Association of Advanced Glycosylation End products Receptor (RAGE) polymorphisms with coronary heart disease in post menopausal women

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 758-779-Cardiometabolic Risk & Vascular Biology
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-767
Xenofon Xyrafis*1, Sarantis Livadas2, Athanasios Karachalios1, Evangelos Marinakis3, Claire Christakou3, Christina Piperi4, Panagiotis Kokkoris5, Neoklis Georgopoulos6 and Evanthia Diamanti-Kandarakis7
1Sotiria Hospital, Athens University Medical School, Athens, Greece, 2Unit of Endocrinology, Metabolism and Diabetes, Athens, Greece, 3Sotiria Hospital, Athens University Medical School, Greece, 4Univ of Athens Medical Sch, Athina, Greece, 5Hellenic Air Force General Hos, Athens, Greece, 6University of Patras, Medical School, Patras, Greece, 7Medical School University of Athens, Athens, Greece
Background: Recent studies have suggested an important role of  Advanced Glycosylation End products Receptor (RAGE) in the developmnet of atherosclerosis. However, investigation of the relationship between RAGE polymorphisms (-429T/C, -374T/A) and coronary heart disease (CHD) has shown contradictory results. Furthemore, hyperandrogenemia in women post menopause has been associated with an adverse CHD risk profile.

Aim of the study : To investigate any possible relationship between RAGE polymorphisms with CHD and the association of RAGE polymorphisms with cardiovascular risk factors in postmenopausal women.

Methods: 96 menopausal women (28 diabetics - 68 non diabetics, mean age: 68,34yrs) who underwent coronary angiography were genotyped for the -429T/C and -374T/A variants of RAGE. In this group androgen and estrogen levels, lipid parameters, glucose, HbA1c and insulin were determined and Free Androgen Index was calculated.


Results: Τhere was no significant difference in RAGE polymorphisms frequencies between women with CHD confirmed in coronary angiography and those without CHD, although a cardioprotective trend was disclosed for  374AA polymorhism. Regarding hormonal/metabolic profile, women with homozygosity for the -429 allele (TT) had significantly lower levels of HDL (43,7 ± 17,16 vs. 52,95 ± 14,47, P=0.036) and SHBG (42,73 ± 18,17 vs 52,55 ± 20,71, P=0.038) compared to eterozygotic subjects (TC) and significantly higher levels of triglycerides (151,75 ± 50,65 vs. 125,89 ± 36,64, P=0.042), FAI (1,85 ± 1,43 vs. 1,17 ± 0,84, P=0.042) and Androstenedione (1,61 ± 1,01 vs. 1,22± 0,58, P=0.031). Women with homozygosity for the -374 allele (AA) had significantly lower LDL levels (83,8 ± 21,96 vs 105 ± 42,97, P=0.046) compared to eterozygotic (AT) subjects.


Conclusion: Our data did not demonstrate an association between polymorphisms of the RAGE gene and CHD in menopausal women. However, homozygosity for the -429 allele (TT) of RAGE is associated with an adverse lipid profile and hyperandrogenemia and its role as a predisposing factor of atherosclerosis needs further evaluation.

Nothing to Disclose: XX, SL, AK, EM, CC, CP, PK, NG, ED

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