Blood Oxidant Ties: The Evolving Concepts in Myocardial Injury and Cardiovascular Disease

Prevention of Reperfusion Injury in Acute Myocardial Infarction: A “flashback” Journey of Novel Strategies Based on the Potential Therapeutic Role of Antioxidants

Author(s): Francisco Salazar-Cornejo, Abraham Gajardo, Marcelo J. Kogan and Ramón Rodrigo * .

Pp: 128-147 (20)

DOI: 10.2174/9789815165012123010010

* (Excluding Mailing and Handling)


It has been recognized that oxidative stress plays a key role in the development of cardiac alterations derived from events of ischemia followed by reperfusion, such as in the clinical setting of acute myocardial infarction of patients subjected to coronary angioplasty. During ischemia, due to the occlusion of a coronary branch, biochemical events responsible for anaerobic metabolism, ATP availability and impairment of cell ionic homeostasis are the major deleterious effects. Following the onset of reperfusión, a burst of reactive oxygen species occurs, thus accounting for increased tissue damage due to the endovascular intervention. This iatrogenic damage has not been adequately treated to date. Among the many pharmacological attempts, cardioprotection with antioxidants should be mentioned; however, the experimental studies have not been translated into successful clinical trials aimed to prevent this enhancement of cardiac damage, despite some beneficial effects have been reported in the clinical outcome of the patients. This chapter aimed to present the hypothesis that the combination of antioxidant effects should improve the cardioprotection of the patients subjected to coronary angioplasty following acute myocardial infarction. Therefore, we present an update of previous attempts at cardioprotection with an antioxidant alone and give the basis for the expected improved protection by using two or more antioxidant compounds exerting different mechanisms that could enhance the beneficial protective effect.

Keywords: Acute myocardial infarction, Antioxidant enzymes, Antioxidants, Apoptosis, Combined antioxidant treatment, Ischemia/Reperfusion injury, Lipid peroxidation, Necrosis, Oxidative stress, Reactive oxygen species.

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