Hyperhomocysteinemia An Additional Risk Factor in White Coat Hypertension
The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension an...
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Published in | International Heart Journal Vol. 46; no. 2; pp. 245 - 254 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Japan
International Heart Journal Association
01.03.2005
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Subjects | |
Online Access | Get full text |
ISSN | 1349-2365 1349-3299 |
DOI | 10.1536/ihj.46.245 |
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Abstract | The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension and a daytime ambulatory blood pressure of < 135/85 mmHg. Plasma levels of homocysteine were determined in patients with WCH, hypertension, and normotension (NT). The study group included 100 subjects, 33 with WCH (16 males, 17 females) aged 49.1 ± 1.9; 35 sustained hypertensives (17 males,18 females) aged 48.5 ± 1.7 and 32 normotensive control subjects (15 males, 17 females) aged 48.8 ± 2.2. The subjects were matched for age, gender, and body mass index. Patients with a smoking habit, dyslipidemia, or diabetes mellitus were not included in the study. Homocysteine levels were analyzed by ELISA. Plasma homocysteine levels were significantly higher in the WCH group compared to the controls (12.32 ± 1.07 versus 5.35 ± 1.38 μmol/L; P < 0.001) and the WCH group had significantly lower homocysteine values than the hypertensives (19.03 ± 0.76 μmol/L P < 0.001). Total cholesterol and tri-glycerides were not different among the groups. There were no statistically significant differences in urinary albumin excretion (UAE) or creatinine clearence between the three groups. Hypertensive retinopathy was observed in the WCH group, but was less severe and less frequent compared to HTs. LVMI was greater in the WCH group compared to the NTs, but significantly less than HTs. The data demonstrate that WCH is associated with high levels of homocysteine. The increase in homocysteine level in WCH is not as high as in SHT. Since an elevated plasma homocysteine level is a strong risk factor for coronary artery disease and there was target organ damage in our WCH group, we conclude that WCH should not be considered to be an innocent trait. |
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AbstractList | The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension and a daytime ambulatory blood pressure of < 135/85 mmHg. Plasma levels of homocysteine were determined in patients with WCH, hypertension, and normotension (NT). The study group included 100 subjects, 33 with WCH (16 males, 17 females) aged 49.1 +/- 1.9; 35 sustained hypertensives (17 males,18 females) aged 48.5 +/- 1.7 and 32 normotensive control subjects (15 males, 17 females) aged 48.8 +/- 2.2. The subjects were matched for age, gender, and body mass index. Patients with a smoking habit, dyslipidemia, or diabetes mellitus were not included in the study. Homocysteine levels were analyzed by ELISA. Plasma homocysteine levels were significantly higher in the WCH group compared to the controls (12.32 +/- 1.07 versus 5.35 +/- 1.38 micromol/L; P < 0.001) and the WCH group had significantly lower homocysteine values than the hypertensives (19.03 +/- 0.76 micromol/L P < 0.001). Total cholesterol and tri-glycerides were not different among the groups. There were no statistically significant differences in urinary albumin excretion (UAE) or creatinine clearance between the three groups. Hypertensive retinopathy was observed in the WCH group, but was less severe and less frequent compared to HTs. LVMI was greater in the WCH group compared to the NTs, but significantly less than HTs. The data demonstrate that WCH is associated with high levels of homocysteine. The