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(Hypertension. 1996;28:719-724.)
© 1996 American Heart Association, Inc.
Articles |
A New Classification Scheme for Hypertension Based on Relative and Absolute Risk With Implications for Treatment and Reimbursement
the Department of Preventive Medicine, Rush–Presbyterian–St Luke's Medical Center, Rush Medical College of Rush University, Chicago, Ill.
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Abstract |
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Top
Abstract
IntroductionClassification schemes for hypertension are necessary. They provide us with definitions for when hypertension begins and help us to assess risk, determine prognosis, and guide management. Systems in current use rely on either the level of blood pressure (diastolic, systolic, or both) and classify patients based on the level of relative risk (the proportional likelihood of cardiovascular events occurring as blood pressure rises), absolute risk (the actual odds that a patient or a population will develop an event), or both. Absolute risk reflects the sum of all the factors that contribute to the likelihood that a patient will experience cardiovascular disease. The system we propose stages hypertensive individuals on the basis of blood pressure level (as does the Fifth Joint National Committee report on the detection, evaluation, and treatment of high blood pressure [JNC-V] and the World Health Organization/International Society of Hypertension guidelines) but uses different levels for each stage than do the previous systems and then modifies the numerical stage with the subscript "c" for complicated (when target-organ damage and/or other cardiovascular risk factors are present) or "u" for uncomplicated (when they are absent). The data obtained from a complete medical history and physical examination and a few inexpensive laboratory tests provide the information a provider needs to classify an individual as being complicated or uncomplicated. This system also provides a guide to treatment, as drug therapy would be used sooner in individuals with complicated hypertension, and we propose that compensation for providers be higher when they are caring for a patient with complicated rather than uncomplicated hypertension.
Key Words: blood pressure classification • risk assessment
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Introduction |
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The objective of defining and classifying hypertension is not simply to ascertain when hypertension starts and normotension ends. Classification schemes are necessary because they provide us with definitions as to when hypertension begins and help us assess risk, determine prognosis, and ascertain when and how aggressively to treat. If clinicians are better able to select individuals at high risk, their therapeutic efforts to prevent complications are much more likely to be effective and spare those at low risk from the potential harm of unnecessary or overaggressive therapy.1
The ideal classification scheme should be simple but comprehensive. It should identify those individuals at high risk and provide a guide to management. Since hypertension is both a disease (a disturbance in normal physiology) and a risk factor (a characteristic that increases the likelihood that an individual will develop a disease), the scheme should provide a guide to prognosis and help identify people who can expect to benefit most from treatment—an especially valuable feature from medical and economic perspectives.2
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Current and Previous Classification Schemes for Hypertension |
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There are four basic ways to classify hypertensive individuals. The first uses only the level of BP—DBP, SBP, or both. Such a system is based on the increase in the relative risk (the proportional likelihood) of cardiovascular events occurring as BP rises.3 Estimates of relative risk have been obtained from observational studies, such as the Framingham Heart Study.4
The risks and ultimate outcomes in hypertensive individuals, however, are much more closely related to the presence of other cardiovascular risk factors and/or TOD than to BP level.5 Therefore, other systems based on absolute risk have emerged.5 6 7 8 Absolute risk—the actual odds that a patient (or population) will develop an event—reflects the sum of all the factors that contribute to the risk of cardiovascular disease. Such classification systems use BP level but also account for the effect of TOD and/or other cardiovascular risk factors on prognosis.
A third type of system classifies hypertensive individuals on the basis of the expected benefit of treatment as demonstrated in clinical trials of antihypertensive therapy. Although most systems rely heavily on such data, none use it exclusively. This approach might be more cost-effective but would be exceedingly difficult to validate and would not necessarily be superior to a system based on relative or absolute risk. It would be more complicated to use and may not be any more generalizable than current systems. Many populations with hypertension have not been adequately represented in clinical trials, and a substantial amount of extrapolation of the relative value of treating these individuals would still be necessary. Furthermore, clinical trials are usually efficacy studies (data obtained from a nonrepresentative cohort treated in an idealized fashion) rather than effectiveness studies (treatment of "real" patients under "real-world" conditions), and so the data obtained may not apply to the general hypertensive population.9
The final way to classify hypertensive individuals would be to use some genetic, biochemical, or physiological parameter such as plasma renin activity or the renin-sodium index to denote those at high risk.10 Although in some studies a high plasma renin activity or renin-sodium index was shown to confer a poor prognosis, the use of such parameters for the selection of high-risk hypertensive individuals and choice of therapy has not fulfilled its promise and has not replaced more traditional classification systems. Whether genetic markers, such as angiotensin-converting enzyme gene polymorphism, will significantly improve our ability to select which people are at risk remains to be proved.11
Since no classification system in common use relies only on clinical trial–derived evidence of benefit or on clinical, biochemical, or genetic markers of risk, these approaches will not be discussed further.
