- Email: [email protected]
Diagnostic evaluation
Journal of the American Society of Hypertension 8(9) (2014) 680–681
American Society of Hypertension Self-Assessment Guide
Diagnostic evaluation Classification of hypertension Barry J. Materson, MD, MBA To purchase and complete the ASH Hypertension Self-Assessments please use the following link: https://secure.ptcny.com/webtest
There is no generally accepted definition of hypertension. Attempts to define it have often included the concept of hypertension as a disease with blood pressure elevation as a symptom, that the higher the pressure above 115 mm Hg systolic and the greater the duration of that elevation, the higher the risk of cardiovascular, renal, and cerebral target organ events, and that reducing the blood pressure conveys a reduction in target organ damage. Many definitions attempt to coordinate both the blood pressure level and the patient’s cardiovascular risk factors.1–5 Blood pressure is traditionally estimated by the indirect assessment of intraarterial pressure. This demands that personnel be appropriately trained, instruments be calibrated, and that automated devices be validated and intermittently calibrated. In general, devices that estimate intraarterial pressure from the finger or wrist should not be used. Equally important is that the patients be seated with back supported, feet on the floor (legs not crossed) arm at heart level, and the patient rested for a minimum of 5 minutes. The American Heart Association and Joint National Committee (JNC) 7 have published the standards for blood pressure determination.1,6 Clinicians must be aware that automated devices will produce visible readouts that may be interpreted as accurate even if the patients were not positioned correctly. This could be as dangerous as accepting a laboratory test value without validation. Hypertension may be systolic (isolated systolic hypertension), diastolic (isolated diastolic hypertension), or systolic– diastolic. Systolic hypertension is uncommon in young This article is part of the American Society of Hypertension Self-Assessment Guide series. For other articles in this series, visit the JASH home page at www.ashjournal.com. *Corresponding author: Barry J. Materson, MD, MBA, University of Miami Miller School of Medicine (M-854), Post Office Box 016960, Physical location: CRB 935, Miami, FL 33101. Tel: (305) 243-7221; Fax: (305) 243-9902. E-mail: [email protected]
individuals but becomes increasingly common after age 50. After 75 years of age, the prevalence is about 23%.7,8 Systolic hypertension reflects a decrease in major vascular compliance and loss of elasticity due to arteriosclerotic disease. It is not at all ‘‘natural’’ and conveys an increased risk of stroke, decreased cognitive function, and other target organ damage. Systolic blood pressure tends to be highly variable and is sensitive to changes in sympathetic nervous system activity.9 On occasion, relief of a cause of stress to a patient may be more appropriate than adjusting drug therapy.10,11 Diastolic hypertension is more common in younger individuals. It clearly conveys risk of future target organ damage, but the decision to treat younger subjects with other than lifestyle modification must be predicated on their cardiovascular risk factors. Multiple readings over up to 3 months may be necessary to establish that the diastolic pressure is consistently elevated. If untreated, many of these patients will go on to develop systolic–diastolic hypertension.8 Systolic–diastolic hypertension is by far the most common; it is defined by having both the systolic and diastolic blood pressure above the established normal levels. Normal values are established by examination of epidemiological data, data from the life insurance industry and from observation of the risk of target organ damage from controlled clinical trials. The values are agreed upon by committees or national societies and are not always in total agreement. Such values are always arbitrary because there are no natural biological breakpoints and individual variability is high. Of particular concern are the groups of patients with coexisting risk factors such as diabetes mellitus, chronic kidney disease, and established coronary heart disease. At the time of this writing, systolic blood pressure <120 mm Hg and diastolic pressure <80 mm Hg define normal. JNC 7 defined blood pressure from 120–139 mm Hg systolic and 81–89 mm Hg diastolic as ‘‘prehypertension’’. The intent was to recognize that prehypertension carried the risk of developing fixed hypertension and a low but
1933-1711/$ - see front matter Ó 2014 American Society of Hypertension. All rights reserved. http://dx.doi.org/10.1016/j.jash.2014.07.031
