Metabolic disturbances as a factor of the pathogenesis of hypertensive disease and its clinical outcomes


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Abstract

Aim. To identify and determine the mechanisms of an association between arterial hypertension (AH) and proatherogenic systemic metabolic disturbances in hypertensive disease (HD), as well as the possibility of eliminating these disturbances by antihypertensive therapy. Subjects and methods. Fifty-four patients with HD and 64 persons randomly selected from an unorganized urban population were examined. Systolic and diastolic blood pressure (BP), insulin sensitivity, the most important metabolic parameters of lipids, lipoproteins, and glucose, the degree of systemic inflammation and oxidative stress, and the rate of lipoprotein proatherogenic and immunogenic modification were determined. Results. All the patients with HD were found to have a regular concurrence of AH with systemic inflammation and activated free-radical reactions, metabolic abnormalities, such as atherogenic dyslipidemia, insulin resistance, atherogenic and immunogenic modified lipoproteins. Antihypertensive treatment failed to eliminate metabolic disturbances even when BP control was fully restored. Conclusion. AH and systemic metabolic disturbances in HD have a common pathogenetic basis and the treatment of hypertensive patients should provide the normalization of not only BP, but also inflammatory and oxidative status and systemic metabolism.

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Нарушение метаболизма как фактор патогенеза гипертонической болезни и ее клинических исходов. - Резюме. Цель исследования. Выявление и определение механизмов связи между артериальной гипертонией (АГ) и системными метаболическими нарушениями проатерогенного характера при гипертонической болезни (ГБ), а также возможности устранения метаболических нарушений при антигипертензивной терапии. Материалы и методы. Обследовали 54 пациентов с ГБ и 64 лиц, отобранных методом случайной выборки из неорганизованной городской популяции. Определяли систолическое и диастолическое АД, чувствительность к инсулину, важнейшие показатели обмена липидов, липопротеинов и глюкозы, выраженность системного воспаления и оксидантного стресса, интенсивность проатерогенной и иммуногенной модификации липопротеинов крови. Результаты. У всех больных ГБ констатировано закономерное сочетание АГ с системным воспалением и активацией свободнорадикальных реакций, метаболическими нарушениями типа атерогенной дислипидемии, инсулинорезистентности, атерогенной и иммуногенной модификацией липопротеинов. Антигипертензивная терапия не устраняла нарушения метаболизма даже при полном восстановлении контроля АД. Заключение. АГ и нарушения системного метаболизма при ГБ имеют единую патогенетическую основу, и лечение больных ГБ должно предусматривать нормализацию не только АД, но и провоспалительного и прооксидатного статуса, системного метаболизма.
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References

