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High breath pentane concentrations during acute myocardial infarction
Z W Weitz1, A J Birnbaum, P A Sobotka
1Department of Medicine/Rheumatology, University of Illinois, Chicago.
Lancet (London, England)
|April 20, 1991
Summary
Reperfusion after heart attack causes lipid peroxidation, indicated by higher breath pentane levels. This suggests oxygen radicals contribute to heart tissue damage during myocardial infarction.
Area of Science:
- Cardiology
- Biochemistry
- Free Radical Biology
Background:
- Myocardial infarction (MI) involves ischemia and reperfusion.
- Reperfusion may trigger oxidative stress and cell damage.
- Lipid peroxidation is a marker of oxidative damage.
Purpose of the Study:
- To investigate if reperfusion after myocardial ischemia causes free-radical-mediated lipid peroxidation.
- To measure pentane, a marker of lipid peroxidation, in breath samples.
- To assess the role of oxygen radicals in myocardial infarction pathogenesis.
Main Methods:
- Breath pentane levels were measured in three groups: healthy controls, patients with suspected MI but no ECG changes (patient controls), and patients with confirmed acute MI.
- Groups were matched for age, sex, underlying disease, and smoking habits.
- Time from chest pain onset to breath collection was standardized.
Main Results:
- Breath pentane concentration was significantly higher in the acute MI group (4.96 nmol/l) compared to patient controls (1.96 nmol/l) and healthy controls (1.71 nmol/l).
- The difference was statistically significant (p < 0.0001).
- Higher pentane indicates increased lipid peroxidation during acute MI.
Conclusions:
- Reperfusion following myocardial ischemia leads to increased lipid peroxidation.
- Elevated breath pentane suggests significant oxygen radical activity during acute MI.
- Oxygen radicals likely contribute to the pathogenesis of myocardial tissue damage.
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