B.J. Materson / Journal of the American Society of Hypertension 8(9) (2014) 680–681
higher risk of target organ damage. The range from 130–129 and/or 85–89 mm Hg carries increased risk that can be reduced by single drug therapy in a group of subjects that had one or more cardiovascular risk factors.12 The European societies continue to refer to this range as ‘‘high normal’’. JNC 7 classified the range of 140–159/90–99 as stage 1 hypertension and the range of 160/100 mm Hg as stage 2 hypertension. The committee reasoned that all stage 2 hypertensive patients should be treated and that there was no value to defining higher pressure levels. Note that when blood pressure is determined by repeated home readings or ambulatory blood pressure monitoring (ABPM), the definition values should be reduced by 5/5 mm Hg. Goal blood pressures had been set arbitrarily at <130/80 mm Hg for patients with diabetes mellitus, chronic kidney disease, and established cardiovascular disease. The evidence base is not clearly established and these goals have been challenged because solid evidence from randomized prospective trials does not exist. As of May 2014, generally accepted definitive goals have not yet been established. ‘‘White coat’’ or clinic hypertension is defined by persistently elevated readings in the office setting and persistently normal readings at home or by ABPM. It is not benign in that there is an increased risk for evolving into fixed hypertension and, over time, may convey an increased risk of stroke.13 ‘‘Masked hypertension’’ refers to elevated pressures obtained at home or by ABPM despite persistently normal office pressures. Both masked hypertension and loss of the normal reduction of blood pressure during sleep (dipping) confer an increased risk of target organ damage.14 Two new guidelines have been published.15,16 The American Heart Association and the American Society of Hypertension may team to develop a new, definitive set of guidelines based on the best evidence then available. The goal is 2015. Suggested References 1. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al; and the National High Blood Pressure Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7— Complete Version). Hypertension 2003;42:1206–52. 2. Materson BJ. Commentary on ‘‘Expanding the definition and classification of hypertension’’. J Clin Hypertens 2005;7:540–1. 3. Giles TD, Materson BJ, Cohn JN, Kostis JB. Definition and classification of hypertension: an update. J Clin Hypertens 2009;11:611–4.
681
4. Izzo JL Jr, Giles TD, Materson BJ. Chapter C107: defining the syndrome of hypertension. In: Izzo JL Jr, Black HR, editors. Hypertension primer. 4th ed. Lippincott: Williams & Wilkins, Philadelphia; 2008. P. 351–5. 5. Giles TD, Materson BJ. Chapter 4. Defining hypertension. In Black HR, Elliott WJ (Eds): Hypertension: A companion to Braunwald’s heart disease, Second Edition. Elsevier, Philadelphia, (scheduled publication late 2011 or 2012). 6. Materson BJ, Chandra S. Inconsistency of intra-arterial pressure estimation. Therapy 2011;8:215–25. 7. Vardan S, Mookherjee S. Perspectives on isolated systolic hypertension in elderly patients. Arch Fam Med 2000;9:319–23. 8. Franklin SS, Jacobs MJ, Wong ND, L’Italien GJ, Lapuerta P. Predominance of isolated systolic hypertension among middle-age and elderly US hypertensive: Analysis based on National Health and Nutrition Examination Survey (NHANES) III. Hypertension 2001;37: 869–74. 9. Franklin SS, Mitchell GF. Aging, arterial function, and systolic hypertension. In: Izzo JL Jr, Sica DA, Black HR, editors. Hypertenssion primer. 4th ed. Philadelphia: Lippincott Wiliams & Wilkins; 2008. P. 144–8. 10. Materson BJ. Easily ‘‘curable’’ anxiety-induced hypertension. J Clin Hypertens 2009;11:646–7. 11. Pickering TG, Chernow L. Paroxysmal hypertension: the role of stress and psychological factors. J Clin Hypertens 2008;10:575–81. 12. Julius S, Nesbitt SD, Egan BM, Weber MA, Michelson EL, Kaciroti N, et al. Trial of Preventing Hypertension (TROPHY) Study Investigators. Feasibility of treating prehypertension with an angiotensinreceptor blocker. NEJM 2006;354:1685–97. 13. Pickering TG, White WB. When and how to use self (home) and ambulatory blood pressure monitoring. J Am Soc Hypertens 2008;2:119–24. 14. Pickering TG, Eguchi K, Kario K. Maksed hypertension: a review. Hypertens Res 2007;30:479–88. 15. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). 2013 ESH/ESC guidelines for the management of arterial hypertension. J Hypertens 2013;31:1281–357. 16. Weber MA, Schiffrin EL, White WB, Mann S, Lindholm LH, Kenerson JG, et al. Clinical practice guidelines for the management of hypertension in the community. A statement by the American Society of Hypertension and the International Society of Hypertension. J Clin Hypertens 2014;16:14–26.
