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Клинические и генетические факторы, определяющие поражения органов-мишеней у пациентов с артериальной гипертензией среди населения Горной Шории
Клинические и генетические факторы, определяющие поражения органов-мишеней у пациентов с артериальной гипертензией среди населения Горной Шории
Мулерова Т.А. Клинические и генетические факторы, определяющие поражения органов-мишеней у пациентов с артериальной гипертензией среди населения Горной Шории. Системные гипертензии. 2017; 14 (3): 42–50. DOI: 10.26442/2075-082X_14.3.42-50
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Аннотация
Цель исследования – установить ассоциации клинических и генетических факторов риска с поражениями органов-мишеней (сердце, сосуды, почки) у пациентов с артериальной гипертензией (АГ) населения Горной Шории в зависимости от этнической принадлежности.
Материалы и методы. Проведено клинико-эпидемиологическое исследование компактно проживающего населения в труднодоступных районах Горной Шории. Данный регион среднегорья расположен на юге Западной Сибири. Обследованы 1409 человек: 901 – представители коренной национальности (шорцы), 508 – представители некоренной национальности (90% из них европеоиды). Диагноз АГ выставлялся в соответствии с рекомендациями Всероссийского научного общества кардиологов и Российского медицинского общества по артериальной гипертонии (2010 г.). Оценка структурно-функционального состояния миокарда и дуплексное сканирование брахицефальных артерий пациентам с АГ проведены методом эхокардиографии. Фотометрическим методом исследовали уровень альбумина мочи. Полиморфизмы генов ACE (I/D, rs4340), АGT (c.803T>C, rs699), AGTR1 (А1166С, rs5186), ADRB1 (с.145A>G, Ser49Gly, rs1801252), ADRA2B (I/D, rs28365031), MTHFR (c.677С>Т, Ala222Val, rs1801133) и NOS3 (VNTR, 4b/4a) тестировали с помощью полимеразной цепной реакции.
Результаты. В коренной этнической группе гипертрофия миокарда левого желудочка (ГЛЖ) ассоциировалась с особенностями течения самой АГ (ее степени и длительности), курением, генотипами I/D гена АСЕ среди мужчин и Т/Т и С/Т гена MTHFR; увеличенная толщина комплекса интима–медиа (ТКИМ) – с особенностями течения самой АГ (ее длительности), мужским полом, возрастом, генотипами Т/С гена АGT и С/T гена MTHFR; повышенный уровень альбуминурии – с особенностями течения самой АГ (ее степени и длительности), нарушениями липидного обмена (гипоальфахолестеринемия, гипертриглицеридемия, гипербетахолестеринемия), генотипами D/D и I/D гена АСЕ, D/D гена ADRA2B и С/Т гена MTHFR среди лиц возрастной группы 18–64 лет. Протективные эффекты оказывали генотип Т/С гена AGT в отношении ГЛЖ, генотипы G/G и А/G гена ADRB1 в отношении увеличения ТКИМ и альбуминурии. В некоренной этнической группе ГЛЖ взаимосвязана с особенностями течения самой АГ (ее длительности), гипертриглицеридемией, абдоминальным ожирением, генотипами D/D гена АСЕ и 4b/4а и 4а/4а гена NOS3; увеличенная ТКИМ – с особенностями течения самой АГ (ее длительности), возрастом и генотипами Т/С и С/С гена АGT; повышенный уровень альбуминурии – с особенностями течения самой АГ (ее степени и длительности), ожирением, включая абдоминальное, генотипами С/С гена AGTR1, D/D гена ADRA2B и Т/Т гена MTHFR. Протективный эффект оказывал генотип I/D гена ADRA2B в отношении увеличения ТКИМ.
Заключение. Данное исследование продемонстрировало актуальность проблемы этногенетических механизмов развития мультифакториальной патологии, что требует проведения дальнейших исследований и выделения лиц с АГ и поражением органов-мишеней для последующего контроля при проведении профилактических осмотров и диспансеризации населения.
Ключевые слова: этнос, гипертрофия миокарда левого желудочка, атеросклероз каротидных артерий, альбуминурия, гены-кандидаты артериальной гипертензии.
Matherials and methods. A clinical and epidemiological study of compactly living population in the remote areas of the Mountain Shoria was carried out. This middle altitude region is located in the south of Western Siberia. 1409 people were examined (901 representatives of the indigenous ethnic group – the Shors, 508 representatives of the non-indigenous ethnic group – 90% of them being Caucasian). The diagnosis of AH was set in accordance with the recommendations of the Society of Cardiology of the Russian Federation / Medical Society of the Russian Federation on the Problem of Arterial Hypertension, 2010. Assessment of the structural and functional state of the cardiac muscle and duplex scanning of brachiocephalic arteries among the patients with AH was made by echocardiography. A photometric method was used to examine the urinary albumin concentration level. The polymorphisms of the genes ACE (I/D, rs4340), АGT (c.803T>C, rs699), AGTR1 (А1166С, rs5186), ADRB1 (с.145A>G, Ser49Gly, rs1801252), ADRA2B (I/D, rs28365031), MTHFR (c.677С>Т, Ala222Val, rs1801133) and NOS3 (VNTR, 4b/4a) were tested by the PCR method.