  1. Rahmouni K., Correia M.L., Haynes W.G., Mark A.L. Obesity-associated hypertension. New insights into mechanisms. Hypertension 2005; 45: 9-16.
  2. Levick S.P., McLarty J.L., Murray D.B. et al. Cardiac mast cells mediate left ventricular fibrosis in the hypertensive rat heart. Hypertension 2009; 53: 1041-1047.
  3. Qureshi A.I., Suri M.F., Kirmani J.F. et al. Is prehypertension a risk factor for cardiovascular diseases? Stroke 2005; 36: 1859-1863.
  4. Ferranini E. The phenomenon of insulin resistance: its possible relevance to hypertensive disease. In: Laragh J.H., Brenner B.M. (eds). Hypertension: pathophysiology, diagnosis and management. New-York: Raven-Press 1995: 2281-2300.
  5. De Bacquer D., De Backer G., Ostör E. et al. Predictive value of classical risk factors and their control in coronary patients: a follow-up of the EUROASPIRE I cohort. Eur J Cardiovasc Prev Rehabil 2003; 10: 289-295.
  6. Brunner H.R., Laragh J.H., Baer I. et al. Essential hypertension: renin and aldosterone, heart attack and stroke. New Engl J Med 1972; 286: 441-449.
  7. Alderman M., Madhaven S., Ooi W.L. et al. Association of renin-sodium profile with the risk of myocardial infarction in patients with hypertension. New Engl J Med 1991; 324: 1098-1104.
  8. De Luca N., Asmar R., London G.M. et al. Selective reduction of cardiac mass and central blood pressure on low-dose combination perindopril/indapamide in hypertensive subjects. J Hypertens 2004; 22: 1623-1630.
  9. Franklin S.S., Khan S.A., Wong N.D. et al. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham Heart Study. Circulation 1999; 100: 354-360.
  10. Lüders S., Hammersen F., Kulschewski A. et al. Diagnosis of impaired glucose tolerance in hypertensive patients in daily clinical practice. Int J Clin Pract 2005; 59: 632-638.
  11. Chae C.U., Lee R.T., Rifai N., Ridker P.M. Blood pressure and inflammation in apparently healthy men. Hypertension 2002; 38: 399-403.
  12. Abramson J.L., Weintraub W.S., Vaccarino V. Association between pulse pressure and C-reactive protein among apparently healthy US adults. Hypertension 2002; 39:197-202.
  13. Dzau V.J., Antman E.M., Black H.R. et al. The cardiovascular disease continuum validated: clinical evidence of improved patients outcomes: part II. Clinical trial evidence (acute coronary syndromes through renal disease) and future directions. Circulation 2006; 114: 2781-2791.
  14. Dahlof B., Devereux R.B., Kielsen S.E. et al. For the LIFE study group. Cardiobvascular morbidity and mortality in the Losartan In-tervention For Endpoint reduction in hypertension study (LIFE): a randomized trial against atenolol. Lancet 2002; 359: 995-1003.
  15. Schillaci G., Pasqualini L., Vaudo G. et al. Effect of body weight changes on 24-hour blood pressure and left ventricular mass in hypertension: a 4-year follow-up. Am J Hypertens 2003; 16: 634-639.
  16. Vasan R.S., Larson M.G., Leip E.P. et al. Impact of high-normal pressure on the risk of cardiovascular disease. N Engl J Med 2001; 345: 1291-1297.
  17. Behr T.M., Willette R.N., Coatney R.W. et al. Eprosartan improves cardiac performance, reduces cardiac hypertrophy and mortality and downregulates myocardial chemoattractant protein-1 and inflammation in hypertensive heart disease. J Hypertens 2004; 22: 583-592.
  18. Giles T.D., Berk B.C., Black H.R. et al. Pathophysiologic, diagnostic, and therapeutic aspects of the metabolic syndrome. J Clin Hypertens (Greenwich) 2005; 7: 505-512.
  19. Papagiotakos D.B., Kromhout D., Menotti A. et al. The relation between pulse pressure and cardiovascular mortality in 12.763 middle-aged men from various parts of the world: a 25-year follow-up of the seven countries study. Arch Int Med 2005; 165: 2142-2147.
  20. Manabe S., Okura T., Watanabe S., Higaki J. Association between carotid haemodynamics and inflammation in patients with essential hypertension. J Hum Hypertens 2005; 19: 787-791.
  21. Wang Z.V., Scherer P.E. Adiponectin, cardiovascular function, and hypertension. Hypertension 2008; 51: 8-16.
  22. Neter J.E., Stam B.E., Kok F.J. et al. Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension 2003; 42: 878-884.
  23. Williams B., Lacy P.S., Thom S.M. et al. Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation 2006; 113: 1213-1225.
  24. Rossi R., Turco V., Origliani G., Modena M.G. Type 2 diabetes mellitus is a risk factor for the development of hypertension in postmenopausal women. J Hypertens 2006; 24: 2017-2022.
  25. Weber M. Should treatment of hypertension be driven by blood pressure or total cardiovascular risk? Renin-Angiotensin System In Cardiovascular Medicine 2006; 2 (3): 16-19.
  26. Gaillard T., Schuster D., Osei K. Independent role of blood pressure on cardiovascular risk factors in nondiabetic, obese African-American women with family history of type 2 diabetes: Implications for metabolic syndrome components. Hypertension 2009; 3: 25-34.
  27. Korhonen P., Aarnio P., Saaresranta T. et al. Glucose homeostasis in hypertensive subjects. Hypertension 2008; 51: 945-952.
  28. Jeng J.-R. Plasma adiponectin, T94G gene polymorphism and PAI-1 in patients with and without hypertension. Cardiology 2007; 107: 30-37.
  29. Iwashima Y., Katsuya T., Ishikawa K. et al. Hypoadiponectinemia is an independent risk factor for hypertension. Hypertension 2004; 43: 1318-1323.
  30. Chow W.-S., Cheung B.M.Y., Tso A.W.K. et al. Hypoadiponectinemia as a predictor for the development of hypertension: a 5-year prospective study. Hypertension 2007; 49: 1455-1461.
  31. Neaton J.D., Wentworth D. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease. Overall findings and differences by age for 316 099 white men. Arch Int Med 1992; 152: 56-64.
  32. Leibowitz A., Grossman E. How to define prehypertension in diabetes/metabolic syndrome. Diabetes Care 2009; 32 (2): S275-S279.
  33. Mainous A.G., Everett C.J., Loszka H. et al. Prehypertension and mortality in a nationally representative cohort. Am J Cardiol 2004; 94: 1496-1500.
  34. De Lano F.A., Schmid-Schönbein G.W. Proteinase аctivity and receptor cleavage. Mechanism for insulin resistance in the spontaneously hypertensive rat. Hypertension 2008; 52: 415-423.
  35. Талаева Т.В., Братусь В.В., Амброскина В.В. и др. Системный характер нарушений метаболизма, активности воспаления, оксидантного стресса и атерогенности плазмы у больных с ишемической болезнью сердца. Укр Кардиол Журн 2007; 12: 8-19.
  36. Бойцов С.А. Взаимосвязи артериосклероза, атеросклероза и артериальной гипертонии - старый вопрос в свете новых данных. Тер арх 2009; 12: 5-11.
  37. Modena M.G., Bonetti L., Coppi F. et al. Prognostic role of reversibile endothelial dysfunction in hypertensive postmenopausal women. J Am Coll Cardiol 2002; 40: 505-510.
  38. Su T.C., Chien K.L., Jeng J.S. et al. Pulse pressure, aortic regurgitation and carotid atherosclerosis: a comparison between hypertensives and normotensives. Int J Clin Pract 2006; 60: 134-140.
  39. Rahmouni K., Correia M.L., Haynes W.G., Mark A.L. Obesity-associated hypertension. New insights into mechanisms. Hypertension 2005; 45: 9-16.

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