Markers of oxidative stress in acute myocardial infarction treated by percutaneous coronary intervention

• Autorzy: Eva Sedláková , Oliver Rácz , Eva Lovásová , Roman Beòaèka , Martin Kurpas , Anna Chmelárová , Ján Sedlák , Martin Studenèan
• Języki publikacji: EN

Abstrakty

EN

In the current study, we evaluated the dynamics of oxidative stress markers in patients with acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention (PCI). Thirty consecutive patients with AMI with ST elevation were included. Plasma lipid peroxidation end product malondialdehyde (MDA) and total antioxidant capacity (TAC) in blood plasma were evaluated. Peripheral venous blood samples were obtained prior to reperfusion and at five time points after reperfusion. The control group consisted of 20 ischemic patients without acute coronary syndrome. TAC in the AMI group at admission was lower than in control patients (1.26 + 0.32 vs. 1.52 + 0.24 mmol/l). Within 1 h after reperfusion, in most cases, values significantly declined (1 min, 1.10 + 0.33 mmol/l; 1 h, 1.06 + 0.21 mmol/l [p= 0.03]). After 3 h, values began to increase (1.14 + 0.29 mmol/l) and returned to basal values after 3 d (1.29 + 0.24 mmol/l). MDA levels in AMI patients at admission were higher than in control patients (1.66 + 0.55 vs. 1.44 + 0.55 mmol/l) but showed a sustained decrease over the 3 h after reperfusion of the occluded artery (1 min, 1.57 + 0.37 mmol/l; 1 h, 1.50 + 0.35 μmol/l; 3 h, 1.35 + 0.59 μmol/l [p = 0.03]). Reperfusion of the occluded coronary artery by PCI in AMI lead to an immediate decrease in TAC, suggesting formation of reactive oxygen species. However, the MDA level significantly decreased after reperfusion. This may suggests less reperfusion injury after PCI.

Słowa kluczowe

EN

Acute myocardial infarction; Reperfusion; Oxidative stress; Total antioxidant capacity; Malondialdehyde

• Czasopismo: Open Medicine
• Rocznik: 2009
• Tom: 4
• Numer: 1
• Strony: 26-31

Daty

wydano

2009-03-01

online

2009-02-11

Twórcy

autor

Eva Sedláková

• Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia,

autor

Oliver Rácz

• Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia

autor

Eva Lovásová

• Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia

autor

Roman Beòaèka

• Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia

autor

Martin Kurpas

• Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia

autor

Anna Chmelárová

• Department of Experimental Medicine, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia

autor

Ján Sedlák

• Eastern Slovak Cardiovascular Institute, 04001, Košice, Slovakia

autor

Martin Studenèan

• Eastern Slovak Cardiovascular Institute, 04001, Košice, Slovakia

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Identyfikatory

DOI

10.2478/s11536-009-0015-8