Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Abstract

[247][248][249][250][251][252][253][254][255] Acute myocardial infarction causing cardiac ischemia is responsible for the majority of cardiac related deaths. Medical interventions that ensure rapid reperfusion, such as percutaneous coronary intervention, are aimed to allow myocardial re-oxygenation. However, this generates reactive oxygen species, resembling ischemiareperfusion type of injury based on oxidative stress. In the present study we monitored dynamic changes of total serum peroxides, total antioxidant capacity and soluble intercellular adhesion molecule-1 as well as the titer of antibodies against oxidized low-density lipoproteins in the blood during the convalescence period of 32 patients with acute myocardial infarction treated by percutaneous coronary intervention. Samples were taken at admittance and at two hours, four hours, three days and seven days following percutaneous coronary intervention. Total antioxidant capacity dropped to 82% ( p < 0.05). The titer of antibodies against oxidized low-density lipoproteins transiently decreased within the first three days, and increased afterwards. The values of serum peroxides and soluble intercellular adhesion molecule-1 increased continuously in respect to the initial levels reaching the maximum at the time of release from hospital. These findings indicate a persistent oxidative stress that might be associated with intravascular inflammation in patients during convalescence and release from hospital. myocardial infarction; percutaneous coronary intervention; inflammation; soluble intercellular adhesion molecule-1; lipid peroxidation © 2006 Tohoku University Medical Press While oxidative stress has been shown to be related with the age and living habits (Ozbay and Dulker 2002), it plays an important role in the development of vascular diseases that affect vital organs, in particular brain and heart (Zarkovic 2003;Zarkovic et al. 2004;Madamanchi et al.

Competitive and seasonal oxidative stress in elite alpine ski racers

“…This was associated with a concomitant decrease in the oLAb titers, because excess peroxides generated epitopes for these antibodies, which consequently decreased through binding to these epitopes. These harmful peroxides reduce fitness in American football players (Schippinger et al, 2002) and increase under pathological conditions (Nikolic‐Heitzler et al, 2006). Just peroxides are harmful oxidants; they were also reported as signalling molecules in both healthy and inflammatory T lymphocytes, which respond differently to this agent (Nindl et al, 2004).…”

Ergometry Induces Systemic Oxidative Stress in Healthy Human Subjects

“…The total antioxidant capacity of serum was determined as described before by a commercially available assay (TAC LND, Germany) (Nikolic-Heitzler et al 2006). The assay is based on serum antioxidant consumption after addition of hydrogen peroxide.…”

Serum sphingolipids level as a novel potential marker for early detection of human myocardial ischaemic injury

“…It is not clear whether sphingolipids are markers of the inflammatory process associated with atherosclerotic CAD and/or are markers of cardiac ischaemia associated with flow obstructive coronary artery lesions. During coronary occlusion and subsequent reperfusion such as occurs during treatment of MI with percutaneous coronary intervention (PCI), reactive oxygen species (ROS) are formed that mediate ischaemia-reperfusion injury based on oxidative stress (Nikolic-Heitzler et al, 2006). ROS regulate S1P levels through changes in the function of sphingosine kinase, the final rate limiting step in S1P synthesis (Maceyka et al, 2007).…”