increase in homocysteine level in WCH is not as high as in SHT. Since an elevated plasma homocysteine level is a strong risk factor for coronary artery disease and there was target organ damage in our WCH group, we conclude that WCH should not be considered to be an innocent trait. The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension and a daytime ambulatory blood pressure of < 135/85 mmHg. Plasma levels of homocysteine were determined in patients with WCH, hypertension, and normotension (NT). The study group included 100 subjects, 33 with WCH (16 males, 17 females) aged 49.1 ± 1.9; 35 sustained hypertensives (17 males,18 females) aged 48.5 ± 1.7 and 32 normotensive control subjects (15 males, 17 females) aged 48.8 ± 2.2. The subjects were matched for age, gender, and body mass index. Patients with a smoking habit, dyslipidemia, or diabetes mellitus were not included in the study. Homocysteine levels were analyzed by ELISA. Plasma homocysteine levels were significantly higher in the WCH group compared to the controls (12.32 ± 1.07 versus 5.35 ± 1.38 μmol/L; P < 0.001) and the WCH group had significantly lower homocysteine values than the hypertensives (19.03 ± 0.76 μmol/L P < 0.001). Total cholesterol and tri-glycerides were not different among the groups. There were no statistically significant differences in urinary albumin excretion (UAE) or creatinine clearence between the three groups. Hypertensive retinopathy was observed in the WCH group, but was less severe and less frequent compared to HTs. LVMI was greater in the WCH group compared to the NTs, but significantly less than HTs. The data demonstrate that WCH is associated with high levels of homocysteine. The increase in homocysteine level in WCH is not as high as in SHT. Since an elevated plasma homocysteine level is a strong risk factor for coronary artery disease and there was target organ damage in our WCH group, we conclude that WCH should not be considered to be an innocent trait. The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension and a daytime ambulatory blood pressure of < 135/85 mmHg. Plasma levels of homocysteine were determined in patients with WCH, hypertension, and normotension (NT). The study group included 100 subjects, 33 with WCH (16 males, 17 females) aged 49.1 +/- 1.9; 35 sustained hypertensives (17 males,18 females) aged 48.5 +/- 1.7 and 32 normotensive control subjects (15 males, 17 females) aged 48.8 +/- 2.2. The subjects were matched for age, gender, and body mass index. Patients with a smoking habit, dyslipidemia, or diabetes mellitus were not included in the study. Homocysteine levels were analyzed by ELISA. Plasma homocysteine levels were significantly higher in the WCH group compared to the controls (12.32 +/- 1.07 versus 5.35 +/- 1.38 micromol/L; P < 0.001) and the WCH group had significantly lower homocysteine values than the hypertensives (19.03 +/- 0.76 micromol/L P < 0.001). Total cholesterol and tri-glycerides were not different among the groups. There were no statistically significant differences in urinary albumin excretion (UAE) or creatinine clearance between the three groups. Hypertensive retinopathy was observed in the WCH group, but was less severe and less frequent compared to HTs. LVMI was greater in the WCH group compared to the NTs, but significantly less than HTs. The data demonstrate that WCH is associated with high levels of homocysteine. The increase in homocysteine level in WCH is not as high as in SHT. Since an elevated plasma homocysteine level is a strong risk factor for coronary artery disease and there was target organ damage in our WCH group, we conclude that WCH should not be considered to be an innocent trait.The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension and a daytime ambulatory blood