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Systems Based on Relative Risk (Use of BP Level Alone) |
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Since we were first able to accurately measure BP noninvasively, we have defined and classified hypertension on the basis of BP level alone.12 This is appropriate because the rate of cardiovascular events rises as BP rises. In 1977, the initial report of the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure (JNC-I) classified hypertension only by DBP.13 In JNC-II (1980), hypertension was first classified in the United States as mild (DBP from 90 to 104 mm Hg), moderate (DBP from 105 to 114), or severe (DBP
115).14 SBP was again not considered. JNC-III in 1984 refined the classification system further by introducing the term high-normal for those individuals with DBP values from 85 to 89 mm Hg, recognizing the excess risk for cardiovascular disease and premature mortality in individuals with this DBP level.15 JNC-III also introduced the terms isolated systolic hypertension and borderline isolated systolic hypertension for individuals with SBP 160 mm Hg and 140 to 159 mm Hg, respectively, and DBP <90 mm Hg. This belatedly acknowledged the evidence that individuals with elevated SBP were at increased risk of cardiovascular disease regardless of DBP level. We had known for some time that SBP was a better predictor than DBP of mortality and virtually all of the cardiovascular complications attributable to hypertension.16 |
Systems Based on Absolute Risk (Use of BP and/or Comorbidity) |
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Since Janeway,17 authors have classified hypertensive individuals primarily by the amount of TOD noted, particularly in the optic fundus and kidney. Keith et al18 divided hypertensive individuals into four groups, now called grades, on the basis of retinal arteriolar changes and the presence or absence of exudates, hemorrhages, or papilledema. This system was very effective at defining prognosis. Individuals with group IV retinopathy (hemorrhages, exudates, and papilledema) had a dramatically worse prognosis, with a mortality rate of 76% at 1 year, than those in groups I and II (with only arterial tortuosity or arteriovenous nicking), in which only 10% to 12% died in 1 year.
In 1993, JNC-V modified the classification systems from earlier reports in two very important ways.6 It not only provided arbitrary cut points for both SBP and DBP, including both or either in the definition of hypertension, but also added individuals with SBPs of 130 to 139 mm Hg to the group with high-normal BP and specified <120 mm Hg SBP and <80 mm Hg DBP as optimal BP. The data from the Multiple Risk Factor Intervention Trial (MRFIT) screenees made it obligatory to recognize SBP and highlight the risk in individuals with SBP from 120 to 139 mm Hg.19
JNC-V also adopted the word "stage" to categorize hypertension severity, abandoning the designations of borderline, mild, moderate, and severe. The committee felt that the term "mild" hypertension implied to both providers and patients that hypertensive individuals with BPs in that range had a benign condition that did not require excessive concern. Although the risk of complications from an elevated BP is certainly higher and more immediate in people with stage III or IV hypertension (moderate and severe hypertension in the old nomenclature), the majority of events occur in those with stage I or II hypertension (and in those with high-normal BP readings) because so many more people have this BP level.20 The data from the MRFIT screenees reiterated the importance of other risk factors and TOD on absolute risk.19 Although JNC-V did note the importance of comorbidity and detailed the need for specific mention of whether TOD or other risk factors were present, such was not emphasized in that classification system and few clinicians appear to have adopted that recommendation.
The 1993 revision of the WHO/ISH guidelines retained the terms "mild," "moderate," and "severe" and also "borderline" hypertension and expanded the staging system that had been used since 1962.7 8 21 Individuals with stage I hypertension have no objective signs of TOD. Those with stage II have one or more of the following: grade I or II retinopathy, proteinuria, and/or plasma creatinine levels between 1.2 and 2.0 mg/dL and/or evidence of atherosclerosis. Stage III includes individuals with symptoms and signs of more advanced TOD than those with stage II. This system is valuable because it forces the clinician to consider TOD and other risk factors rather than just BP, but it is too complicated for general use and may require extensive and expensive testing for establishment of the degree of TOD. Furthermore, the WHO/ISH system classifies hypertensive individuals by both BP level and TOD and does not provide adequate guidance as to how to use either in risk assessment.
