Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction

Berg, Kirsti; Jynge, Per; Bjerve, Kristian S.; Skarra, Sissel; Basu, Samar; Wiseth, Rune

doi:10.1080/10715760400028027

Cited by 50 publications

(39 citation statements)

References 23 publications

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“…MDA levels in AMI patients were higher than in the control group, and TAC levels were lower. This indicates that oxidative stress is already elevated during ischemia, which is in agreement with previous studies [3,15].…”

Section: Discussionsupporting

confidence: 82%

“…In contrast, starting at the third hour, there was an increase in the TAC level up to the third day. These findings are similar to those reported by Beard et al [11] and Berg et al [15]. Beard reported a decrease in plasma glutathione peroxidase lasting 2 h after reperfusion, followed by a continuous increase for up to 2 d. The decrease in TAC after reperfusion may indicate a depletion of antioxidants as a consequence of overproduction of ROS in the damaged area.…”

Section: Discussionsupporting

confidence: 81%

“…All previous studies reported an increase in the MDA level following thrombolytic opening of infarct-related arteries, and Berg et al reported an increase in oxidative stress as measured by 8-iso-PGF2α levels following PCI [15]. Although we expected a rise in the plasma MDA level, it fell significantly after PCI in this study.…”

Section: Discussioncontrasting

confidence: 55%

“…Similarly, Berg et al [15] did not find a direct relationship between 8-iso-PGF2α, a marker of oxidative stress, and troponin T, a marker of myocardial injury.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2009

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AbstractIn 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.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 81%

Section: Discussioncontrasting

confidence: 55%

“…Similarly, Berg et al [15] did not find a direct relationship between 8-iso-PGF2α, a marker of oxidative stress, and troponin T, a marker of myocardial injury.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2009

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“…Consumption of antioxidants was previously shown in patients with peripheral arterial disease after ischemia-reperfusion as well as after vascular surgery (Berg et al 2005;Wonisch et al 2005). It should be mentioned that interpretation of data on total serum antioxidant capacity is not easy, as it is not certain which antioxidants have major impact on the overall capacity under different circumstances of acute or chronic oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Nikolić-Heitzler

Rabuzin

Tatzber

et al. 2006

Tohoku J. Exp. Med.

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[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.

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Identification of LPS‐inducible genes downregulated by ubiquinone in human THP‐1 monocytes

Schmelzer

Döring

2010

BioFactors

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Coenzyme Q(10) (CoQ(10)) is an obligatory element in the respiratory chain and functions as a potent antioxidant of lipid membranes. More recently, anti-inflammatory effects as well as an impact of CoQ(10) on gene expression have been observed. To reveal putative effects of Q(10) on LPS-induced gene expression, whole genome expression analysis was performed in the monocytic cell line THP-1. Thousand one hundred twenty-nine and 710 probe sets have been identified to be significantly (P

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Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction

Cited by 50 publications

References 23 publications

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

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

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Identification of LPS‐inducible genes downregulated by ubiquinone in human THP‐1 monocytes

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