2.50
Hdl Handle:
http://hdl.handle.net/10755/159355
Type:
Presentation
Title:
Genetic Polymorphisms, Homocysteinemia and Risk of Coronary Artery Disease
Abstract:
Genetic Polymorphisms, Homocysteinemia and Risk of Coronary Artery Disease
Conference Sponsor:Midwest Nursing Research Society
Conference Year:2003
Author:Hayashi, Satomi
Contact Address:Nursing Practice, 1305 North Martin Avenue, Room 402, Tucson, AZ, 85721-0203, USA
Co-Authors:Shu-Fen Wung
Coronary artery disease (CAD) is the leading cause of mortality and morbidity for both men and women in the western countries. However, only 50% of traditional risk factors account for causes of CAD. New risk factors have been investigated to explain the pathogenesis of CAD. Among these new risk factors, elevated homocysteinemia is considered an important and independent risk factor for CAD. More than two-thousand articles were published on homocysteinemia in 2001 alone. Studies in vitro and in vivo have indicated that homocysteine can impair endothelial function thus increase risk of CAD. An elevated plasma homocysteine level may interact with conventional risk factors to further increase risk of CAD. The purpose of this presentation is to discuss current knowledge on genetic polymorphisms in key enzymes involved in homocysteine metabolism and their relationship to CAD. These common polymorphisms include C677T in the methylenetertrahydrofolate reductase (MTHFR) gene, A66G in the methionine synthase reductase (MTRR) gene, and T833C and G919A in the cystathionine ß-synthase (CBS) gene. In particular, the results of recent salient studies that provided evidence of significant associations of these genetics polymorphisms and CAD in various populations will be discussed. Potential gene-environment interactions that may elevate homocysteine level and increase the risk of CAD will be addressed. In summary, gene polymorphisms of key enzymes in homocysteine metabolism and the risk of CAD have been intensively investigated in different populations. Knowledge from these recent studies is important for nurse clinicians and researchers to be able to incorporate cardiovascular genetic information in their practice and research. AN: MN030180
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Midwest Nursing Research Society

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleGenetic Polymorphisms, Homocysteinemia and Risk of Coronary Artery Diseaseen_GB
dc.identifier.urihttp://hdl.handle.net/10755/159355-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Genetic Polymorphisms, Homocysteinemia and Risk of Coronary Artery Disease </td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Midwest Nursing Research Society</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2003</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Hayashi, Satomi</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">Nursing Practice, 1305 North Martin Avenue, Room 402, Tucson, AZ, 85721-0203, USA</td></tr><tr class="item-co-authors"><td class="label">Co-Authors:</td><td class="value">Shu-Fen Wung</td></tr><tr><td colspan="2" class="item-abstract">Coronary artery disease (CAD) is the leading cause of mortality and morbidity for both men and women in the western countries. However, only 50% of traditional risk factors account for causes of CAD. New risk factors have been investigated to explain the pathogenesis of CAD. Among these new risk factors, elevated homocysteinemia is considered an important and independent risk factor for CAD. More than two-thousand articles were published on homocysteinemia in 2001 alone. Studies in vitro and in vivo have indicated that homocysteine can impair endothelial function thus increase risk of CAD. An elevated plasma homocysteine level may interact with conventional risk factors to further increase risk of CAD. The purpose of this presentation is to discuss current knowledge on genetic polymorphisms in key enzymes involved in homocysteine metabolism and their relationship to CAD. These common polymorphisms include C677T in the methylenetertrahydrofolate reductase (MTHFR) gene, A66G in the methionine synthase reductase (MTRR) gene, and T833C and G919A in the cystathionine &szlig;-synthase (CBS) gene. In particular, the results of recent salient studies that provided evidence of significant associations of these genetics polymorphisms and CAD in various populations will be discussed. Potential gene-environment interactions that may elevate homocysteine level and increase the risk of CAD will be addressed. In summary, gene polymorphisms of key enzymes in homocysteine metabolism and the risk of CAD have been intensively investigated in different populations. Knowledge from these recent studies is important for nurse clinicians and researchers to be able to incorporate cardiovascular genetic information in their practice and research. AN: MN030180 </td></tr></table>en_GB
dc.date.available2011-10-26T21:56:18Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T21:56:18Z-
dc.description.sponsorshipMidwest Nursing Research Societyen_GB
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