087 Oxidative stress implication in cardiogenic shock with ischemic or idiopathic severe left ventricular dysfunction: role of etiologies of cardiomyopathies

Abstract

Oxidative stress (OS) implication is paramount in pathology: ischemia reperfusion sequence (acute coronary syndrome, cardiac surgery, transplantation). Involvement of OS in heart failure (HF) is less known but is increased in the failing heart, and this might contribute to the pathogenesis of myocardial remodeling and HF. Prospective study to identify OS in plasma from patients with a cardiogenic shock and to evaluate the role of etiologies of cardiomyopathy: ischemia or no. Consecutive patients hospitalized in the cardiology unit with a first cardiogenic shock that complicated an idiopathic or ischemic dilated cardiomyopathy (DCM) with left ventricular (LV) dysfunction. Exclusion criteria: known cardiomyopathy, acute coronary syndrome, septic or anaphylactic or hypovolemic shock, treatment with angiotensin converting enzyme inhibitors (ACEI) or angiotensin II antagonists (AA II). OS was evaluated in blood samples at the admission (T 0 ) and one month later: thiobarbituric acid-reactive substances (TBARS), total antioxidant status (TAS), protein carbonyls (PC) and LDL oxidized; superoxide dismutase (SOD), glutathione peroxidase(GSH and GSSG/GSH) and catalase activities; plasma α tocopherol, vitamin A and β carotene. 23 consecutive patients (90% men), mean age 59±11y. Follow-up of 15 months. The aetiologies of CMD were ischemic (n=6), idiopathic (n=15), toxic (n=1) or restrictive (n=1). The mean LV ejection fraction was 23.3±8%. The NT-proBNP level was 9600±2000ng/ml. T o 1 MONTH NORMAL VALUE PC (μmol/g prot) 0.16 (0.05-0.41) 0.14 (0.07-0.29) < 0.10 TBARS (nmol/gHb) 2.2 (1.3-17.3) 2.5 (1.1-6.5) 0.7-1.6 LDLox (UI/L) 48 (20-83) 49 (26-98) 16-18 GSH (μmol/g Hb) 2.1 (0.8-3.1) 2.2 (1.7-4) 3.3-6.9 GSSG/GSH 0.19 (0.09-0.93) 0.13 (0.07-0.29) < 0.08 Acute heart failure was associated with an increased OS. OS was more important in patients with arrhythmia. Acute heart failure increased the level of oxygen free radicals. We hypothetized that modifications of OS could be implied in arrhythmias and complications of acute heart failure.