OXIDATIVE STRESS MARKERS IN ACUTE MYOCARDIAL INFARCTION TREATED BY PRIMARY PERCUTANEOUS CORONARY INTERVENTION

Abstract

The current study analysed the dynamics of oxidative stress markers in patients with acute ST-elevation myocardial infarction treated by primary percutaneous intervention. Excessive reactive oxygen species production is known to induce myocardial reperfusion injury. There are few studies that evaluated oxidative stress markers in the interventional era, the historical papers were all based on thrombolysis as a mean of reperfusion. Thirty-seven patients were included. Peripheral venous blood samples were obtained prior to coronary angioplasty, at 1 hour and 24 hours after that. Plasma malondialdehyde, reduced glutathione / oxidised glutathione ratio and total antioxidant capacity were determined. Malondialdehyde was significantly lower at 1 hour (3.1 ± 0.96 nmol/ml vs 2.68 ± 0.81 nmol/ml, p<0.01) and 24 hours (3.1 ± 0.96 nmol/ml vs 2.15 ± 0.95 nmol/ml, p<0.01). Also, reduced glutathione / oxidised glutathione ratio dropped significantly at 1 hour (3.25 Q1-Q3 2.17-5.19 vs 2.33 Q1-Q3 1.53-2.82, p<0.01) and at 24 hours (3.25 Q1-Q3 2.17-5.19 vs 1.96 Q1-Q3 1.28-2.85, p<0.01). Total antioxidant capacity had non-significant variation. There was no correlation between these markers and time from symptom-onset or left ventricular ejection fraction. Reperfusion of the occluded coronary artery by percutaneous coronary intervention in acute myocardial infarction led to a rapid decrease of reduced glutathione / oxidised glutathione ratio, that may indicate a depletion of antioxidants as a consequence of overproduction of reactive oxygen species in the damaged area. However, the malondialdehyde level significantly decreased after vessel opening. This may suggest low reperfusion injury after angioplasty.