Severity of Cardiovascular Remodeling in Type 2 Diabetes and Essential Hypertension in the Presence of Unfavorable Genetic Polymorphism

Presentation Number: LB SAT 81
Date of Presentation: April 1st, 2017

Anna S Shalimova*1, Oleksandr Bilovol2, Lesya Bobronnikova2 and Olena Al-Trawneh2
1Kharkiv National Medical University, Kharkiv, Ukraine, 2Kharkiv National Medical University


The aim: to establish the association of genetic polymorphism of angiotensin II receptor type 1 gene (AGTR1), peroxisome proliferator-activating receptor-γ2 (PPARγ2), insulin receptor substrate-1 (IRS-1), transcription factor 7-like 2 gene (TCF7L2) with the severity of cardiovascular remodeling in comorbidity of type 2 diabetes (DM2) and essential hypertension (EH).

Methods: echocardiography evaluation of mitral diastolic blood flow and tissue Doppler spectral modes, reactive hyperemia, color Doppler mapping, genotyping of A1166C polymorphism of AGTR1, Pro12Ala polymorphism of PPARγ2, rs1801278 polymorphism of IRS-1, rs7903146 polymorphism of TCF7L2. We examined 320 patients with EH stage II, grade 2 and DM2 moderate, subcompensated aged 45-60 years.

Patients with A/C and C/C genotypes of AGTR1 had significantly larger left ventricle (LV) dimensions, higher myocardial mass index (MMI) LV and lower values E/A as compared to A/A genotype (p<0.01). The influence of specified genetic polymorphisms in vascular remodeling was confirmed by significantly higher intima-media thickness (IMT) and lower degree of endothelium-dependent vasodilatation (EDVD) in A/C and C/C genotypes (p<0.001).

Patients with Pro/Pro genotype of PPARγ2 had significantly larger LV dimensions (p<0.01) and MMILV (p<0.05), higher IMT (p<0.001) and pulse wave velocity in carotid artery (p<0.05), lower EDVD (p<0.001) than patients with Pro12Ala/Ala12Ala genotype.

In patients with Arg/Arg and Gly/Arg genotypes of IRS-1 significantly lower value of E/A (p<0.05) and higher value of integrated indicator of diastolic dysfunction E/e (p<0.05) were established (as compared to Gly/Gly genotype).

Diastolic function index E/A was differed depending on genotype of TCF7L2: it was significantly lower in C/T and T/T genotypes as compared to C/C genotype (p<0.001). The evaluation of vascular condition did not show significant differences in parameters depending on TCF7L2 polymorphism.

It was found that patients with 3-4 crossed «unfavorable» genotypes had significantly more pronounced cardiovascular remodeling than patients with 1-2 crossed «unfavorable» genotypes.

Conclusions: cardiovascular remodeling in DM2 and EH is associated with genotype of AGTR1, PPARγ2, IRS-1 and TCF7L2. Severity of cardiovascular remodeling in specified comorbidity is more pronounced in the presence of 3-4 crossed «unfavorable» genotypes.


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