pressure of < 135/85 mmHg. Plasma levels of homocysteine were determined in patients with WCH, hypertension, and normotension (NT). The study group included 100 subjects, 33 with WCH (16 males, 17 females) aged 49.1 +/- 1.9; 35 sustained hypertensives (17 males,18 females) aged 48.5 +/- 1.7 and 32 normotensive control subjects (15 males, 17 females) aged 48.8 +/- 2.2. The subjects were matched for age, gender, and body mass index. Patients with a smoking habit, dyslipidemia, or diabetes mellitus were not included in the study. Homocysteine levels were analyzed by ELISA. Plasma homocysteine levels were significantly higher in the WCH group compared to the controls (12.32 +/- 1.07 versus 5.35 +/- 1.38 micromol/L; P < 0.001) and the WCH group had significantly lower homocysteine values than the hypertensives (19.03 +/- 0.76 micromol/L P < 0.001). Total cholesterol and tri-glycerides were not different among the groups. There were no statistically significant differences in urinary albumin excretion (UAE) or creatinine clearance between the three groups. Hypertensive retinopathy was observed in the WCH group, but was less severe and less frequent compared to HTs. LVMI was greater in the WCH group compared to the NTs, but significantly less than HTs. The data demonstrate that WCH is associated with high levels of homocysteine. The increase in homocysteine level in WCH is not as high as in SHT. Since an elevated plasma homocysteine level is a strong risk factor for coronary artery disease and there was target organ damage in our WCH group, we conclude that WCH should not be considered to be an innocent trait. |
Author | Ertürk, Nurver Simsek, Gönül Kutlu, Ayse Karter, Yesari Öztürk, Esin Uzun, Hafize Çurgunlu, Asll Erdine, Serap Vehid, Suphi Aydin, Seval |
Author_xml | – sequence: 1 fullname: Çurgunlu, Asll organization: Department of Internal Medicine, Taksim Public Hospital – sequence: 1 fullname: Aydin, Seval organization: Department of Biochemistry, Taksim Public Hospital – sequence: 1 fullname: Ertürk, Nurver organization: Department of Family Medicine, Taksim Public Hospital – sequence: 1 fullname: Vehid, Suphi organization: Department of Public Health, Taksim Public Hospital – sequence: 1 fullname: Uzun, Hafize organization: Department of Biochemistry, Taksim Public Hospital – sequence: 1 fullname: Karter, Yesari organization: Department of Internal Medicine, Taksim Public Hospital – sequence: 1 fullname: Kutlu, Ayse organization: Department of Neurology, Taksim Public Hospital – sequence: 1 fullname: Erdine, Serap organization: Cardiology Institute, Cerrahpasa Medical Faculty, Istanbul University – sequence: 1 fullname: Simsek, Gönül organization: Department of Physiology, Cerrahpasa Medical Faculty – sequence: 1 fullname: Öztürk, Esin organization: Department of Internal Medicine, Taksim Public Hospital |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15876808$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_2478_ahem_2021_0002 crossref_primary_10_1097_MBP_0000000000000171 crossref_primary_10_1536_ihj_49_671 crossref_primary_10_1038_sj_jhh_1002325 crossref_primary_10_1536_ihj_49_87 crossref_primary_10_1536_ihj_48_605 crossref_primary_10_2169_internalmedicine_47_0787 crossref_primary_10_1097_HJH_0000000000000416 crossref_primary_10_1080_10641960802251958 crossref_primary_10_1111_1440_1681_12114 crossref_primary_10_1017_S0029665109991728 crossref_primary_10_1111_j_1440_1681_2008_04886_x crossref_primary_10_1007_s11010_007_9434_5 crossref_primary_10_3109_08037051_2011_575577 crossref_primary_10_1536_ihj_49_449 crossref_primary_10_1097_MD_0000000000016085 crossref_primary_10_1111_j_1742_1241_2006_00959_x crossref_primary_10_5662_wjm_v4_i3_144 |