American Society of Hypertension Self-Assessment Guide
Diagnostic evaluation Classification of hypertension Barry J. Materson, MD, MBA To purchase and complete the ASH Hypertension Self-Assessments please use the following link: https://secure.ptcny.com/webtest
There is no generally accepted definition of hypertension. Attempts to define it have often included the concept of hypertension as a disease with blood pressure elevation as a symptom, that the higher the pressure above 115 mm Hg systolic and the greater the duration of that elevation, the higher the risk of cardiovascular, renal, and cerebral target organ events, and that reducing the blood pressure conveys a reduction in target organ damage. Many definitions attempt to coordinate both the blood pressure level and the patient’s cardiovascular risk factors.1–5 Blood pressure is traditionally estimated by the indirect assessment of intraarterial pressure. This demands that personnel be appropriately trained, instruments be calibrated, and that automated devices be validated and intermittently calibrated. In general, devices that estimate intraarterial pressure from the finger or wrist should not be used. Equally important is that the patients be seated with back supported, feet on the floor (legs not crossed) arm at heart level, and the patient rested for a minimum of 5 minutes. The American Heart Association and Joint National Committee (JNC) 7 have published the standards for blood pressure determination.1,6 Clinicians must be aware that automated devices will produce visible readouts that may be interpreted as accurate even if the patients were not positioned correctly. This could be as dangerous as accepting a laboratory test value without validation. Hypertension may be systolic (isolated systolic hypertension), diastolic (isolated diastolic hypertension), or systolic– diastolic. Systolic hypertension is uncommon in young This article is part of the American Society of Hypertension Self-Assessment Guide series. For other articles in this series, visit the JASH home page at www.ashjournal.com. *Corresponding author: Barry J. Materson, MD, MBA, University of Miami Miller School of Medicine (M-854), Post Office Box 016960, Physical location: CRB 935, Miami, FL 33101. Tel: (305) 243-7221; Fax: (305) 243-9902. E-mail: [email protected]
individuals but becomes increasingly common after age 50. After 75 years of age, the prevalence is about 23%.7,8 Systolic hypertension reflects a decrease in major vascular compliance and loss of elasticity due to arteriosclerotic disease. It is not at all ‘‘natural’’ and conveys an increased risk of stroke, decreased cognitive function, and other target organ damage. Systolic blood pressure tends to be highly variable and is sensitive to changes in sympathetic nervous system activity.9 On occasion, relief of a cause of stress to a patient may be more appropriate than adjusting drug therapy.10,11 Diastolic hypertension is more common in younger individuals. It clearly conveys risk of future target organ damage, but the decision to treat younger subjects with other than lifestyle modification must be predicated on their cardiovascular risk factors. Multiple readings over up to 3 months may be necessary to establish that the diastolic pressure is consistently elevated. If untreated, many of these patients will go on to develop systolic–diastolic hypertension.8 Systolic–diastolic hypertension is by far the most common; it is defined by having both the systolic and diastolic blood pressure above the established normal levels. Normal values are established by examination of epidemiological data, data from the life insurance industry and from observation of the risk of target organ damage from controlled clinical trials. The values are agreed upon by committees or national societies and are not always in total agreement. Such values are always arbitrary because there are no natural biological breakpoints and individual variability is high. Of particular concern are the groups of patients with coexisting risk factors such as diabetes mellitus, chronic kidney disease, and established coronary heart disease. At the time of this writing, systolic blood pressure <120 mm Hg and diastolic pressure <80 mm Hg define normal. JNC 7 defined blood pressure from 120–139 mm Hg systolic and 81–89 mm Hg diastolic as ‘‘prehypertension’’. The intent was to recognize that prehypertension carried the risk of developing fixed hypertension and a low but
1933-1711/$ - see front matter Ó 2014 American Society of Hypertension. All rights reserved. http://dx.doi.org/10.1016/j.jash.2014.07.031
B.J. Materson / Journal of the American Society of Hypertension 8(9) (2014) 680–681
