ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 26 of 56
УЖМБС 2018, 3(6): 154–159
Clinical Medicine

Features of Сlinical-metabolic Disorders and Structural-functional Changes of Heart in Patients with Essential Hypertension with Abdominal Obesity and Heart Hypertrophy

Starchenko T. G., Snigurska I. O., Myloslavsky D. K., Bozhko V. V.

The purpose of the study was to find the relationship between the nature of structural and functional changes in the heart and metabolic factors in patients with hypertension with obesity and determining their role in the progression of HS in this category of patients. Material and methods. 82 patients took part in our study. We compared the data of 66 patients with essential hypertension (main group), abdominal obesity and hypertrophy of the heart and 16 patients with essential hypertension with obesity without heart hypertrophy (control group). The scope of the examination included: general clinical, anthropometric and echocardioscopic methods, blood glucose (fasting and after glucose loading), lipid levels, uric acid, glomerular filtration rate. Results and discussion. In the course of study, we noticed that patients with essential hypertension, abdominal obesity and heart hypertrophy differed from patients with essential hypertension with abdominal obesity without heart hypertrophy. The differences were in age, longer duration of hypertension, more severe heredity for hypertension, more severe clinical course of hypertension, more frequent disorders of carbohydrate metabolism in the main group. The lipid metabolism disorders included elevated the blood triglycerides levels, higher plasma levels of uric acid, frequent occurrence of hyperuricemia, disorders of the functional state of the kidneys. Conclusions. The most common causes affecting the level of SC are obesity, IR, and hypertension. In the patients whom we examined, the plasma level of SC was significantly higher in the main group than in the control group. This can be explained by disorders of the renal secretion of SC, which is probably due to an increase in tubular reabsorption of sodium, induced by insulin. In turn, hyperuricemia leads to the exhausting production of free radicals, to increase the level of TG and to accelerate the processes of LDL oxidation in the artery wall, which also contributes to the progression of atherosclerosis, fibrosis and HS.

Keywords: hypertension, abdominal obesity, cardiac hypertrophy, metabolic disorders