Cites_doi | 10.1161/01.CIR.90.5.2291 10.1038/sj.jhh.1000917 10.1016/S0735-1097(01)01492-9 10.1016/S0735-1097(02)01717-5 10.1161/01.HYP.16.6.617 10.1038/sj.jhh.1001524 10.1161/01.CIR.96.6.1745 10.1001/jama.274.19.1526 10.1161/01.CIR.0000019737.87850.5A 10.1016/0002-9149(86)90771-X 10.1161/01.HYP.0000101690.58391.13 10.1161/01.HYP.24.1.101 10.1055/s-2000-8096 10.1016/S0161-6420(82)34664-3 10.1515/CCLM.2003.216 10.1136/bmj.322.7285.531 10.1016/0021-9150(89)90118-4 10.1001/jama.261.6.873 10.1016/S0895-7061(00)01321-2 10.1161/01.HYP.21.6.836 10.1001/jama.1988.03720020027031 10.1093/ajh/5.4.207 10.1136/bmj.320.7242.1128 10.1016/S0895-7061(02)02984-9 10.1093/aje/kwf157 10.1055/s-2000-8472 10.1016/0895-7061(96)00203-8 10.1177/0091270003258190 10.1007/s003950070012 |
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References | 19. Ramsay L, Williams B, Johnston G, et al. Guidelines for management of hypertension: report of the third working party of the British Hypertension Society. J Hum Hypertens 1999; 13: 569-92. (Review) 28. Rodrigo R, Passalacqua W, Araya J, Orellana M, Rivera G. Homocysteine and essential hypertension. J Clin Pharmacol 2003; 43: 1299-306. (Review) 5. Hoegholm A, Bang LE, Kristensen KS, Nielsen JW, Holm J. Microalbuminuria in 411 untreated individuals with established hypertension, white coat hypertension, and normotension. Hypertension 1994; 24: 101-5. 23. Walsh JB. Hypertensive retinopathy. Description, classification, and prognosis. Ophthalmology 1982; 89: 1127-31. 13. van Guldener C, Stehouwer CD. Hyperhomocysteinemia, vascular pathology, and endothelial dysfunction. Semin Tromb Hemost 2000; 26: 281-9. (Review) 12. Nygard O, Vollset SE, Refsum H, et al. Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study. JAMA 1995; 274: 1526-33. 27. Boers GH. Mild hyperhomocysteinemia is an independent risk factor of arterial vascular disease. Semin Thromb Hemost 2000; 26: 291-5. (Review) 20. Guidelines Subcommittee. 1999 World Health Organization - International Society of Hypertension Guidelines for the Management of Hypertension. J Hypertens 1999; 17: 151-83. 4. Cardillo C, De Felice F, Campia U, Folli G. Psychological reactivity and cardiac end-organ changes in white coat hypertension. Hypertension 1993; 21: 836-44. 25. Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left venticular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57: 450-8. 16. Lip GY, Edmunds E, Martin SC, Jones AF, Blann AD, Beevers DG. A pilot study of homocyst(e)ine levels in essential hypertension: relationship to von Willebrand factor, an index of endothelial damage. Am J Hypertens 2001; 14: 627-31. 33. Kahleova R, Palyzova D, Zvara K, et al. Essential hypertension in adolescents: association with insulin resistance and with metabolism of homocysteine and vitamins. Am J Hypertens 2002; 15: 857-64. 9. Lim U, Cassano PA. Homocysteine and blood pressure in the Third National Health and Nutrition Examination Survey, 1988-1994. Am J Epidemiol 2002; 156: 1105-13. 2. Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension? JAMA 1988; 259: 225-8. 26. Sainani GS, Sainani R. Homocysteine and its role in the pathogenesis of atherosclerotic vascular disease. J Assoc Physicians India 2002; 50 (Suppl): 5-8. 14. Virdis A, Ghiadoni L, Cardinal H, et al. Mechanisms responsible for endothelial dysfunction induced by fasting hyperhomocysteinemia in normotensive subjects and patients with essential hypertension. J Am Coll Cardiol 2001; 38: 1106-15. 24. Ferrier KE, Muhlmann MH, Baguet JP, et al. Intensive cholesterol reduction lowers blood pressure and large artery stiffness in isolated systolic hypertension. J Am Coll Cardiol 2002; 39: 1020-5. 