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Transmyocardial Laser Revascularization and Stem Cell Therapy to Remodel an Infarcted Heart

Transmyocardial revascularization (TMR) has emerged as an additional therapeutic option for patients suffering from diffuse coronary artery disease (CAD), providing immediate angina relief. The current potential of this therapy focuses on the injection of stem cells, in order to create a synergistic angiogenic effect while increasing myocardial repair and regeneration. Although TMR procedures provide increased vascularization within the myocardium, patients suffering from ischemic cardiomyopathy may not benefit from angiogenesis alone. Therefore, the goal of introducing stem cells is to restore the functional state of a failing heart by providing stem cells with a favorable microenvironment that will enhance their engraftment. Since the therapeutic effect of stem cells is dependent on their capacity to survive and retain in the myocardium, laser therapy may provide a strategy for increasing stem cell engraftment. If so, these cells may have the potential to act as mitochondrial donors or as sources of paracrine factors, aiding in the recovery from oxidative stress and providing antioxidant reserves. Furthermore, laser therapy may also play an influential role in regulating cardiac repair and regeneration via epithelial-mesenchymal transition (EMT). By interacting with specific transcription factors TMR may provide another pathway by which it can offer reparative effects. Cumulatively, paracrine release, denervation, and angiogenesis contribute to the therapeutic benefits experienced by TMR patients, including a significant reduction in angina, with increases in myocardial perfusion and survival rates. With the addition of stem cells, these effects may be further augmented, thus providing increased symptomatic relief in patients.

Identiferoai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/620838
Date January 2016
CreatorsIwanski, Jessika, Iwanski, Jessika
ContributorsKhalpey, Zain, Wong, Raymond K., Runyan, Raymond B.
PublisherThe University of Arizona.
Source SetsUniversity of Arizona
Languageen_US
Detected LanguageEnglish
Typetext, Electronic Thesis
RightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.

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