Results. Among the members of the indigenous ethnic group left ventricle hypertrophy (LVH) correlated with the AG progression features (extent and duration), smoking, genotypes I/D of the ACE gene among men and T/T and C/T of the MTHFR gene; increased intima-media complex thickness (IMT) correlated with the AG progression features (duration), male sex, age, genotypes T/C of the AGT gene and C/T of the MTHFR gene; high level of albuminuria (AU) correlated with the AG progression features (extent and duration), lipid disorders (hypoalphacholesterolemia, hypertriglyceridemia, hyperbetacholesterolemia), genotypes D/D and I/D of the ACE gene, D/D of the ADRA2B gene and the C/T of the MTHFR gene among 18–64-year-olds. Genotype T/C of the AGT gene had a protective effect on LVH, genotypes G/G and A/G of the ADRB1 gene had protective effects on IMT and AU levels. In the nonindigenous ethnic group LVH correlated with the AG progression features (duration), hypertriglyceridemia, abdominal obesity, genotypes D/D of the ACE gene, 4b/4a and 4a/4a of the NOS3 gene; increased IMT correlated with the AG progression features (duration), age and genotypes T/C and C/C of the AGT gene; AU high level correlated with the AG progression features (extent and duration), obesity, abdominal including, genotypes C/C of the AGTR1 gene, D/D of the ADRA2B gene and T/T of the MTHFR gene. Genotype I/D of the ADRA2B gene had protective effect on IMT.
Conclusion. The study demonstrated the importance of the ethnogenetic mechanisms in the multifactorial pathology development. The problem requires further research, also identification of people with AH and target lesions is needed for monitoring during the prophylactic medical examination of the population.
Key words: ethnic group, left ventricle hypertrophy, carotid artery atherosclerosis, albuminuria, arterial hypertension candidate genes.
Материалы и методы. Проведено клинико-эпидемиологическое исследование компактно проживающего населения в труднодоступных районах Горной Шории. Данный регион среднегорья расположен на юге Западной Сибири. Обследованы 1409 человек: 901 – представители коренной национальности (шорцы), 508 – представители некоренной национальности (90% из них европеоиды). Диагноз АГ выставлялся в соответствии с рекомендациями Всероссийского научного общества кардиологов и Российского медицинского общества по артериальной гипертонии (2010 г.). Оценка структурно-функционального состояния миокарда и дуплексное сканирование брахицефальных артерий пациентам с АГ проведены методом эхокардиографии. Фотометрическим методом исследовали уровень альбумина мочи. Полиморфизмы генов ACE (I/D, rs4340), АGT (c.803T>C, rs699), AGTR1 (А1166С, rs5186), ADRB1 (с.145A>G, Ser49Gly, rs1801252), ADRA2B (I/D, rs28365031), MTHFR (c.677С>Т, Ala222Val, rs1801133) и NOS3 (VNTR, 4b/4a) тестировали с помощью полимеразной цепной реакции.
Результаты. В коренной этнической группе гипертрофия миокарда левого желудочка (ГЛЖ) ассоциировалась с особенностями течения самой АГ (ее степени и длительности), курением, генотипами I/D гена АСЕ среди мужчин и Т/Т и С/Т гена MTHFR; увеличенная толщина комплекса интима–медиа (ТКИМ) – с особенностями течения самой АГ (ее длительности), мужским полом, возрастом, генотипами Т/С гена АGT и С/T гена MTHFR; повышенный уровень альбуминурии – с особенностями течения самой АГ (ее степени и длительности), нарушениями липидного обмена (гипоальфахолестеринемия, гипертриглицеридемия, гипербетахолестеринемия), генотипами D/D и I/D гена АСЕ, D/D гена ADRA2B и С/Т гена MTHFR среди лиц возрастной группы 18–64 лет. Протективные эффекты оказывали генотип Т/С гена AGT в отношении ГЛЖ, генотипы G/G и А/G гена ADRB1 в отношении увеличения ТКИМ и альбуминурии. В некоренной этнической группе ГЛЖ взаимосвязана с особенностями течения самой АГ (ее длительности), гипертриглицеридемией, абдоминальным ожирением, генотипами D/D гена АСЕ и 4b/4а и 4а/4а гена NOS3; увеличенная ТКИМ – с особенностями течения самой АГ (ее длительности), возрастом и генотипами Т/С и С/С гена АGT; повышенный уровень альбуминурии – с особенностями течения самой АГ (ее степени и длительности), ожирением, включая абдоминальное, генотипами С/С гена AGTR1, D/D гена ADRA2B и Т/Т гена MTHFR. Протективный эффект оказывал генотип I/D гена ADRA2B в отношении увеличения ТКИМ.
Заключение. Данное исследование продемонстрировало актуальность проблемы этногенетических механизмов развития мультифакториальной патологии, что требует проведения дальнейших исследований и выделения лиц с АГ и поражением органов-мишеней для последующего контроля при проведении профилактических осмотров и диспансеризации населения.
Ключевые слова: этнос, гипертрофия миокарда левого желудочка, атеросклероз каротидных артерий, альбуминурия, гены-кандидаты артериальной гипертензии.
________________________________________________
Matherials and methods. A clinical and epidemiological study of compactly living population in the remote areas of the Mountain Shoria was carried out. This middle altitude region is located in the south of Western Siberia. 1409 people were examined (901 representatives of the indigenous ethnic group – the Shors, 508 representatives of the non-indigenous ethnic group – 90% of them being Caucasian). The diagnosis of AH was set in accordance with the recommendations of the Society of Cardiology of the Russian Federation / Medical Society of the Russian Federation on the Problem of Arterial Hypertension, 2010. Assessment of the structural and functional state of the cardiac muscle and duplex scanning of brachiocephalic arteries among the patients with AH was made by echocardiography. A photometric method was used to examine the urinary albumin concentration level. The polymorphisms of the genes ACE (I/D, rs4340), АGT (c.803T>C, rs699), AGTR1 (А1166С, rs5186), ADRB1 (с.145A>G, Ser49Gly, rs1801252), ADRA2B (I/D, rs28365031), MTHFR (c.677С>Т, Ala222Val, rs1801133) and NOS3 (VNTR, 4b/4a) were tested by the PCR method.