22. O'Brien E, Coats A, Owens P, et al. Use and interpretation of ambulatory blood pressure monitoring: recommendations of the British Hypertension Society. BMJ 2000; 320: 1128-34. (Review) 30. Stehouwer CD, van Guldener C. Does homocysteine cause hypertension? Clin Chem Lab Med 2003; 41: 1408-11. (Review) 3. White WB, Schulman P, McCabe EJ, Dey HM. Average daily blood pressure, not office blood pressure, determines cardiac function in patients with hypertension. JAMA 1989; 261: 873-7. 10. Araki A, Sako Y, Fukusimma Y, Matsumoto M, Asada T, Kita T. Plasma sulfhydryl-containing amino acids in patients with cerebral infarction and in hypertensive subjects. Atherosclerosis 1989; 79: 139-46. 17. Pierdomenico SD, Bucci A, Lapenna D, et al. Circulating homocysteine levels in sustained and white coat hypertension. J Hum Hypertens 2003; 17: 165-70. 6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period: a population-based study of elderly men. Circulation 2002; 106: 63-8. 1. Soma J, Aakhus S, Dahl K, et al. Hemodynamics in white coat hypertension compared to ambulatory hypertension and normotension. Am J Hypertens 1996; 9: 1090-8. 11. Sutton-Tyrrell K, Bostom A, Sefhub J, Zeigler-Johnson C. High homocysteine levels are independently related to isolated systolic hypertension in older adults. Circulation 1997; 96: 1745-9. 21. O'Brien E, Waeber B, Parati G, Staessen J, Myers MJ. Blood pressure measuring devices: recommendations of the European Society of Hypertension. BMJ 2001; 322: 531-6. 29. Sundstrom J, Sullivan L, D'Agostino RB, et al. Plasma homocysteine, hypertension incidence, and blood pressure tracking: the Framingham Heart Study. Hypertension 2003; 42: 1100-5. 34. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period: a population-based study of elderly men. Circulation 2002; 106: 63-8. 31. Pierdomenico SD, Bucci A, Lapenna D, et al. Circulating homocysteine levels in sustained and white coat hypertension. J Hum Hypertens 2003; 17: 165-70. 8. Weber MA, Neutel JM, Smith DH, Graettinger WF. Diagnosis of mild hypertension by ambulatory blood pressure monitoring. Circulation 1994; 90: 2291-8. 15. Maxwell SR. Coronary artery disease-free radical damage, antioxidant protection and the role of homocysteine. Basic Res Cardiol 2000; 95 Suppl 1: 165-71. 32. Brunelli T, Pepe G, Marcucci R, et al. Comparison of three methods for total homocysteine plasma determination. Clin Lab 2001; 47: 393-7. 7. Julius S, Mejia A, Jones K, et al. ‘White coat’ versus ‘sustained’ borderline hypertension in Tecumseh, Michigan. Hypertension 1990; 16: 617-23. 18. American Society of Hypertension. Recommendations for routine blood pressure measurement by indirect cuff sphygmomanometry. Am J Hypertens 1992; 5: 207-9. 23 24 25 26 27 28 29 (22) 1982; 89 (7) 1994; 90 (9) 1989; 79 30 31 10 32 11 33 12 13 14 15 16 17 18 19 (5) 1994; 24 1 3 8 (2) 1988; 259 (4) 1993; 21 20 (6) 1990; 16 21 |
References_xml | – reference: 12. Nygard O, Vollset SE, Refsum H, et al. Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study. JAMA 1995; 274: 1526-33. – reference: 21. O'Brien E, Waeber B, Parati G, Staessen J, Myers MJ. Blood pressure measuring devices: recommendations of the European Society of Hypertension. BMJ 2001; 322: 531-6. – reference: 7. Julius S, Mejia A, Jones K, et al. ‘White coat’ versus ‘sustained’ borderline hypertension in Tecumseh, Michigan. Hypertension 1990; 16: 617-23. – reference: 18. American Society of Hypertension. Recommendations for routine blood pressure measurement by indirect cuff sphygmomanometry. Am J Hypertens 1992; 5: 207-9. – reference: 3. White WB, Schulman P, McCabe EJ, Dey HM. Average daily blood pressure, not office blood pressure, determines cardiac function in patients with hypertension. JAMA 1989; 261: 873-7. – reference: 6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period: a population-based study of elderly men. Circulation 2002; 106: 63-8. – reference: 2. Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension? JAMA 1988; 259: 225-8. – reference: 31. Pierdomenico SD, Bucci A, Lapenna D, et al. Circulating homocysteine levels in sustained and white coat hypertension. J Hum Hypertens 2003; 17: 165-70. – reference: 33. Kahleova R, Palyzova D, Zvara K, et al. Essential hypertension in adolescents: association with insulin resistance and with metabolism of homocysteine and vitamins. Am J Hypertens 2002; 15: 857-64. – reference: 23. Walsh JB. Hypertensive retinopathy. Description, classification, and prognosis. Ophthalmology 1982; 89: 1127-31. – reference: 26. Sainani GS, Sainani R. Homocysteine and its role in the pathogenesis of atherosclerotic vascular disease. J Assoc Physicians India 2002; 50 (Suppl): 5-8. – reference: 4. Cardillo C, De Felice F, Campia U, Folli G. Psychological reactivity and cardiac end-organ changes in white coat hypertension. Hypertension 1993; 21: 836-44. – reference: 27. Boers GH. Mild hyperhomocysteinemia is an independent risk factor of arterial vascular disease. Semin Thromb Hemost 2000; 26: 291-5. (Review) – reference: 15. Maxwell SR. Coronary artery disease-free radical damage, antioxidant protection and the role of homocysteine. Basic Res Cardiol 2000; 95 Suppl 1: 165-71. – reference: 29. Sundstrom J, Sullivan L, D'Agostino RB, et al. Plasma homocysteine, hypertension incidence, and blood pressure tracking: the Framingham Heart Study. Hypertension 2003; 42: 1100-5. – reference: 5. Hoegholm A, Bang LE, Kristensen KS, Nielsen JW, Holm J. Microalbuminuria in 411 untreated individuals with established hypertension, white coat hypertension, and normotension. Hypertension 1994; 24: 101-5. – reference: 14. Virdis A, Ghiadoni L, Cardinal H, et al. Mechanisms responsible for endothelial dysfunction induced by fasting hyperhomocysteinemia in normotensive subjects and patients with essential hypertension. J Am Coll Cardiol 2001; 38: 1106-15. – reference: 19. Ramsay L, Williams B, Johnston G, et al. Guidelines for management of hypertension: report of the third working party of the British Hypertension Society. J Hum Hypertens 1999; 13: 569-92. (Review) – reference: 22. O'Brien E, Coats A, Owens P, et al. Use and interpretation of ambulatory blood pressure monitoring: recommendations of the British Hypertension Society. BMJ 2000; 320: 1128-34. (Review) – reference: 17. Pierdomenico SD, Bucci A, Lapenna D, et al. Circulating homocysteine levels in sustained and white coat hypertension. J Hum Hypertens 2003; 17: 165-70. – reference: 32. Brunelli T, Pepe G, Marcucci R, et al. Comparison of three methods for total homocysteine plasma determination. Clin Lab 2001; 47: 393-7. – reference: 30. Stehouwer CD, van Guldener C. Does homocysteine cause hypertension? Clin Chem Lab Med 2003; 41: 1408-11. (Review) – reference: 25. Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left venticular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57: 450-8. – reference: 16. Lip GY, Edmunds E, Martin SC, Jones AF, Blann AD, Beevers DG. A pilot study of homocyst(e)ine levels in essential hypertension: relationship to von Willebrand factor, an index of endothelial damage. Am J Hypertens 2001; 14: 627-31. – reference: 24. Ferrier KE, Muhlmann MH, Baguet JP, et al. Intensive cholesterol reduction lowers blood pressure and large artery stiffness in isolated systolic hypertension. J Am Coll Cardiol 2002; 39: 1020-5. – reference: 11. Sutton-Tyrrell K, Bostom A, Sefhub J, Zeigler-Johnson C. High homocysteine levels are independently related to isolated systolic hypertension in older adults. Circulation 1997; 96: 1745-9. – reference: 13. van Guldener C, Stehouwer CD. Hyperhomocysteinemia, vascular pathology, and endothelial dysfunction. Semin Tromb Hemost 2000; 26: 281-9. (Review) – reference: 1. Soma J, Aakhus S, Dahl K, et al. Hemodynamics in white coat hypertension compared to ambulatory hypertension and normotension. Am J Hypertens 1996; 9: 1090-8. – reference: 34. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period: a population-based study of elderly men. Circulation 2002; 106: 63-8. – reference: 8. Weber MA, Neutel JM, Smith DH, Graettinger WF. Diagnosis of mild hypertension by ambulatory blood pressure monitoring. Circulation 1994; 90: 2291-8. – reference: 10. Araki A, Sako Y, Fukusimma Y, Matsumoto M, Asada T, Kita T. Plasma sulfhydryl-containing amino acids in patients with cerebral infarction and in hypertensive subjects. Atherosclerosis 1989; 79: 139-46. – reference: 20. Guidelines Subcommittee. 1999 World Health Organization - International Society of Hypertension Guidelines for the Management of Hypertension. J Hypertens 1999; 17: 151-83. – reference: 28. Rodrigo R, Passalacqua W, Araya J, Orellana M, Rivera G. Homocysteine and essential hypertension. J Clin Pharmacol 2003; 43: 1299-306. (Review) – reference: 9. Lim U, Cassano PA. Homocysteine and blood pressure in the Third National Health and Nutrition Examination Survey, 1988-1994. Am J Epidemiol 2002; 156: 1105-13. – volume: 90 start-page: 2291 issn: 0009-7322 year: 1994 ident: 7 publication-title: Circulation doi: 10.1161/01.CIR.90.5.2291 – ident: 18 doi: 10.1038/sj.jhh.1000917 – ident: 13 doi: 10.1016/S0735-1097(01)01492-9 – ident: 23 doi: 10.1016/S0735-1097(02)01717-5 – volume: 16 start-page: 617 issn: 0194-911X year: 1990 ident: 6 publication-title: Hypertension doi: 10.1161/01.HYP.16.6.617 – ident: 30 doi: 10.1038/sj.jhh.1001524 – ident: 10 doi: 10.1161/01.CIR.96.6.1745 – ident: 11 doi: 10.1001/jama.274.19.1526 – ident: 33 doi: 10.1161/01.CIR.0000019737.87850.5A – ident: 31 – ident: 24 doi: 10.1016/0002-9149(86)90771-X – ident: 28 doi: 10.1161/01.HYP.0000101690.58391.13 – volume: 24 start-page: 101 issn: 0194-911X year: 1994 ident: 5 publication-title: Hypertension doi: 10.1161/01.HYP.24.1.101 – ident: 26 doi: 10.1055/s-2000-8096 – volume: 89 start-page: 1127 issn: 0161-6420 year: 1982 ident: 22 publication-title: Ophthalmology doi: 10.1016/S0161-6420(82)34664-3 – ident: 29 doi: 10.1515/CCLM.2003.216 – ident: 20 doi: 10.1136/bmj.322.7285.531 – volume: 79 start-page: 139 issn: 0021-9150 year: 1989 ident: 9 publication-title: Atherosclerosis doi: 10.1016/0021-9150(89)90118-4 – ident: 3 doi: 10.1001/jama.261.6.873 – ident: 15 doi: 10.1016/S0895-7061(00)01321-2 – volume: 21 start-page: 836 issn: 0194-911X year: 1993 ident: 4 publication-title: Hypertension doi: 10.1161/01.HYP.21.6.836 – volume: 259 start-page: 225 issn: 0098-7484 year: 1988 ident: 2 publication-title: JAMA The Journal of the American Medical Association doi: 10.1001/jama.1988.03720020027031 – ident: 17 doi: 10.1093/ajh/5.4.207 – ident: 19 – ident: 21 doi: 10.1136/bmj.320.7242.1128 – ident: 32 doi: 10.1016/S0895-7061(02)02984-9 – ident: 8 doi: 10.1093/aje/kwf157 – ident: 12 doi: 10.1055/s-2000-8472 – ident: 1 doi: 10.1016/0895-7061(96)00203-8 – ident: 27 doi: 10.1177/0091270003258190 – ident: 14 doi: 10.1007/s003950070012 – ident: 16 doi: 10.1038/sj.jhh.1001524 – ident: 25 |
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Snippet | The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat... |
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SubjectTerms | Blood Pressure Monitoring, Ambulatory Body Mass Index Coronary Artery Disease - complications Endothelium, Vascular - pathology Female Homocysteine Homocysteine - blood Humans Hyperhomocysteinemia - complications Hypertension - etiology Male Middle Aged Office Visits Retinal Diseases - etiology Risk Factors Smoking Target organ damage White coat hypertension |
Subtitle | An Additional Risk Factor in White Coat Hypertension |
Title | Hyperhomocysteinemia |
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