Role of oxidative stress in heart failure subsequent to myocardial infarction
| dc.contributor.author | Hill, Michael F. | en_US |
| dc.date.accessioned | 2007-05-17T12:39:23Z | |
| dc.date.available | 2007-05-17T12:39:23Z | |
| dc.date.issued | 1998-05-01T00:00:00Z | en_US |
| dc.degree.discipline | Physiology | en_US |
| dc.degree.level | Doctor of Philosophy (Ph.D.) | en_US |
| dc.description.abstract | Congestive heart failure (CHF) following myocardial infarction (MI) continues to be an important clinical problem. Although the etiology of heart failure is multifactorial, one mechanism that appears to play a key role is an increase in oxidative stress. We have earlier demonstrated that mild, moderate and severe stages of heart failure subsequent to MI are accompanied by an antioxidant deficit and elevated oxidative stress in the myocardium. The objective of the present research was to characterize regional changes in antioxidants and oxidative stress in the right and viable left ventricles separately in relation to the hemodynamic function in each of the respective ventricles. Another goal of this rese rch was to establish whether a relative deficit in the antioxidant reserve is the cause or simply an effect of the CHF due to MI. The hypothesis tested was that an increase in oxidative stress aided by a deficit in the antioxidant reserve plays a role in the pathogenesis of heart failure subsequent to MI and that chronic antioxidant therapy involving vitamin E may modulate the development of heart failure. Characteristic hemodynamic and biochemical changes demonstrated that ventricular failure subsequent to MI is associated with an antioxidant deficit and increased oxidative stress first in the LV, followed by the RV. These oxidative stress changes also correlated with the hemodynamic function in each of the ventricles. In order to establish a "cause and effect" relationship for oxidative stress, beneficial effects of dietary supplementation with vitamin E (a strong biological antioxidant) were analyzed. Improved cardiac function in each of the respective ventricles withg vitamin E treatment was associated with an enhanced antioxidant status, improved redox ratio and reduced lipid peroxidation. In conclusion, it is suggested that decreased antioxidants and increased oxidative stress may have a causative role in the pathogenesis of heart failure subsequent to myocardial infarction. Clinical potential and applicability of these findings in surviving patients with myocardial infarction needs to be addressed. (Abstract shortened by UMI.) | en_US |
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| dc.format.extent | 184 bytes | |
| dc.format.mimetype | application/pdf | |
| dc.format.mimetype | text/plain | |
| dc.identifier.uri | http://hdl.handle.net/1993/1525 | |
| dc.language.iso | eng | en_US |
| dc.rights | open access | en_US |
| dc.title | Role of oxidative stress in heart failure subsequent to myocardial infarction | en_US |
| dc.type | doctoral thesis | en_US |