higher risk of target organ damage. The range from 130–129 and/or 85–89 mm Hg carries increased risk that can be reduced by single drug therapy in a group of subjects that had one or more cardiovascular risk factors.12 The European societies continue to refer to this range as ‘‘high normal’’. JNC 7 classified the range of 140–159/90–99 as stage 1 hypertension and the range of 160/100 mm Hg as stage 2 hypertension. The committee reasoned that all stage 2 hypertensive patients should be treated and that there was no value to defining higher pressure levels. Note that when blood pressure is determined by repeated home readings or ambulatory blood pressure monitoring (ABPM), the definition values should be reduced by 5/5 mm Hg. Goal blood pressures had been set arbitrarily at <130/80 mm Hg for patients with diabetes mellitus, chronic kidney disease, and established cardiovascular disease. The evidence base is not clearly established and these goals have been challenged because solid evidence from randomized prospective trials does not exist. As of May 2014, generally accepted definitive goals have not yet been established. ‘‘White coat’’ or clinic hypertension is defined by persistently elevated readings in the office setting and persistently normal readings at home or by ABPM. It is not benign in that there is an increased risk for evolving into fixed hypertension and, over time, may convey an increased risk of stroke.13 ‘‘Masked hypertension’’ refers to elevated pressures obtained at home or by ABPM despite persistently normal office pressures. Both masked hypertension and loss of the normal reduction of blood pressure during sleep (dipping) confer an increased risk of target organ damage.14 Two new guidelines have been published.15,16 The American Heart Association and the American Society of Hypertension may team to develop a new, definitive set of guidelines based on the best evidence then available. The goal is 2015. Suggested References 1. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al; and the National High Blood Pressure Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7— Complete Version). Hypertension 2003;42:1206–52. 2. Materson BJ. Commentary on ‘‘Expanding the definition and classification of hypertension’’. J Clin Hypertens 2005;7:540–1. 3. Giles TD, Materson BJ, Cohn JN, Kostis JB. Definition and classification of hypertension: an update. J Clin Hypertens 2009;11:611–4.
681
4. Izzo JL Jr, Giles TD, Materson BJ. Chapter C107: defining the syndrome of hypertension. In: Izzo JL Jr, Black HR, editors. Hypertension primer. 4th ed. Lippincott: Williams & Wilkins, Philadelphia; 2008. P. 351–5. 5. Giles TD, Materson BJ. Chapter 4. Defining hypertension. In Black HR, Elliott WJ (Eds): Hypertension: A companion to Braunwald’s heart disease, Second Edition. Elsevier, Philadelphia, (scheduled publication late 2011 or 2012). 6. Materson BJ, Chandra S. Inconsistency of intra-arterial pressure estimation. Therapy 2011;8:215–25. 7. Vardan S, Mookherjee S. Perspectives on isolated systolic hypertension in elderly patients. Arch Fam Med 2000;9:319–23. 8. Franklin SS, Jacobs MJ, Wong ND, L’Italien GJ, Lapuerta P. Predominance of isolated systolic hypertension among middle-age and elderly US hypertensive: Analysis based on National Health and Nutrition Examination Survey (NHANES) III. Hypertension 2001;37: 869–74. 9. Franklin SS, Mitchell GF. Aging, arterial function, and systolic hypertension. In: Izzo JL Jr, Sica DA, Black HR, editors. Hypertenssion primer. 4th ed. Philadelphia: Lippincott Wiliams & Wilkins; 2008. P. 144–8. 10. Materson BJ. Easily ‘‘curable’’ anxiety-induced hypertension. J Clin Hypertens 2009;11:646–7. 11. Pickering TG, Chernow L. Paroxysmal hypertension: the role of stress and psychological factors. J Clin Hypertens 2008;10:575–81. 12. Julius S, Nesbitt SD, Egan BM, Weber MA, Michelson EL, Kaciroti N, et al. Trial of Preventing Hypertension (TROPHY) Study Investigators. Feasibility of treating prehypertension with an angiotensinreceptor blocker. NEJM 2006;354:1685–97. 13. Pickering TG, White WB. When and how to use self (home) and ambulatory blood pressure monitoring. J Am Soc Hypertens 2008;2:119–24. 14. Pickering TG, Eguchi K, Kario K. Maksed hypertension: a review. Hypertens Res 2007;30:479–88. 15. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). 2013 ESH/ESC guidelines for the management of arterial hypertension. J Hypertens 2013;31:1281–357. 16. Weber MA, Schiffrin EL, White WB, Mann S, Lindholm LH, Kenerson JG, et al. Clinical practice guidelines for the management of hypertension in the community. A statement by the American Society of Hypertension and the International Society of Hypertension. J Clin Hypertens 2014;16:14–26.