The National Advisory Committee on Core Health and Disability Support Services from New Zealand tied estimates of absolute risk to therapeutic recommendations and strongly advised that hypertension treatment be based on absolute risk rather than BP level.5 Individuals with an absolute risk for a cardiovascular event of more than 20% in 10 years (for example, a 60-year-old man with a BP of 160/95 mm Hg and two other risk factors) should be treated, whereas someone whose risk is lower (a 40-year-old woman whose BP is 170/100 mm Hg with one other risk factor) should not. The risk predictions are based on data from the Framingham Heart Study that demonstrate the substantial increase in the absolute risk of cardiovascular disease events in individuals with SBP 170 mm Hg and/or DBP 100 and also indicate the effect that other cardiovascular risk factors, TOD, and symptomatic cardiovascular disease have on prognosis.22 Unfortunately, the value of this classification system and the recommendations on treatment that result are weakened because Framingham Heart Study risk predictions may not apply to other populations and are not universally accepted or widely enough known to be used in individualized therapy.
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A New Scheme for Classifying High BP |
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Although the new classification schemes proposed by JNC-V, WHO/ISH, and New Zealand are improvements over prior systems, further modifications are necessary. JNC-V does not adequately highlight the importance of absolute risk as defined by comorbidity, and the WHO/ISH system and New Zealand recommendations are too cumbersome for routine use. Furthermore, neither system pays adequate attention to the growing body of knowledge on the risks inherent in people with a wide pulse pressure and otherwise modest elevations of SBP.
The system we propose also stages hypertensive individuals, although the cut points of BP chosen for each of the stages are somewhat different from those in JNC-V (Table 1
).6 As in JNC-V, individuals would be classified according to the higher of the stages into which they fall.
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This system agrees that optimal SBP is <120 mm Hg and DBP is <80.6 20 Individuals with SBP levels from 120 to 134 and DBP levels from 80 to 84 are classified as having normal BP. For all others, we feel it is necessary to note whether other cardiovascular risk factors, TOD, or both are present. To do so, we suggest modifying the numerical stage with the subscript "c" for complicated and "u" for uncomplicated. This simple device will point out to the provider and patient that comorbidity is present (subscript "c") and prognosis worse. Thus, more concern and earlier and more aggressive therapy would be warranted. In those hypertensive individuals without other cardiovascular risk factors and/or TOD (subscript "u"), the approach to treatment at the same BP level would be less aggressive (Table 2).
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The ascertainment of evidence that other risk factors and TOD are present can be costly and if invasive tests are done, could potentially add risk to the evaluation of the hypertensive individual. The data obtained from a complete medical history and physical examination together with a few inexpensive laboratory tests provide most of the information a physician would need to classify a hypertensive person as being complicated or uncomplicated. The simple and inexpensive initial evaluation recommended by JNC-V, for example, will inform the clinician about the presence of prior cardiovascular disease events and risk factors such as cigarette smoking; determine whether symptomatic cardiovascular disease is present; and measure lipid levels (including total serum cholesterol, high-density lipoprotein cholesterol, and serum triglycerides), serum glucose, and renal function as well as indicate whether electrocardiographic left ventricular hypertrophy or proteinuria is present.6 Although this basic evaluation will undoubtedly misclassify some complicated hypertensive individuals as being free of TOD and/or other risk factors, the need to limit healthcare expenditures dictates that the use of procedures such as limited echocardiography, carotid ultrasound, and ultrafast computerized tomography of the heart as well as measurement of other risk factors such as microalbuminuria, serum fibrinogen, or homocysteine levels not be routinely performed, even if important subclinical disease is missed in some individuals.23 24 25
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Therapeutic Implications |
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We also suggest modifying the BP levels used for assignment of hypertensive individuals to various stages in the JNC-V classification so the system can serve as a guide to therapy. Although data from the MRFIT screenees and considerable data from earlier epidemiological surveys have clearly shown that cardiovascular risk increases as BP rises above 120/80 mm Hg, we do not feel it is justified to label people with SBP levels from 120 to 134 mm Hg and DBP levels from 80 to 84 as having anything but a normal BP.19 20 At present, no data support attempts to lower BP in such individuals, even though other risk factors and/or hypertension-related TOD might be present. In certain situations, such as in diabetics or people with chronic renal disease, lowering BP further may turn out to be justified.26 27
Hypertensive individuals with SBP from 135 to 149 mm Hg and/or DBP from 86 to 95 (stage 1 in the proposed classification system) do not warrant drug therapy initially unless TOD or other cardiovascular risk factors are present.28 29 Those with stage 1u hypertension should be treated with lifestyle modification (reduction of weight and salt intake, increase in exercise, and moderation of alcohol intake) for at least 6 months.6 Since the data from the Treatment of Mild Hypertension Study (TOMHS) suggest that pharmacological therapy for hypertensive individuals in this range prevents events significantly better than even effective lifestyle modification, drug therapy is appropriate in those with stage 1u hypertension should lifestyle modification fail to reduce BP to below goal (135 mm Hg SBP and 85 DBP) after that time period.30 Hypertensive individuals with stage 1c hypertension and those with SBP from 150 to 180 mm Hg or DBP from 96 to 110 (the remainder of JNC-V stages 1 and 2) should probably receive pharmacological therapy after a shorter trial (3 to 6 months) of lifestyle modification unless BP is successfully reduced to goal. In some, both lifestyle modification and pharmacological therapy will be appropriate at the initiation of treatment.