Results. Among the members of the indigenous ethnic group left ventricle hypertrophy (LVH) correlated with the AG progression features (extent and duration), smoking, genotypes I/D of the ACE gene among men and T/T and C/T of the MTHFR gene; increased intima-media complex thickness (IMT) correlated with the AG progression features (duration), male sex, age, genotypes T/C of the AGT gene and C/T of the MTHFR gene; high level of albuminuria (AU) correlated with the AG progression features (extent and duration), lipid disorders (hypoalphacholesterolemia, hypertriglyceridemia, hyperbetacholesterolemia), genotypes D/D and I/D of the ACE gene, D/D of the ADRA2B gene and the C/T of the MTHFR gene among 18–64-year-olds. Genotype T/C of the AGT gene had a protective effect on LVH, genotypes G/G and A/G of the ADRB1 gene had protective effects on IMT and AU levels. In the nonindigenous ethnic group LVH correlated with the AG progression features (duration), hypertriglyceridemia, abdominal obesity, genotypes D/D of the ACE gene, 4b/4a and 4a/4a of the NOS3 gene; increased IMT correlated with the AG progression features (duration), age and genotypes T/C and C/C of the AGT gene; AU high level correlated with the AG progression features (extent and duration), obesity, abdominal including, genotypes C/C of the AGTR1 gene, D/D of the ADRA2B gene and T/T of the MTHFR gene. Genotype I/D of the ADRA2B gene had protective effect on IMT.
Conclusion. The study demonstrated the importance of the ethnogenetic mechanisms in the multifactorial pathology development. The problem requires further research, also identification of people with AH and target lesions is needed for monitoring during the prophylactic medical examination of the population.
Key words: ethnic group, left ventricle hypertrophy, carotid artery atherosclerosis, albuminuria, arterial hypertension candidate genes.
Полный текст
Список литературы
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41. Abd El-Aziz TA, Mohamed RH. Influence of MTHFR C677T gene polymorphism in the development of cardiovascular disease in Egyptian patients with rheumatoid arthritis. Gene 2017; 610: 127–32.
42. Saitou M, Osonoi T, Kawamori R et al. Genetic risk factors and the anti-atherosclerotic effect of pioglitazone on carotid atherosclerosis of subjects with type 2 diabetes a retrospective study. J Atheroscler Thromb 2010; 17 (4): 386–94.
43. Koo HS, Lee HS, Hong YM. Methylenetetrahydrofolate reductase TT genotype as a predictor of cardiovascular risk in hypertensive adolescents. Pediatr Cardiol 2008; 29 (1): 1.
44. Ukinc K, Ersoz HO, Karahan C et al. Methyltetrahydrofolate reductase C677T gene mutation and hyperhomocysteinemia as a novel risk factor for diabetic nephropathy. Endocrine 2009; 36 (2): 255–61.
45. El-Baz R, Settin A, Ismaeel A et al. MTHFR C677T, A1298C and ACE I/D polymorphisms as risk factors for diabetic nephropathy among type 2 diabetic patients. J Renin Angiotensin Aldosterone Syst 2012; 13 (4): 472–7.
2. Sehestedt T, Jeppesen J, Hansen TW et al. Thresholds for pulse wave velocity, urine albumin creatinine ratio and left ventricular mass index using SCORE, Framingham and ESH/ESC risk charts. J Hypertens 2012; 30: 1928–36.
3. Sumin A.N., Osokina A.V., Shcheglova A.V. et al. Assessment of cardio-ankle vascular index in patients with coronary artery disease with a different type of diastolic dysfunction of the left ventricle. Complex Issues of Cardiovascular Diseases. 2016; (2): 51–8. [in Russian]
4. Kristensen SD, Baumgartner H, Casadeiet B et al. Highlights of the 2008 scientific sessions of the European Society of Cardiology. J Am Coll Cardiol 2008; 52 (24): 2032–42.
5. Barsukov A.V., Zobnina M.Р., Talanzeva M.S. Retrospective prognostic assessment of essential hypertensive patients with different types of left ventricular hypertrophy in dependence of obesity presence. Arterialnaia gipertenziya. 2012; 5 (18): 385–98. [in Russian]
6. Chambless LE, Folsom AR, Clegg LX et al. Carotid wall thickness is predictive of incident clinical stroke: The Atherosclerosis Risk in Communities (ARIC) study. Am J Еpidemiology 2000; 151 (5): 478–87.
7. Dijk JM, van der Graaf Y, Bots ML et al. Carotid intima-media thickness and the risk of new vascular events in patients with manifest atherosclerotic disease: the SMART study. Eur Heart J 2006; 27 (16): 1971–78.
8. Murakami S, Otsuka K, Hotta N et al. Common carotid intima-media thickness is predictive of all-cause and cardiovascular mortality in elderly community-dwelling people: Longitudinal Investigation for the Longevity and Aging in Hokkaido County (LILAC) study. Biomed Pharmacother 2005; 59 (Suppl. 1): S49–53.
9. Hitha B, Pappachan JM, Pillai HB et al. Microalbuminuria in patients with essential hypertension and its relationship to target organ damage: an Indian experience. Saudi J Kidney Dis Transpl 2008; 19 (3): 411–9.
10. Kuznetsova T.Yu., Gavrilov D.V., Samoсhodskaya L.M. et al. Clinical and genetic risk factors for microalbuminuria in hypertension. Systemic Hypertension. 2010; 1: 15–21. [in Russian]
11. Hu DC, Zhao XL, Shao JC et al. Interaction of six candidate genes in essential hypertension. Genet Mol Res 2014; 13 (4): 8385–95.
12. Devereux RB, Alonso DR, Lutas EM et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57 (6): 450–8.
13. Snapir A, Scheinin M, Groop LC et al. The insertion/deletion variation in the a2B-adrenoceptor does not seem to modify the risk for acute myocardial infarction, but may modify the risk for hypertension in sib-pairs from families with type 2 diabetes. Cardiovasc Diabetol 2003; 24 (2): 15.
