HYPERHOMOCYSTEINEMIA AS A RISK FACTOR OF CARDIOVASCULAR DISEASES
Cardiovascular diseases are the leading cause of death. In this regard, the importance of the prevention problem increases, which is aimed at the identification and elimination of risk factors, which include elevated levels of homocysteine in the blood.
In recent years, actively studying the possibility of the use of B vitamins in vascular and neurodegenerative diseases. One of the main factors of hyperhomocysteinemia is the deficiency of vitamins B6, B12, B9 resulting from the features of the diet and impaired absorption. It was found that the use of preparations of B vitamins can reduce hyperhomocysteinemia in the blood. On the basis of the theory of homocysteic atherosclerosis development the presence of possible association hyperhomocysteinemia with the vascular disease formation is explained. It was found that the use of high doses of B vitamins contribute to a significant reduction in the progression of atherosclerosis in the early stages.
The article describes the role of hyperhomocysteinemia as a risk factor for cardiovascular disease. A review of the evidence base and domestic research is prepared. The conclusions recognizing regional specificities and influence of radiation factor are drawn.
Objective: To conduct a literature search on the study of hyperhomocysteinemia as a risk factor for cardiovascular disease.
Materials and methods: To achieve this goal was performed a systematic literature search in an online resource. 278 sources were found of which 63 sources were selected for subsequent analysis. Key points forming search queries to search for literature were presented to the following elements: homocysteine, vitamin B, folic acid, cardiovascular risk.
Results and conclusions: For high-risk patients, which include patients with personal or family history of early cardiovascular failure, and those with malnutrition (reduced absorption syndrome), hypothyroidism, kidney disease, systemic lupus erythematosus; taking drugs such as nicotinic acid, theophylline, methotrexate dopamine, and those who are exposed to nitric oxide, it is necessary to carry out the definition of plasma homocysteine.
Liudmila K. Karazhanova, http://orcid.org/0000-0002-4719-6034
Aisulu S. Zhunuspekova, http://orcid.org/0000-0003-1496-3281
Semey State Medical University,
The Department of internship in internal medicine
Semey, Kazakhstan.
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31. Heinz J., et al., B vitamins and the risk of total mortality and cardiovascular disease in end-stage renal disease: results of a randomized controlled trial. J. Lipid. Res. 2008, 305(24) рр.86-90.
32. Halvorsen В., Waehre T., Scholz H.et al. Interleukin-10 enhances the oxidized LDL-induced foam cell formation of macrophages by antiapoptotic mechanism. J. Lipid. Res. 2005.Vol. 46, № 2.рр. 211-219.
33. .Harb T.S., Zareba W., Moss A.J. et al. Association of C-reactive protein and serum amyloid A with recurrent coronary events in stable patients after healing of acute myocardial infarction. Am J Cardiol, 2002. Vol.89. Р. 216-221.
34. Hamrick M.W, Pennington C, Newton D, Xie D, Isales C Leptin deficiency produces contrasting phenotypes in bones of the limb and spine. Bone. 2004. рр. 376–383
35. Homocysteine Studies Collaboration. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA. 2002. 288(16) рр.2015-2022
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42. Malinow M.R, Stampfer M.J. Role of plasma homocyst(e)ine in arterial occlnsive diseases. Clin Gmn, 1994. рр.857-858.
43. Marti-Carvajal A.J. et al., Homocysteine lowering interventions for preventing cardiovascular events (Review). Cochrane Collaboration and published in The Cochrane Library 2009.
44. National institutes of health consensus development panel on osteoporosis prevention, diagnosis and therapy 2001. JAMA. 285 (6) рр.785–795
45. PACIFIC Study Group. Dose-dependent effects of folic acid on plasma homocysteine in a randomized trial conducted among 723 individuals with coronary heart disease. EHJ 2002;23:1509–15. [MEDLINE: 12395803]
46. Pepine C.L., Abrams J., Marks R.G. et al. Characteristics of a contemporary population with angina pectoris. J. Amer. Coll. Cardiol. 1994. V. 74. рр. 226-231.
47. The VITATOPS Trial Study Group. B-vitamins in patients with recent transient ischaemic attack or stroke in the VITAmins TO Prevent Stroke (VITATOPS) trial: a randomised, double-blind, parallel, placebo-controlled trial. Lancet Neurology. 2010;9:855-65
48. Schnyder G, et al. Effect of homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin B6 on clinical outcome after percutaneous coronary intervention: the Swiss Heart study: a randomized controlled trial. JAMA. 2002;288:973-9.
49. Savonitto S., Ardissiono D., Egstrup K. et al. Combination therapy with metoprolol and nifedipine versus monotherapy in patients with stable angina pectoris. J. Amer. Coll. Cardiol. 1996. V. 27. рр. 311-316.
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Каражанова Л.К., Жунуспекова А.С. Гипергомоцистеинемия как фактор риска сердечно-сосудистых заболеваний (Обзор литературы) / / Наука и Здравоохранение. 2016. №4. С. 129-144. Karazhanova L.K., Zhunuspekova A.S. Hyperhomocysteinemia as a risk factor of cardiovascular diseases (Literature review). Nauka i Zdravookhranenie [Science & Healthcare]. 2016, 4, pp. 129-144. Қаражанова Л.Қ., Жүніспекова А.С. Гипергомоцистеинемия жүрек – қантамыр ауруларының қауіп-қатер факторы ретінде (Әдебиеттерге шолу) / / Ғылым және Денсаулық сақтау. 2016. №4. Б. 129-144.Related publications:
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