fluid and plasma and whether they correlate with cardiac function indexes. The purpose of the study was to investigate whether oxidative stress markers in pericardial fluid and plasma are associated with left ventricular function. Methods and results: Twenty-eight consecutive patients (class I or II NYHA) scheduled for myocardial revascularization, valve replacement, valve repair or closure of atrial septal defect. Plasma and pericardial fluid were collected and malondialdehyde, catalase, superoxide dismutase and glutathione peroxidase were determined. Left ventricular ejection fraction, left ventricular end diastolic diameter and left ventricular end systolic diameter were determined as echocardiographic indexes of ventricular function. We found that oxidative stress determined by a simple malondialdehyde (MDA) assay, correlated in plasma and pericardial fluid, and this parameter was associated with left ventricular end systolic diameter. Conclusion: Plasma and pericardial fluid malondialdehyde levels can be used as an early marker of ventricular dysfunction. D 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Pericardial fluid; Oxidative stress; Malondialdehyde; Antioxidant enzymes; Ventricular function; Heart failure 1. Introduction Evidences from different sources suggest that an exces- sive increase in reactive oxygen species contributes to the pathogenesis of a variety of cardiovascular diseases [1,2]. Under normal conditions, there is a fine balance between reactive oxygen species and a variety of antioxidant defense systems. Any alteration in this balance in favor of reactive oxygen species causes an increase in oxidative stress and initiate cellular changes that may lead to heart failure [3]. Lipid peroxidation generates several unsaturated aldehydes, such as malondialdehyde and 4-OH-nonenal, which may interact with and modify the function of other molecules that are of biological importance. Although heart failure is a state of generalized oxidative stress, the resultant spectrum of saturated and unsaturated aldehydes has not been sys- tematically characterized in this condition in both plasma and pericardial fluid. However, it cannot be ruled out that malondialdehyde is only a marker for increased myocardial damage in these patients. Oxidative stress has traditionally been evaluated by mea- suring plasma levels of malondialdehyde and the assessment of antioxidant enzymes such as catalase, superoxide dismu- tase and glutathione peroxidase [3]. However, no definite information is available concerning the actual relationship of oxidative stress assessed by these methods in plasma with what is actually taking place at the myocardial level. Peri- cardial fluid is not merely an ultrafiltrate of plasma, but also a transudate from the cardiac interstitium, reflecting the com- position of cardiac interstitium and the production and release of macromolecules in normal and diseased myocardium [4]. We determined pericardial fluid malondialdehyde levels as well as their correlations with plasma malondialdehyde levels 0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2004.03.013 * Corresponding authors. Jose Luis Vukasovic is to be contacted at Department of Cardiovascular Diseases, Faculty of Medicine, University of Chile. Av. Salvador 364 Santiago, Chile. Fax: +56-2-269-6263. Sergio Lavandero, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Olivos 1007, Santiago 6640750 Chile. Fax: +56-2-737-8920. E-mail addresses: vukasovic@terra.cl (J.L. Vukasovic), slavander@uchile.cl (S. Lavandero). www.elsevier.com/locate/ijcard International Journal of Cardiology 101 (2005) 197 – 201