14. Lima JJ, Feng H, Duckworth L et al. Association analyses of adrenergic receptor polymorphisms with obesity and metabolic alterations. Metabolism 2007; 56 (6): 757–65.
15. Salimi S, Firoozrai M, Nourmohammadi I et al. Endothelial nitric oxide synthase gene intron4 VNTR polymorphism in patients with coronary artery disease in Iran. Indian J Med Res 2006; 124 (6): 683–8.
16. Ehret GB, Munroe PB, Rice KM et al. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Nature 2011; 478 (7367): 103–9.
17. Coutinho T, Turner ST, Kullo I. Aortic pulse wave velocity is associated with measures of subclinical target organ damage. JACC Cardiovasc Imaging 2011; 4 (7): 754–61.
18. Frigo G, Bertolo O, Roman E et al. Relationship of left ventricular mass with clinic blood pressure measured over a six month period vs. ambulatory blood pressure (abstract). J Hypertens 2000; 18 (2): 44.
19. Nambi V, Chambless L, Folsom AR et al. Carotid intima-media thickness and presence or absence of plaque improves prediction of coronary heart disease risk: the ARIC (Atherosclerosis Risk In Communities) study. J Am Coll Cardiol 2010; 55: 1600–07.
20. Peters SA, den Ruijter HM, Bots ML, Moons KG. Improvements in risk stratification for the occurrence of cardiovascular disease by imaging subclinical atherosclerosis: a systematic review. Heart 2012; 98 (3): 177–84.
21. Reboldi G, Gentile G, Angeli F, Verdecchia P. Microalbuminuria and hypertension. Minerva Medica 2005; 96 (4): 261–75.
22. Payne JR, Eleftheriou KI, James LE et al. Left ventricular growth response to exercise and cigarette smoking: data from LARGE Heart. Heart 2006; 92 (12): 1784–88.
23. Grandi AM, Zanzi P, Piantanida E et al. Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives. Int J Obes Relat Metab Disord 2000; 24 (8): 954–58.
24. Falqui V, Viazzi F, Leoncini G et al. Blood pressure load, vascular permeability and target organ damage in primary hypertension. J Nephrol 2007; 20 (Suppl. 12): S63–7.
25. Bonnet F, Marre M, Halimi JM et al. Waist circumference and the metabolic syndrome predict the development of elevated albuminuria in non-diabetic subjects: the DESIR study. J Hypertens 2006; 24 (6): 1157–63.
26. Frangogiannis NG. The immune system and cardiac repair. Pharmacol Res 2008; 58 (2): 88–111.
27. Aggoun Y, Bonnet D, Sidi D et al. Arterial mechanical changes in children with familial hypercholesterolemia. Arteriocler Thromb Vasc Biol 2000; 20: 2070–75.
28. Wilkinson IB, Prasad K. Hall IR et al. Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia. J Am Coll Cardiol 2002; 39: 1005–11.
29. Li X, Li Y, Jia N et al. Angiotensin-converting enzyme gene deletion allele increases the risk of left ventricular hypertrophy: evidence from a meta-analysis. Mol Biol Rep 2012; 39 (12): 10063–75.
30. Di Mauro M, Izzicupo P, Santarelli F et al. ACE and AGTR1 polymorphisms and left ventricular hypertrophy in endurance athletes. Med Sci Sports Exerc 2010; 42–(5): 915–21.
31. Park EY, Ahn HM, Lee JA, Hong YM. Insertion/deletion polymorphism of angiotensin converting enzyme gene in Korean hypertensive adolescents. Heart Vessels 2009; 24 (3): 193–8.
32. Imbalzano E, Vatrano M, Quartuccio S et al. Clinical impact of angiotensin I converting enzyme polymorphisms in subjects with resistant hypertension. Mol Cell Biochem 2017 Feb 11.
33. Pedrinelli R, Dell'Omo G, Penno G et al. Alpha-adducin and angiotensin-converting enzyme polymorphisms in hypertension: evidence for a joint influence on albuminuria. J Hypertens 2006; 24 (5): 931–7.
34. Parchwani DN, Palandurkar KM, Hema Chandan Kumar D, Patel DJ. Genetic Predisposition to Diabetic Nephropathy: Evidence for a Role of ACE (I/D) Gene Polymorphism in Type 2 Diabetic Population from Kutch Region. Indian J Clin Biochem 2015; 30 (1): 43–54.
35. Ott C, Schwarz T, Hilgers KF et al. Left-ventricular structure and function are influenced by angiotensinogen gene polymorphism (-20 A/C) in young male patients. Am J Hypertens 2007; 20 (9): 974–80.
36. Eliseeva MR, Srozhidinova NZ, Khamidullaeva GA, Abdullaeva GZh. Genetic determinants of cardiovascular remodeling in Uzbek patients with essential hypertension. Ter. Arkhiv. 2009; 81 (1): 64–9. [Russian]
37. Kelly M, Bagnall RD, Peverill RE et al. A polymorphic miR-155 binding site in AGTR1 is associated with cardiac hypertrophy in Friedreich ataxia. J Mol Cell Cardiol 2011; 51 (5): 848–54.
38. Jin Y, Kuznetsova T, Thijs L et al. Association of left ventricular mass with the AGTR1 A1166C polymorphism. Am J Hypertens 2012; 25 (4): 472–8.
39. Buraczynskа M, Ksiazek P, Lopatynski J et al. Association of the reninangiotensin system gene polymorphism with nephropathy in type II diabetes. Polskie archiwum medycyny wewnetrznej 2002; 108 (2): 725–30.