We have designated individuals with SBP >180 mm Hg and/or DBP >110 as stage 3 and would recommend that both lifestyle modification and pharmacological therapy be used at the outset. Such would be the case whether the individual was stage 3u or stage 3c. Since the third National Health and Nutrition Survey showed that only 1.0% of Americans have JNC-V stages 3 and 4 hypertension, it is not necessary to have two different stages.31
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The Importance of a Wide Pulse Pressure |
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Numerous population studies have shown that although SBP increases as a population ages, DBP peaks at approximately age 55 and falls thereafter, so pulse pressure rises.31 32 This may be a healthy survivor effect (those with significant diastolic hypertension had died), but it is much more likely that the widening of pulse pressure is a result of structural changes in large blood vessels leading to reduced arterial compliance and greater stiffness.33 34 More recently, Madhavan et al35 showed that people in the upper tertile of pretreatment pulse pressure (
63 mm Hg) had a greater mortality than those in the lower tertiles and that pulse pressure but not SBP or DBP was an independent predictor of outcome, particularly myocardial infarction. Other researchers have shown that a wide pulse pressure (60 mm Hg) was associated with carotid artery stenosis, end-stage renal disease, renovascular hypertension, thickened resistance vessels, left ventricular hypertrophy, cardiovascular events, and mortality.24 36 37 38 39 40 41 42 43 The importance of a wide pulse pressure seems not to be limited to the elderly. In the MRFIT screenees, men with DBP <70 mm Hg and SBP >160 had the highest coronary artery disease death rate noted.19 In young and middle-aged (35 to 57 years) white men, there was a substantially higher coronary artery disease death rate in 12 years for those with a BP of >160/<70 mm Hg than of >160/>100 (80.6 of 10 000 versus 48.3 of 10 000).19 These data provide an explanation for the phenomenon of a J-shaped or U-shaped relationship between DBP and morbidity and mortality, first described by Stewart in 197944 and later confirmed by Cruickshank and many others.45 46 47 The increase in coronary heart disease in individuals with a low DBP was originally attributed to excessive lowering of DBP with treatment, but now it is clear that individuals with a low DBP and elevated SBP are those at particularly high risk regardless of whether they received antihypertensive therapy.48 49
None of the classification systems currently in use, including the one we propose here, specifically highlights the importance of a wide pulse pressure. In this proposed system, hypertensive individuals with a wide pulse pressure will be classified by their SBP level and associated TOD and/or risk factors and treated accordingly. If clinicians assess and treat their patients on the basis of whether a patient has hypertension with complications, not simply on the basis of BP level, they may not need a specific reminder that a hypertensive individual with an elevated SBP and "low" or "normal" DBP probably has generalized atherosclerosis and a potentially poor prognosis rather than a satisfactory DBP.24 50 Unfortunately, none of the clinical trials that provide the evidence on which we should base our treatment recommendations has used pulse pressure level for assessment of the benefit of antihypertensive therapy. Therefore, we cannot be certain that directing our therapeutic efforts at those hypertensive individuals with a wide pulse pressure will necessarily be more successful than treating according to DBP or SBP. We do know from the Systolic Hypertension in the Elderly Program (SHEP) that elderly people with isolated systolic hypertension (stages 2-3u or 2-3c in the current proposed system) and an average pulse pressure of 94 mm Hg at baseline had dramatic reductions in fatal and nonfatal stroke, coronary heart disease, and congestive heart failure with therapy.51 These data convincingly showed that reducing DBP in the elderly did not precipitate coronary heart disease or stroke but instead prevented them. We do not have data yet on the benefit or risks of treatment in individuals with stage 1 systolic hypertension.
