Background: 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.
Aim: Prospective study to identify OS in plasma from patients with a cardiogenic shock and to evaluate etiologies of cardiomyopathy: ischemia or no.
Methods: consecutive patients hospitalized in the department of cardiology 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 (AAII).
OS was evaluated in blood samples at the admission (T0) and one month later: thiobarbituric acid-reactive substances (TBARS), total antioxidant status (TAS), protein carbonyls (PC) and oxidized LDL; superoxide dismutase (SOD), glutathione peroxidase (GSH and GSSG/GSH) and catalase activities: plasma α-tocopherol, vitamin A and β-carotene.
Results: 23 consecutive patients (90% men), mean age 59±11y. Follow-up 15 months. Acute heart failure was associated with an increased OS. OS was more important in patients with arrhythmia.
Acute heart failure due to ischemic or idiopathic CM was associated with increased OS. Etiologies of CM did not modify OS status.
Ischemic CM Non ischemic CM
endothelial TBARS (nmol/gHb) 3.22 ± 0.84 4.8 ± 1.1
plasmatic TBARS (μmol/L) 2.23 ± 0.4 2.19 ± 0.5
ox LDL (UI/L) 0.45 ± 012 0.5 ± 0.12
protein carbonyls (μmol/gprot) 0.185 ± 0.09 0.188 ± 0.01
Vitamin A (μmol/l) 0.66 ± 0.28 0.56 ± 0.28
α-tocopherol (mg/L) 11.1 ± 3.2 9.9 ± 2.7
GSH (μmol /gHb) 2.2 ± 0.7 2.1 ± 0.7
GSSG (μmol /gHb) 0.85 ± 0.06 0.7 ± 0.07
Cu/Zn SOD (UI/g Hb) 1363.1 ± 233.5 1409.8 ± 304.8
GPx (UI/g Hb) 50.5 ± 5 59.7 ± 8.7
Catalase (UI/g Hb) 125 ± 6 133 ± 8
Conclusion: Acute heart failure increased levels of oxygen free radicals independently of CM etiologies. We hypothetized that modifications of OS could be implied in arrhythmias and complications of acute heart failure