40. Fabris B, Bortoletto M, Candido R et al. Genetic polymorphisms of the renin-angiotensin-aldosterone system and renal insufficiency in essential hypertension. J Hypertens 2005; 23 (2): 309–16.
41. Abd El-Aziz TA, Mohamed RH. Influence of MTHFR C677T gene polymorphism in the development of cardiovascular disease in Egyptian patients with rheumatoid arthritis. Gene 2017; 610: 127–32.
42. Saitou M, Osonoi T, Kawamori R et al. Genetic risk factors and the anti-atherosclerotic effect of pioglitazone on carotid atherosclerosis of subjects with type 2 diabetes a retrospective study. J Atheroscler Thromb 2010; 17 (4): 386–94.
43. Koo HS, Lee HS, Hong YM. Methylenetetrahydrofolate reductase TT genotype as a predictor of cardiovascular risk in hypertensive adolescents. Pediatr Cardiol 2008; 29 (1): 1.
44. Ukinc K, Ersoz HO, Karahan C et al. Methyltetrahydrofolate reductase C677T gene mutation and hyperhomocysteinemia as a novel risk factor for diabetic nephropathy. Endocrine 2009; 36 (2): 255–61.
45. El-Baz R, Settin A, Ismaeel A et al. MTHFR C677T, A1298C and ACE I/D polymorphisms as risk factors for diabetic nephropathy among type 2 diabetic patients. J Renin Angiotensin Aldosterone Syst 2012; 13 (4): 472–7.
2. Sehestedt T, Jeppesen J, Hansen TW et al. Thresholds for pulse wave velocity, urine albumin creatinine ratio and left ventricular mass index using SCORE, Framingham and ESH/ESC risk charts. J Hypertens 2012; 30: 1928–36.
3. Сумин А.Н., Осокина А.В., Щеглова А.В. и др. Оценка сердечно-лодыжечного сосудистого индекса у больных ИБС с различным типом диастолической дисфункции левого желудочка. Комплексные проблемы сердечно-сосудистых заболеваний. 2016; (2): 51–8. / Sumin A.N., Osokina A.V., Shcheglova A.V. et al. Assessment of cardio-ankle vascular index in patients with coronary artery disease with a different type of diastolic dysfunction of the left ventricle. Complex Issues of Cardiovascular Diseases. 2016; (2): 51–8. [in Russian]
4. Kristensen SD, Baumgartner H, Casadeiet B et al. Highlights of the 2008 scientific sessions of the European Society of Cardiology. J Am Coll Cardiol 2008; 52 (24): 2032–42.
5. Барсуков А.В., Зобнина М.П., Таланцева М.С. Гипертрофия левого желудочка и прогноз: данные пятилетнего ретроспективного наблюдения за пациентами с эссенциальной артериальной гипертензией. Артериальная гипертензия. 2012; 18 (5): 385–98. / Barsukov A.V., Zobnina M.Р., Talanzeva M.S. Retrospective prognostic assessment of essential hypertensive patients with different types of left ventricular hypertrophy in dependence of obesity presence. Arterialnaia gipertenziya. 2012; 5 (18): 385–98. [in Russian]
6. Chambless LE, Folsom AR, Clegg LX et al. Carotid wall thickness is predictive of incident clinical stroke: The Atherosclerosis Risk in Communities (ARIC) study. Am J Еpidemiology 2000; 151 (5): 478–87.
7. Dijk JM, van der Graaf Y, Bots ML et al. Carotid intima-media thickness and the risk of new vascular events in patients with manifest atherosclerotic disease: the SMART study. Eur Heart J 2006; 27 (16): 1971–78.
8. Murakami S, Otsuka K, Hotta N et al. Common carotid intima-media thickness is predictive of all-cause and cardiovascular mortality in elderly community-dwelling people: Longitudinal Investigation for the Longevity and Aging in Hokkaido County (LILAC) study. Biomed Pharmacother 2005; 59 (Suppl. 1): S49–53.
9. Hitha B, Pappachan JM, Pillai HB et al. Microalbuminuria in patients with essential hypertension and its relationship to target organ damage: an Indian experience. Saudi J Kidney Dis Transpl 2008; 19 (3): 411–9.
10. Кузнецова Т.Ю., Гаврилов Д.В., Самоходская Л.М. и др. Клинико-генетические факторы риска развития микроальбуминурии при артериальной гипертензии. Системные гипертензии. 2010; 1: 15–21. / Kuznetsova T.Yu., Gavrilov D.V., Samoсhodskaya L.M. et al. Clinical and genetic risk factors for microalbuminuria in hypertension. Systemic Hypertension. 2010; 1: 15–21. [in Russian]
11. Hu DC, Zhao XL, Shao JC et al. Interaction of six candidate genes in essential hypertension. Genet Mol Res 2014; 13 (4): 8385–95.
12. Devereux RB, Alonso DR, Lutas EM et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57 (6): 450–8.
13. Snapir A, Scheinin M, Groop LC et al. The insertion/deletion variation in the a2B-adrenoceptor does not seem to modify the risk for acute myocardial infarction, but may modify the risk for hypertension in sib-pairs from families with type 2 diabetes. Cardiovasc Diabetol 2003; 24 (2): 15.
14. Lima JJ, Feng H, Duckworth L et al. Association analyses of adrenergic receptor polymorphisms with obesity and metabolic alterations. Metabolism 2007; 56 (6): 757–65.
15. Salimi S, Firoozrai M, Nourmohammadi I et al. Endothelial nitric oxide synthase gene intron4 VNTR polymorphism in patients with coronary artery disease in Iran. Indian J Med Res 2006; 124 (6): 683–8.
16. Ehret GB, Munroe PB, Rice KM et al. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Nature 2011; 478 (7367): 103–9.