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Link to Reimbursement |
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Although the system suggested here may add time during early visits for hypertension, we feel it is simple and practical enough to be widely used. It should not require additional testing and expense for the clinician to ascertain the presence or absence of TOD or other risk factors. Rather, it relies on data currently collected on each hypertensive individual to classify that individual as complicated or uncomplicated.
The key to whether this or any system like it is adopted may well be the link to reimbursement. If providers received increased compensation when caring for complicated hypertensive individuals, they would spend the additional time to document the fact that complications were present and more carefully follow such patients. If this is true, and if our therapeutic efforts are directed at reducing BP in those whose absolute risk is highest, more complications are likely to be prevented and the overall cost of caring for hypertensive individuals may well go down. Only a prospective evaluation with careful attention to resource utilization and outcomes will convincingly demonstrate whether the use of this system or one like it will save lives and money.
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Conclusion |
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Although we in the medical community have done a superb job of understanding the importance of hypertension as a risk factor and of developing many effective antihypertensive agents, we still are not successfully controlling the majority of hypertensive Americans nor have we reduced the burden of hypertension to its minimum.52 If we can better identify people at risk and apply our treatments more judiciously, we will certainly improve the outcomes of our efforts. Although this proposed classification scheme may not yet meet all of our criteria for an ideal system, we can come closer to that ideal as we hone our skills further and more efficiently define risk.
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Selected Abbreviations and Acronyms |
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Footnotes |
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Reprint requests to Henry R. Black, MD, Department of Preventive Medicine, Rush–Presbyterian–St Luke's Medical Center, 1725 W Harrison St, Suite POB #117, Chicago, IL 60612.
Received April 3, 1996; first decision May 7, 1996; accepted June 20, 1996.
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References |
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- Rose G. Epidemiology. In: Marshall AJ, Barritt DW, eds. The Hypertensive Patient. Kent, UK: Pitman Medical; 1980:1-21.
- Alderman MH, Cushman WC, Hill MN, Krakoff LR. International round table discussion of national guidelines for the detection, evaluation, and treatment of hypertension. Am J Hypertens. 1993;6:974-981.[Medline] [Order article via Infotrieve]
- MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, Abbott R, Godwin J, Dyer A, Stamler J. Blood pressure, stroke, and coronary heart disease, part 1: prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet. 1990;335:765-774.[Medline] [Order article via Infotrieve]
- Kannel WB, Schwartz MJ, McNamara PM. Blood pressure and risk of coronary heart disease: The Framingham Study. Dis Chest. 1969;56:43-52.
- Jackson R, Barham P, Bills J, Birch L, McLennan L, MacMahon S, Maling T. Management of raised blood pressure in New Zealand: a discussion document. BMJ. 1993;307:107-110.
- Joint National Committee on the Detection, Evaluation and Treatment of High Blood Pressure. The fifth report of the Joint National Committee on the detection, evaluation, and treatment of high blood pressure (JNC-V). Arch Intern Med. 1993;153:154-183.[Medline] [Order article via Infotrieve]
- World Health Organization. Arterial Hypertension Report of WHO Expert Committee. Geneva, Switzerland: World Health Organization; 1978. Technical Report Series No. 628.
-
The Guidelines Subcommittee of the WHO/ISH Mild Hypertension Liaison Committee. 1993 guidelines for the management of mild hypertension: memorandum from a World Health Organization/International Society of Hypertension meeting. Hypertension. 1993;22:392-403.
[Free Full Text] - Kupersmith J, Holmes-Rovner M, Hogan A, Rovner D, Gardiner J. Cost-effectiveness analysis in heart disease, part II: preventive therapies. Prog Cardiovasc Dis. 1995;37:243-271.[Medline] [Order article via Infotrieve]
- Alderman MH, Madhavan S, Ooi WL, Cohen H, Sealey JE, Laragh JH. Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension. N Engl J Med. 1991;324:1098-1104.[Abstract]
- Cambien F, Poirier O, Lecerf L, Evans A, Cambou JP, Arveiler D, Luc G, Bard JM, Bara L, Ricard S, Tiret L, Amouel P, Alhenc-Gelas F, Soubrier F. Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction. Nature. 1992;359:641-644.[Medline] [Order article via Infotrieve]
- Korotkoff NC. To the question of methods of determining the blood pressure (from the clinic of professor CP Federoff). Reports of the Imperial Military Academy. 1905;11:365-367.
