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    Genetic variation in the renin–angiotensin–aldosterone system is associated with cardiovascular risk factors and early mortality in established coronary heart disease

    Whalley, Gillian; Ellis, Katrina L.; Palmer, Barry R.; Frampton, Chris M.; Troughton, R. W.; Doughty, Robert N.; Ellis, Chris J.; Pilbrow, Anna P.; Skelton, Lorraine; Yandle, Tim G.; Richards, A. Mark; Cameron, Vicky A.

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    ellis genetics RAAS J HUman Hyper 2012.pdf (381.4Kb)
    Date
    2012
    Citation:
    Ellis, K. L., Palmer, B. R., Frampton, C. M., Troughton, R. W., Doughty, R. N., Whalley, G. A., ... & Cameron, V. A. (2012). Genetic variation in the renin–angiotensin–aldosterone system is associated with cardiovascular risk factors and early mortality in established coronary heart disease. Journal of Human Hypertension.
    Permanent link to Research Bank record:
    https://hdl.handle.net/10652/2120
    Abstract
    This study examined renin–angiotensin–aldosterone (RAAS) system gene variants for associations with cardiovascular risk factors and outcomes in coronary heart disease. Coronary disease patients (n¼1186) were genotyped for 21 single-nucleotide polymorphisms (SNPs) within angiotensinogen (AGT), angiotensin-converting enzyme (ACE), angiotensin-II type-1 receptor (AGTR1) and aldosterone synthase (CYP11B2). Associations with all-cause mortality and cardiovascular readmissions were assessed over a median of 3.0 years. The AGT M235T ‘T’ allele was associated with a younger age of clinical coronary disease onset (P¼0.006), and the AGT rs2478545 minor allele was associated with lower circulating natriuretic peptides (P¼0.0001–P¼0.001) and E/E1 (P¼0.018). Minor alleles of AGT SNPs rs1926723 and rs11122576 were associated with more frequent history of renal disease (Pp0.04) and type-2 diabetes (Pp0.02), higher body mass index (Pp0.02) and greater mortality (Pp0.007). AGT rs11568054 minor allele carriers had more frequent history of renal disease (P¼0.04) and higher plasma creatinine (P¼0.033). AGT rs6687360 minor allele carriers exhibited worse survival (P¼0.02). ACE rs4267385 was associated with older clinical coronary disease onset (P¼0.008) and hypertension (P¼0.013) onset, increased plasma creatinine (P¼0.01), yet greater mortality (P¼0.044). Less history of hypertension was observed with the AGTR1 rs12685977 minor allele (P¼0.039). Genetic variation within the RAAS was associated with cardiovascular risk factors and accordingly poorer survival.
    Keywords:
    Renin–angiotensin–aldosterone system, genetics, coronary disease, mortality
    ANZSRC Field of Research:
    110201 Cardiology (incl. Cardiovascular Diseases)
    Copyright Holder:
    Author
    Copyright Notice:
    Since 2003, ownership of copyright in in original research articles remains with the Authors*, and provided that, when reproducing the Contribution or extracts from it, the Authors acknowledge first and reference publication in the Journal, the Authors retain the following non-exclusive rights: To reproduce the Contribution in whole or in part in any printed volume (book or thesis) of which they are the author(s). They and any academic institution where they work at the time may reproduce the Contribution for the purpose of course teaching. To reuse figures or tables created by them and contained in the Contribution in other works created by them. To post a copy of the Contribution as accepted for publication after peer review (in Word or Tex format) on the Author's own web site, or the Author's institutional repository, or the Author's funding body's archive, six months after publication of the printed or online edition of the Journal, provided that they also link to the Journal article on NPG's web site (eg through the DOI).
    Available Online at:
    http://www.nature.com/jhh/about.html
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    This digital work is protected by copyright. It may be consulted by you, provided you comply with the provisions of the Act and the following conditions of use: Any use you make of these documents or images must be for research or private study purposes only, and you may not make them available to any other person. You will recognise the author's and publishers rights and give due acknowledgement where appropriate.
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