17. Coutinho T, Turner ST, Kullo I. Aortic pulse wave velocity is associated with measures of subclinical target organ damage. JACC Cardiovasc Imaging 2011; 4 (7): 754–61.
18. Frigo G, Bertolo O, Roman E et al. Relationship of left ventricular mass with clinic blood pressure measured over a six month period vs. ambulatory blood pressure (abstract). J Hypertens 2000; 18 (2): 44.
19. Nambi V, Chambless L, Folsom AR et al. Carotid intima-media thickness and presence or absence of plaque improves prediction of coronary heart disease risk: the ARIC (Atherosclerosis Risk In Communities) study. J Am Coll Cardiol 2010; 55: 1600–07.
20. Peters SA, den Ruijter HM, Bots ML, Moons KG. Improvements in risk stratification for the occurrence of cardiovascular disease by imaging subclinical atherosclerosis: a systematic review. Heart 2012; 98 (3): 177–84.
21. Reboldi G, Gentile G, Angeli F, Verdecchia P. Microalbuminuria and hypertension. Minerva Medica 2005; 96 (4): 261–75.
22. Payne JR, Eleftheriou KI, James LE et al. Left ventricular growth response to exercise and cigarette smoking: data from LARGE Heart. Heart 2006; 92 (12): 1784–88.
23. Grandi AM, Zanzi P, Piantanida E et al. Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives. Int J Obes Relat Metab Disord 2000; 24 (8): 954–58.
24. Falqui V, Viazzi F, Leoncini G et al. Blood pressure load, vascular permeability and target organ damage in primary hypertension. J Nephrol 2007; 20 (Suppl. 12): S63–7.
25. Bonnet F, Marre M, Halimi JM et al. Waist circumference and the metabolic syndrome predict the development of elevated albuminuria in non-diabetic subjects: the DESIR study. J Hypertens 2006; 24 (6): 1157–63.
26. Frangogiannis NG. The immune system and cardiac repair. Pharmacol Res 2008; 58 (2): 88–111.
27. Aggoun Y, Bonnet D, Sidi D et al. Arterial mechanical changes in children with familial hypercholesterolemia. Arteriocler Thromb Vasc Biol 2000; 20: 2070–75.
28. Wilkinson IB, Prasad K. Hall IR et al. Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia. J Am Coll Cardiol 2002; 39: 1005–11.
29. Li X, Li Y, Jia N et al. Angiotensin-converting enzyme gene deletion allele increases the risk of left ventricular hypertrophy: evidence from a meta-analysis. Mol Biol Rep 2012; 39 (12): 10063–75.
30. Di Mauro M, Izzicupo P, Santarelli F et al. ACE and AGTR1 polymorphisms and left ventricular hypertrophy in endurance athletes. Med Sci Sports Exerc 2010; 42–(5): 915–21.
31. Park EY, Ahn HM, Lee JA, Hong YM. Insertion/deletion polymorphism of angiotensin converting enzyme gene in Korean hypertensive adolescents. Heart Vessels 2009; 24 (3): 193–8.
32. Imbalzano E, Vatrano M, Quartuccio S et al. Clinical impact of angiotensin I converting enzyme polymorphisms in subjects with resistant hypertension. Mol Cell Biochem 2017 Feb 11.
33. Pedrinelli R, Dell'Omo G, Penno G et al. Alpha-adducin and angiotensin-converting enzyme polymorphisms in hypertension: evidence for a joint influence on albuminuria. J Hypertens 2006; 24 (5): 931–7.
34. Parchwani DN, Palandurkar KM, Hema Chandan Kumar D, Patel DJ. Genetic Predisposition to Diabetic Nephropathy: Evidence for a Role of ACE (I/D) Gene Polymorphism in Type 2 Diabetic Population from Kutch Region. Indian J Clin Biochem 2015; 30 (1): 43–54.
35. Ott C, Schwarz T, Hilgers KF et al. Left-ventricular structure and function are influenced by angiotensinogen gene polymorphism (-20 A/C) in young male patients. Am J Hypertens 2007; 20 (9): 974–80.
36. Елисеева МР, Срожидинова НЗ, Хамидуллаева ГА, Абдуллаева ГЖ. Генетические детерминанты ремоделирования сердечно-сосудистой системы при эссенциальной гипертонии у узбеков. Тер. архив. 2009; 81 (1): 64–9. / Eliseeva MR, Srozhidinova NZ, Khamidullaeva GA, Abdullaeva GZh. Genetic determinants of cardiovascular remodeling in Uzbek patients with essential hypertension. Ter. Arkhiv. 2009; 81 (1): 64–9. [Russian]
37. Kelly M, Bagnall RD, Peverill RE et al. A polymorphic miR-155 binding site in AGTR1 is associated with cardiac hypertrophy in Friedreich ataxia. J Mol Cell Cardiol 2011; 51 (5): 848–54.
38. Jin Y, Kuznetsova T, Thijs L et al. Association of left ventricular mass with the AGTR1 A1166C polymorphism. Am J Hypertens 2012; 25 (4): 472–8.
39. Buraczynskа M, Ksiazek P, Lopatynski J et al. Association of the reninangiotensin system gene polymorphism with nephropathy in type II diabetes. Polskie archiwum medycyny wewnetrznej 2002; 108 (2): 725–30.
40. Fabris B, Bortoletto M, Candido R et al. Genetic polymorphisms of the renin-angiotensin-aldosterone system and renal insufficiency in essential hypertension. J Hypertens 2005; 23 (2): 309–16.
41. Abd El-Aziz TA, Mohamed RH. Influence of MTHFR C677T gene polymorphism in the development of cardiovascular disease in Egyptian patients with rheumatoid arthritis. Gene 2017; 610: 127–32.
