Functional state of endothelium and additional possibilities of its correction with the use of ethylmethylhydroxypyridine succinate in patients with arterial hypertension

August 25, 2021
890
Resume

Objective: to study the functional state of endothelium based on the determination of functional reserve of endothelial progenitor cells (EPC), the rate of endothelium-dependent vasodilation (EDVD) in patients with resistant (RH) and controlled hypertension (CH), and possibility of correction with the use of ethylmethylhydroxypyridine succinate (EMHS).

Object and methods. We studied 50 patients with hypertension, which are divided into groups: intervention (n=26) and comparison (n=24). EMHS (10 days intramuscularly, then 8 weeks orally) was added to standard hypertensive therapy in the intervention group. We assessed the office and 24-h ambulatory blood pressure conducted the test with compression of the brachial artery at the beginning and at the end of the study. Determination of EPC counts in blood (CD45+/CD34+ phenotype) by flow cytometry was studied before and after 60 minutes during exercise tests on a bicycle ergometer.

Results. It was found that patients with RH are characterized by a 25% lower index of EDVD compared with patients with CH (p=0.03). Hypertension was associated with 21% lower EPC counts in blood than in healthy donors (p<0.05), especially with RH. The addition of EMHS contributed to a significant increase in the EDVD index with the most pronounced effect in RH patients and was accompanied by a tendency to increase EPC counts in the initial state, and restore bone marrow reserve function to produce EPC counts in response to ischemia.

Conclusions. The use of EMHS improves the functional state of the endothelium in patients with CH and RH.

References:

  • 1. apps.who.int/iris/bitstream/handle/10665/336643/WHO-EURO-2020-1468-41218-56061-ukr.pdf?sequence=1&isAllowed=y.
  • 2. Versari D., Daghini E., Virdis A. (2009) Endothelial dysfunction as a target for prevention of cardiovascular disease. Diab. Care, 32 (Suppl. 2): 314–321. doi: 10.2337/dc09-S330.
  • 3. Puzik S.G. (2018) Endothelial dysfunction in the pathogenesis of arterial hypertension and the progression of atherosclerosis. Family Med., 2(76): 69–74. (In Rus.).
  • 4. Giannotti G., Doerries C., Mocharla P.S. (2010) Impaired endothelial repair capacity of early endothelial progenitor cells in prehypertensin: relation to endothelial dysfunction. Hypertension, 55: 1389–1397. https://doi.org/10.1161/HYPERTENSIONAHA.109.141614
  • 5. Li Q., Youn J.Y., Cai H. (2015) Mechanisms and consequences of endothelial nitric oxide synthase dysfunction in hypertension. J. Hypertens., 33: 1128–1136. doi: 10.1097/HJH.0000000000000587.
  • 6. Wilcox CS. (2012) Asymmetric dimethylarginine and reactive oxygen species: unwelcome twin visitors to the cardiovascular and kidney disease tables. Hypertension, 59: 375–381. doi: 10.1161/HYPERTENSIONAHA. 111.187310.
  • 7. Harrison D.G., Coffman T.M., Wilcox C.S. (2021) Pathophysiology of Hypertension. The Mosaic Theory and Beyond. Circ. Res., 128: 847–863. DOI: 10.1161/CIRCRESAHA.121.318082.
  • 8. Beraldo D., Cássio J., Rodrigues C.J., Quinto B.M.R. (2020) Role of endothelial function determined by asymmetric dimethylarginine in the prediction of resistant hypertension: а subanalysis of ReHOT trial. J. Clin. Hypertens., 22(11): 2059–2068. DOI: 10.1111/jch.13936.
  • 9. Madhur M.S., Elijovich F., Alexande M. et al. (2021) Hypertension. Do Inflammation and Immunity Hold the Key to Solving this Epidemic? Circ. Res., 128: 908–933. doi: 10.1161/CIRCRESAHA.121.318052.
  • 10. Asahara T., Murohara T., Sullivan A. et al. (1997) Isolation of putative progenitor endothelial cells for angiogenesis. Science, 275(5302): 964–967. doi:10.1126/science.275.5302.964.
  • 11. Corretti M.C., Anderson T.J., Benjamin E.J. et al. (2002) Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J. Am. Coll. Cardiol., 39(6): 1082. J. Am. Coll. Cardiol., 39(2): 257–265. doi:10.1016/s0735-1097(01)01746-6.
  • 12. de Zeeuw D., Parving H.H., Henning R.H. (2006) Microalbuminuria as an early marker for cardiovascular disease. J. Am. Soc. Nephrol., 17(8): 2100–2105. doi:10.1681/ASN.2006050517.
  • 13. Zaremba E.H., Karplyak V.M., Virna M.M. et al. (2018) Pathogenetic rationale for the use of metabolic therapy in patients with chronic coronary heart disease. Medicines of Ukraine, 7(223): 46–50. DOI: https://doi.org/10.37987/1997-9894.2018.7(223).199778. (In Ukr.).
  • 14. Zozulya V.V., Chekman I.S. (2012) Metabolic therapy in geriatric cardiology (pharmaco-epidemiological study). Pharmacology and drug toxicology, 4(29): 67–71. (In Ukr.).