Full text: PDF (Ukr) 208K

  1. Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M, Christiaens T, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension: the Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertension. 2013; 31(7): 1281-357.
  2. Piepoli MF, Hoes AW, Agewall S, Albus C, Brotons C, Catapano AL, Cooney MT, et al. 2016 European Guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts) Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). European Heart Journal. 2016; 37(29): 2315–81.
  3. Belovol AN, Shkolnyk VV, Fadeenko GD, Tveretynov AB. Gypertonycheskaya bolezn y ozhyrenye: monografyya. Ternopol; TGMU; 2013. 344 s. [Russian]
  4. Zhebel VM, Lozynskyy SE. Vid gipertrofiyi livogo shlunochka do gipertenzyvnogo sertsya. Zmina paradygmy. Ukrayinskyy kardiologichnyy zhurnal. 2011; 6: 88-93. [Ukrainian]
  5. Kovalenko VN, Dovzhenko MN, Nasukay EG, Dyachenko YaS. Sravnytelnaya kharakterystyka profylaktyky serdechno-sosudystykh zabolevanyy v Ukrayne y Evrope po dannym EUROASPIRE IV: gospytalnaya lynyya. Arteryalnaya gypertenzyya. 2015; 5(43): 57-61. [Russian]
  6. Mynushkyna LO, Nykytyn AG, Brazhnyk VA, y soavt. Gypertrofyya myokarda u bolnykh gypertonycheskoy boleznyu: rol genetycheskogo polymorfyzma β-adrenoreaktyvnykh struktur. Kardyologyya. 2010; 1: 35-40. [Russian]
  7. Mytchenko EY, Mamedov MN, Kolesnyk TV, Deev AD. Ot ymeny rabochey gruppy Ukraynsko-Rossyyskogo yssledovanyya “Sovremennyy profyl faktorov ryska serdechno-sosudystykh zabolevanyy v gorodskoy populyatsyy Ukrayny”. Ukr kardiologichnyy zhurnal. 2013; 4: 76-83. [Russian]
  8. Mitchenko OI, Mamedov MN, Kolesnyk TV, ta spivavt. Poshyrenist arterialnoyi gipertenziyi u miskiy populyatsiyi Ukrayiny zalezhno vid stupenya ozhyrinnya. Mizhnarodnyy endokrynologichnyy zhurnal. 2015; 3: 13-9. [Ukrainian]
  9. Nedogoda SV. Ozhyrenye y arteryalnaya gypertonyya: teoryya y praktyka vybora optymalnogo gypotenzyvnogo preparata. M; 2012. 80 s. [Ukrainian]
  10. Sertsevo-sudynni zakhvoryuvannya. Rekomendatsiyi z diagnostyky, profilaktyky ta likuvannya. Za red Kovalenko VM, Lutay MI. K: MORION; 2011. 400 s. [Ukrainian]
  11. Fadeenko GD. Ozhyrenye y rysk serdechno-sosudystykh zabolevanyy. Liky Ukrayiny. 2009; 7(133): 55-64. [Russian]
  12. Alderman MH. Serum uric acid as a cardiovascular risk factor for heart desease. Curr Hypertens Reports. 2001; 3(3): 184–9.
  13. Buyck JF, Dufouil C, Mazoyer B, Maillard P, Ducimetière P, Alpérovitch A, Bousser MG, Kurth T, Tzourio C. Cerebral white matter lesions are associated with the risk of stroke but not with other vascular events: the 3C-Dijon study. Stroke. 2009; 40: 2327–31.
  14. Chrostowska M, Szyndler A, Wolf J, Narkiewich K. Obesity and Obstructive Sleep Apnea. In: Manual of Hypertension of the European Society of Hypertension. Ed by Mancia G, Grassi G, Redon J. 2014. p. 47-60.
  15. Coutinho TА, Turner ST, Peyser PA, Bielak LF, Sheedy PF 2nd, Kullo IJ. Associations of serum uric acid with markers of inflammation, metabolic syndrome, andsubclinical coronary atherosclerosis. Am J Hypertens. 2007; 20(1): 83–9. PMID: 17198917.
  16. Drazner МН. The Progression of Hypertensive Heart Disease. Circulation. 2011; 123(3): 327-34.
  17. Ginsberg HN, Zhang YL, Hernandez-Ono A. Metabolic syndrome: focus on dyslipidemia. Obesity. 2006; 14 Suppl 1: 41S–49S.
  18. Wannamethee SG. Serum uric acid is not an independent risk factor for coronary heart desease. Curr Hypertens Reports. 2001; 3: 190-6.
  19. Harazny JM, Ritt M, Baleanu D, Ott C, Heckmann J, Schlaich MP, Michelson G, Schmieder RE. Increased wall: lumen ratio of retinal arterioles in male patients with a history of a cerebrovascular event. Hypertension. 2007; 50(4): 623–9.
  20. Kearney-Schwartz A, Rossignol P, Bracard S, Felblinger J, Fay R, Boivin JM, Lecompte T, et al. Vascular structure and function is correlated to cognitive performance and white matter hyperintensities in older hypertensive patients with subjective memory complaints. Stroke. 2009; 40(4): 1229–36.
  21. Kumar S, O Rahilly S. Insulin Resistance. Insulin action and its disturbances in disease. Wiley; 2005. 616 p.
  22. Richette P, Doherty M, Pascual E, Barskova V, Becce F, Castañeda-Sanabria J, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis. 2017 Jan; 76(1): 29-42.
  23. Schindler C. The metabolic syndrome as an endocrine disease: is there an effective pharmacotherapeutic strategy optimally targeting the pathogenesis? Ther Adv Cardiovasc Dis. 2007 Oct; 1(1): 7-26.