42. Saitou M, Osonoi T, Kawamori R et al. Genetic risk factors and the anti-atherosclerotic effect of pioglitazone on carotid atherosclerosis of subjects with type 2 diabetes a retrospective study. J Atheroscler Thromb 2010; 17 (4): 386–94.
43. Koo HS, Lee HS, Hong YM. Methylenetetrahydrofolate reductase TT genotype as a predictor of cardiovascular risk in hypertensive adolescents. Pediatr Cardiol 2008; 29 (1): 1.
44. Ukinc K, Ersoz HO, Karahan C et al. Methyltetrahydrofolate reductase C677T gene mutation and hyperhomocysteinemia as a novel risk factor for diabetic nephropathy. Endocrine 2009; 36 (2): 255–61.
45. El-Baz R, Settin A, Ismaeel A et al. MTHFR C677T, A1298C and ACE I/D polymorphisms as risk factors for diabetic nephropathy among type 2 diabetic patients. J Renin Angiotensin Aldosterone Syst 2012; 13 (4): 472–7.
________________________________________________
2. Sehestedt T, Jeppesen J, Hansen TW et al. Thresholds for pulse wave velocity, urine albumin creatinine ratio and left ventricular mass index using SCORE, Framingham and ESH/ESC risk charts. J Hypertens 2012; 30: 1928–36.
3. Sumin A.N., Osokina A.V., Shcheglova A.V. et al. Assessment of cardio-ankle vascular index in patients with coronary artery disease with a different type of diastolic dysfunction of the left ventricle. Complex Issues of Cardiovascular Diseases. 2016; (2): 51–8. [in Russian]
4. Kristensen SD, Baumgartner H, Casadeiet B et al. Highlights of the 2008 scientific sessions of the European Society of Cardiology. J Am Coll Cardiol 2008; 52 (24): 2032–42.
5. Barsukov A.V., Zobnina M.Р., Talanzeva M.S. Retrospective prognostic assessment of essential hypertensive patients with different types of left ventricular hypertrophy in dependence of obesity presence. Arterialnaia gipertenziya. 2012; 5 (18): 385–98. [in Russian]
6. Chambless LE, Folsom AR, Clegg LX et al. Carotid wall thickness is predictive of incident clinical stroke: The Atherosclerosis Risk in Communities (ARIC) study. Am J Еpidemiology 2000; 151 (5): 478–87.
7. Dijk JM, van der Graaf Y, Bots ML et al. Carotid intima-media thickness and the risk of new vascular events in patients with manifest atherosclerotic disease: the SMART study. Eur Heart J 2006; 27 (16): 1971–78.
8. Murakami S, Otsuka K, Hotta N et al. Common carotid intima-media thickness is predictive of all-cause and cardiovascular mortality in elderly community-dwelling people: Longitudinal Investigation for the Longevity and Aging in Hokkaido County (LILAC) study. Biomed Pharmacother 2005; 59 (Suppl. 1): S49–53.
9. Hitha B, Pappachan JM, Pillai HB et al. Microalbuminuria in patients with essential hypertension and its relationship to target organ damage: an Indian experience. Saudi J Kidney Dis Transpl 2008; 19 (3): 411–9.
10. Kuznetsova T.Yu., Gavrilov D.V., Samoсhodskaya L.M. et al. Clinical and genetic risk factors for microalbuminuria in hypertension. Systemic Hypertension. 2010; 1: 15–21. [in Russian]
11. Hu DC, Zhao XL, Shao JC et al. Interaction of six candidate genes in essential hypertension. Genet Mol Res 2014; 13 (4): 8385–95.
12. Devereux RB, Alonso DR, Lutas EM et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57 (6): 450–8.
13. Snapir A, Scheinin M, Groop LC et al. The insertion/deletion variation in the a2B-adrenoceptor does not seem to modify the risk for acute myocardial infarction, but may modify the risk for hypertension in sib-pairs from families with type 2 diabetes. Cardiovasc Diabetol 2003; 24 (2): 15.
14. Lima JJ, Feng H, Duckworth L et al. Association analyses of adrenergic receptor polymorphisms with obesity and metabolic alterations. Metabolism 2007; 56 (6): 757–65.
15. Salimi S, Firoozrai M, Nourmohammadi I et al. Endothelial nitric oxide synthase gene intron4 VNTR polymorphism in patients with coronary artery disease in Iran. Indian J Med Res 2006; 124 (6): 683–8.
16. Ehret GB, Munroe PB, Rice KM et al. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Nature 2011; 478 (7367): 103–9.
17. Coutinho T, Turner ST, Kullo I. Aortic pulse wave velocity is associated with measures of subclinical target organ damage. JACC Cardiovasc Imaging 2011; 4 (7): 754–61.
18. Frigo G, Bertolo O, Roman E et al. Relationship of left ventricular mass with clinic blood pressure measured over a six month period vs. ambulatory blood pressure (abstract). J Hypertens 2000; 18 (2): 44.
19. Nambi V, Chambless L, Folsom AR et al. Carotid intima-media thickness and presence or absence of plaque improves prediction of coronary heart disease risk: the ARIC (Atherosclerosis Risk In Communities) study. J Am Coll Cardiol 2010; 55: 1600–07.
20. Peters SA, den Ruijter HM, Bots ML, Moons KG. Improvements in risk stratification for the occurrence of cardiovascular disease by imaging subclinical atherosclerosis: a systematic review. Heart 2012; 98 (3): 177–84.
21. Reboldi G, Gentile G, Angeli F, Verdecchia P. Microalbuminuria and hypertension. Minerva Medica 2005; 96 (4): 261–75.
22. Payne JR, Eleftheriou KI, James LE et al. Left ventricular growth response to exercise and cigarette smoking: data from LARGE Heart. Heart 2006; 92 (12): 1784–88.
