Evidence for antioxidants consumption in the coronary blood of patients with an acute myocardial infarction

Blood flow arrest and reperfusion during myocardial infarction (MI) cause myocyte and endothelium injury through oxidative stress and inflammation, both of which involve Reactive Oxygen Species (ROS) and peroxides that consume antioxidant defenses. The aim of this study was to determine whether serum from the occluded coronary vessel has impaired anti-oxidative defenses as compared to serum from aortic blood or from the periphery of healthy controls. Forty-seven patients (44 men) were included for study. Inclusion criteria were chest pain, ST elevation, and cardiac troponin increase. A photoreaction producing a standardized amount of singlet oxygen (¹O₂), an excited form of oxygen, was performed in serum samples obtained during primary percutaneous coronary intervention (PCI). Immediately after laser light delivery to 5 % sera containing 5 µg/mL rose bengal, dichloro-dihydro-fluorescein (DCFH) was added and its post-oxidation transformation into the fluorescent DCF, was recorded. At least 5 h after the start of symptoms, the mean secondary ROS production after ¹O₂ delivery was increased in coronary sera (p < 0.001), but in aortic blood remained similar to that of healthy controls. The peak troponin value correlated with DCF fluorescence throughout the interval between symptoms onset and PCI. A high fluorescence was associated with a higher risk of MACE. These results show that oxidants secondary to ¹O₂ are increased in occluded vessels during AMI in parallel to c-troponin, demonstrating that antioxidants are consumed. A O₂ increase during reperfusion would thus extend the damage resulting from IDM necrosis. The effect of conditioning during PCI could be studied using the described method.