Prevention of atrial fibrillation following cardiac surgery: Basis for a novel therapeutic strategy based on non-hypoxic myocardial preconditioning
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2008-04Metadata
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Rodrigo Salinas, Ramón
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Prevention of atrial fibrillation following cardiac surgery: Basis for a novel therapeutic strategy based on non-hypoxic myocardial preconditioning
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Abstract
Atrial fibrillation is the most common complication of cardiac surgical procedures performed with cardiopulmonary bypass. It contributes to
increased hospital length of stay and treatment costs. At present, preventive strategies offer only suboptimal benefits, despite improvements in
anesthesia, surgical technique, and medical therapy. The pathogenesis of postoperative atrial fibrillation is considered to be multifactorial.
However oxidative stress is a major contributory factor representing the unavoidable consequences of ischemia/reperfusion cycle occurring in this
setting. Considerable evidence suggests the involvement of reactive oxygen species (ROS) in the pathogenic mechanism of this arrhythmia.
Interestingly, the deleterious consequences of high ROS exposure, such as inflammation, cell death (apoptosis/necrosis) or fibrosis, may be
abrogated by a myocardial preconditioning process caused by previous exposure to moderate ROS concentration known to trigger survival
response mechanisms. The latter condition may be created by n-3 PUFA supplementation that could give rise to an adaptive response
characterized by increased expression of myocardial antioxidant enzymes and/or anti-apoptotic pathways. In addition, a further reinforcement of
myocardial antioxidant defenses could be obtained through vitamins C and E supplementation, an intervention also known to diminish enzymatic
ROS production. Based on this paradigm, this review presents clinical and experimental evidence supporting the pathophysiological and
molecular basis for a novel therapeutic approach aimed to diminish the incidence of postoperative atrial fibrillation through a non-hypoxic
preconditioning plus a reinforcement of the antioxidant defense system in the myocardial tissue.
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This work is supported by the Fondo Nacional de
Investigación Científica y Tecnológica (FONDECYT), grant
no. 1070948.
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PHARMACOLOGY & THERAPEUTICS, Volume: 118, Issue: 1, Pages: 104-127, 2008
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