23. Grandi AM, Zanzi P, Piantanida E et al. Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives. Int J Obes Relat Metab Disord 2000; 24 (8): 954–58.
24. Falqui V, Viazzi F, Leoncini G et al. Blood pressure load, vascular permeability and target organ damage in primary hypertension. J Nephrol 2007; 20 (Suppl. 12): S63–7.
25. Bonnet F, Marre M, Halimi JM et al. Waist circumference and the metabolic syndrome predict the development of elevated albuminuria in non-diabetic subjects: the DESIR study. J Hypertens 2006; 24 (6): 1157–63.
26. Frangogiannis NG. The immune system and cardiac repair. Pharmacol Res 2008; 58 (2): 88–111.
27. Aggoun Y, Bonnet D, Sidi D et al. Arterial mechanical changes in children with familial hypercholesterolemia. Arteriocler Thromb Vasc Biol 2000; 20: 2070–75.
28. Wilkinson IB, Prasad K. Hall IR et al. Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia. J Am Coll Cardiol 2002; 39: 1005–11.
29. Li X, Li Y, Jia N et al. Angiotensin-converting enzyme gene deletion allele increases the risk of left ventricular hypertrophy: evidence from a meta-analysis. Mol Biol Rep 2012; 39 (12): 10063–75.
30. Di Mauro M, Izzicupo P, Santarelli F et al. ACE and AGTR1 polymorphisms and left ventricular hypertrophy in endurance athletes. Med Sci Sports Exerc 2010; 42–(5): 915–21.
31. Park EY, Ahn HM, Lee JA, Hong YM. Insertion/deletion polymorphism of angiotensin converting enzyme gene in Korean hypertensive adolescents. Heart Vessels 2009; 24 (3): 193–8.
32. Imbalzano E, Vatrano M, Quartuccio S et al. Clinical impact of angiotensin I converting enzyme polymorphisms in subjects with resistant hypertension. Mol Cell Biochem 2017 Feb 11.
33. Pedrinelli R, Dell'Omo G, Penno G et al. Alpha-adducin and angiotensin-converting enzyme polymorphisms in hypertension: evidence for a joint influence on albuminuria. J Hypertens 2006; 24 (5): 931–7.
34. Parchwani DN, Palandurkar KM, Hema Chandan Kumar D, Patel DJ. Genetic Predisposition to Diabetic Nephropathy: Evidence for a Role of ACE (I/D) Gene Polymorphism in Type 2 Diabetic Population from Kutch Region. Indian J Clin Biochem 2015; 30 (1): 43–54.
35. Ott C, Schwarz T, Hilgers KF et al. Left-ventricular structure and function are influenced by angiotensinogen gene polymorphism (-20 A/C) in young male patients. Am J Hypertens 2007; 20 (9): 974–80.
36. Eliseeva MR, Srozhidinova NZ, Khamidullaeva GA, Abdullaeva GZh. Genetic determinants of cardiovascular remodeling in Uzbek patients with essential hypertension. Ter. Arkhiv. 2009; 81 (1): 64–9. [Russian]
37. Kelly M, Bagnall RD, Peverill RE et al. A polymorphic miR-155 binding site in AGTR1 is associated with cardiac hypertrophy in Friedreich ataxia. J Mol Cell Cardiol 2011; 51 (5): 848–54.
38. Jin Y, Kuznetsova T, Thijs L et al. Association of left ventricular mass with the AGTR1 A1166C polymorphism. Am J Hypertens 2012; 25 (4): 472–8.
39. Buraczynskа M, Ksiazek P, Lopatynski J et al. Association of the reninangiotensin system gene polymorphism with nephropathy in type II diabetes. Polskie archiwum medycyny wewnetrznej 2002; 108 (2): 725–30.
40. Fabris B, Bortoletto M, Candido R et al. Genetic polymorphisms of the renin-angiotensin-aldosterone system and renal insufficiency in essential hypertension. J Hypertens 2005; 23 (2): 309–16.
41. Abd El-Aziz TA, Mohamed RH. Influence of MTHFR C677T gene polymorphism in the development of cardiovascular disease in Egyptian patients with rheumatoid arthritis. Gene 2017; 610: 127–32.
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Авторы
Т.А.Мулерова
ГБОУ ДПО «Новокузнецкий государственный институт усовершенствования врачей» Минздрава России. 654005, Россия, Новокузнецк, пр-т. Строителей, д. 5;
ФГБНУ «НИИ комплексных проблем сердечно-сосудистых заболеваний». 650002, Россия, Кемерово, Сосновый бульвар, д. 6
mulerova-77@mail.ru
Novokuznetsk State Institute for Postgraduate Training of Physicians of the Ministry of Health of the Russian Federation. 654005, Russian Federation, Novokuznetsk, pr-t. Stroitelei, d. 5;
Research Institute for Complex Issues of Cardiovascular Diseases. 650002, Russian Federation, Kemerovo, Sosnovyi bul., d. 6
mulerova-77@mail.ru
ГБОУ ДПО «Новокузнецкий государственный институт усовершенствования врачей» Минздрава России. 654005, Россия, Новокузнецк, пр-т. Строителей, д. 5;
ФГБНУ «НИИ комплексных проблем сердечно-сосудистых заболеваний». 650002, Россия, Кемерово, Сосновый бульвар, д. 6
mulerova-77@mail.ru
________________________________________________
Novokuznetsk State Institute for Postgraduate Training of Physicians of the Ministry of Health of the Russian Federation. 654005, Russian Federation, Novokuznetsk, pr-t. Stroitelei, d. 5;
Research Institute for Complex Issues of Cardiovascular Diseases. 650002, Russian Federation, Kemerovo, Sosnovyi bul., d. 6
mulerova-77@mail.ru
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