Metformin and left ventricular hypertrophy in patients with comorbidity

How to Cite

Demydenko, G. (2017). Metformin and left ventricular hypertrophy in patients with comorbidity. Inter Collegas, 4(2), 61-64.


Essential hypertension (EH) stays the important public challenge, because of leading positions in morbidity and mortality in not only Ukraine, but also worldwide. Recent studies have suggested that metformin could inhibit cardiomyocyte apoptosis and improve cardiac function.

Aim of the study was to investigate metformin’s influence on left ventricular structure and function in patients with essential hypertension with concomitant type 2 diabetes (T2D).

Materials and methods: 120 patients with essential hypertension (EH) were recruited in the study and were divided into three groups according to comorbid state: 60  - EH and T2D; 30 – EH with prediabetes; 30 – EH without dysglicemia. Carbohydrate parameters, left ventricle structure and function were analyzed before and after 12 weeks of metformin treatment.

Results. Metformin treatment results in fasting glycaemia and insulin resistance diminishing on 21,79 % and 26,84 %.  Echocardiography in 12 weeks metformin treatment showed significant decreasing of left ventricle myocardium mass for 6,1 %, left ventricle posterior wall thickness - 2,3 %. More pronounced changes in patients with EH and T2D are connected with glucotoxicity, lipotoxicity, insulin resistance diminishing and also with pleiotropic metformin’s effects.

Conclusion. Metformin has positive influence to the structure and function of left ventricle with increasing of EDV and LV hypertrophy regress. These findings may provide a potential effectiveness for patients with T2D at risk of developing pathological cardiac hypertrophy.

Key words: essential hypertension, type 2 diabetes, left ventricle hypertrophy, metformin.


Коvalenko V. M., Kornatskyi V. M. (2014). Khvoroby systemy krovoobihy yak medycho-sotcialna I suspilno-politychna problema [Blood circulation system diseases as medical-social and political problem]. Analytical-statistical manual. Kyiv, 280 p.

Demydenko G. V. (2015). Imunozapalennya, endotelialna dysfynchtsia yak fachtory vysokoho kardiometabolichnogo rysyky u chvorych na hipertonichny chovorobu z dysglichemiyeu [Immune inflammation, endothelial dysfunction as factors of high cardiomethabolic risk in patients with essential hypertension with dysglicemia]. Science rise, 10/3 (15), 20-25. DOI: 10.15587/2313-8416.2015.51655.

Palavra F., Reis F., Marado D., Sena A. (2015). Biomarkers of Cardiometabolic Risk, Inflammation and Disease. Springer International Publishing, Switzerland, 165 p.

Wei C., Ranson L., Davidson L. et al. (2014). Metabolically healthy severe obesity and cardiovascular disease risk: a 6-year longitudinal prospective study. J. Am. Coll. Cardiol, 63(12_S). Doi : 10.1016/S0735-1097(14)61353-X.

Davis B.J., Xie Z., Viollet B., Zou M. H. (2006). Activation of the AMP–activated kinase by antidiabetes drug metformin stimulates nitric oxide synthesis in vivo by promoting the association of heat shock protein 90 and endothelial nitric oxide synthase. Diabetes, 55 (2), 496-500.

Order of Ministry of health of Ukraine № 1118 from 21. 12. 2012. –

Rydén L. et al. (2007) Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: executive summary. The Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC) and of the European Association for the Study of Diabetes (EASD). Eur. Heart. J., 28, 88–136.

Mancia G., Laurent S., Agabiti-Rosei E. (2009) Reappraisal of European guidelines on hypertension management : a European Society of Hypertension Task Force document. J. Hypertension, 27, 2121–2158.

Lang R. M., Bierig M., Devereux R. B., Flachskampf F. A., Foster E., and Stewart W. (2006) Recommendations for chamber quantification. Eur. J. Echocardiography, 7, 79–108.

Zhou K., Bellenguez C., Spencer C. C. (2011) GoDARTS and UKPDS Diabetes Pharmacogenetics Study Group, Wellcome Trust Case Control Consortium 2, MAGIC Investigators. Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes. Nat. Genet, 43, 117–120.

Pawlyk A. C., Giacomini K. M., McKeon C., Shuldiner A. R. and Florez J. C. (2014) Metformin Pharmacogenomics: Current Status and Future Directions. Diabetes, 63(8), 2590–2599. Doi : 10.2337/db13-1367.

Sussman J. B., Kent D. M., Nelson J. P., Hayward R. A. (2015) Improving diabetes prevention with benefit based tailored treatment: risk based reanalysis of Diabetes Prevention Program. BMJ, 350, 454. Doi : 10.1136/bmj.h454.

Kumar R., Kerins D. M., Walther T. (2015) Cardiovascular safety of anti-diabetic drugs. European Heart Journal. Cardiovascular Pharmacotherapy, 202–208. Doi : 10.1093/ehjcvp/pvv035/.

Kovalyova O. M., Demydenko G. V., Ambrosova T. V. (2012). Terapevtychnyi potentsial metforminu: vpliv na vuglevodnyi profil ta vasoactyvnyi pul oksidy azoty u chvorych iz poyednanoyu patologiyeyu [Therapeutical potency of metformin: influence on carbohydrate profile and vasoactive nitric oxide pool in patients with comorbidity]. Problems of endocrine pathology, 4, 57-64.

Kovalyova O. M., Demydenko G. V., Ambrosova T. V. (2012). Terapevtychnyi potentsial metforminu: vpliv na vuglevodnyi, lipidnyi, tsytokinovyi profil u chvorych iz poyednanoyu patologiyeyu [Therapeutical potency of metformin: influence on carbohydrate, lipid, cytokine profile in patients with comorbidity]. Problems of endocrine pathology, 3, 35-43.

Inzucchi S. E., Bergenstal R. M., Buse J. B., Diamant M., Ferrannini E., and Matthews D. R. (2015) Management of Hyperglycemia in Type 2 Diabetes: A Patient-Centered Approach: Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care, 38(1), 140–149. Doi : 10.2337/dc14-2441.

Mohan M., McSwiggan S., Baig F., Rutherford L. and Lang C.C. (2015). Metformin and its effects on myocardial dimension and left ventricular hypertrophy in normotensive patients with coronary heart disease (the MET-REMODEL study): rationale and design of the MET-REMODEL study. Cardiovasc Ther, 33(1), 1-8. doi: 10.1111/1755-5922.12101.

Zhang C.X., Pan S.N., Meng R.S., Peng C.Q., Xiong Z.J. and Dong Y.G. (2011). Metformin attenuates ventricular hypertrophy by activating the AMP-activated protein kinase-endothelial nitric oxide synthase pathway in rats. Clin Exp Pharmacol Physiol, 38(1), 55-62. doi: 10.1111/j.1440-1681.2010.05461.x.

Yong-nan Fu, Han Xiao, Xiao-wei Ma, Sheng-yang Jiang, Ming Xu and You-yi Zhang (2011). Metformin attenuates pressure overload-induced cardiac hypertrophy via AMPK activation. Acta Pharmacologica Sinica, 32, 879–887. doi: 10.1038/aps.2010.229.

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