- The Joint National Committee on the Detection, Evaluation and Treatment of High Blood Pressure. Report of the Joint National Committee on detection, evaluation and treatment of high blood pressure: a cooperative study. JAMA. 1977;237:255-261.[Medline] [Order article via Infotrieve]
- The Joint National Committee on the Detection, Evaluation and Treatment of High Blood Pressure. The 1980 report of the Joint National Committee on detection, evaluation and treatment of high blood pressure. Arch Intern Med. 1980;140:1280-1285.[Medline] [Order article via Infotrieve]
- The Joint National Committee on the Detection, Evaluation and Treatment of High Blood Pressure. The 1984 report of the Joint National Committee on detection, evaluation and treatment of high blood pressure. Arch Intern Med. 1984;144:1045-1057.[Medline] [Order article via Infotrieve]
- Kannel WB, Gordon T, Schwartz MJ. Systolic versus diastolic blood pressure and risk of coronary heart disease: the Framingham study. Am J Cardiol. 1971;27:335-346.[Medline] [Order article via Infotrieve]
- Janeway TC. A study of the causes of death in 100 patients with high blood pressure. JAMA. 1912;59:2106-2110.
- Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: their course and prognosis. Am J Med Sci. 1939;197:332-343.
- Neaton JD, Wentworth D, for the Multiple Risk Factor Intervention Trial Research Group. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease: overall findings and differences by age for 316,099 white men. Arch Intern Med. 1992;152:56-64.[Abstract]
- Stamler J, Stamler R, Neaton J. Blood pressure, systolic and diastolic, and cardiovascular risks: US population data. Arch Intern Med. 1993;153:598-615.[Abstract]
- World Health Organization. Arterial Hypertension and Ischemic Heart Disease: Preventive Aspects. Report of an Expert Committee. Geneva, Switzerland: World Health Organization; 1962. Technical Report Series No. 231.
-
Anderson KM, Wilson PWF, Odell PM, Kannel WB. An updated coronary risk profile: a statement for health professionals. Circulation. 1991;83:356-362.
[Free Full Text] - Black HR, Weltin G, Jaffe CC. The limited echocardiogram: a modification of standard echocardiography for use in the routine evaluation of patients with systemic hypertension. Am J Cardiol. 1991;67:1027-1030.[Medline] [Order article via Infotrieve]
- Bots ML, Witteman JCM, Hofman A, deJong PTVM, Grobbee DE. Low diastolic blood pressure and atherosclerosis in elderly subjects. Arch Intern Med. 1996;156:843-848.[Abstract]
- Wong ND, Douwabunpat D, Vo AN, Detrano RC, Eisenberg H, Goel M, Tobis JM. Coronary calcium and atherosclerosis by ultrafast computed tomography in asymptomatic men and women: relation to age and risk factors. Am Heart J. 1994;127:422-430.[Medline] [Order article via Infotrieve]
- Dillon JJ. The relationship between treated blood pressure level and progression of diabetic renal disease. J Am Soc Nephrol. 1992;3:331. Abstract.
- National High Blood Pressure Education Program. National High Blood Pressure Education Program Working Group report on hypertension and chronic renal failure. Arch Intern Med. 1991;151:1280-1287.[Abstract]
- Sever P, Beevers G, Bulpitt C, Lever A, Ramsay L, Reid J, Swales J. Management guidelines in essential hypertension: report of the second working party of the British Hypertension Society. BMJ. 1993;306:983-987.
-
Alderman MH. Blood pressure management: individualized treatment based on absolute risk and the potential for benefit. Ann Intern Med. 1993;119:329-335.
[Abstract/Free Full Text] - Neaton JD, Grimm RH, Prineas RJ, Stamler J, Grandits GA, Elmer PJ, Cutler JA, Flack JM, Schoengerger JA, McDonald R, Lewis CE, Liebson PR. Treatment of mild hypertension study: final results. JAMA. 1993;270:713-724.[Abstract]
-
Burt VL, Whelton P, Roccella EJ, Brown C, Cutler JA, Higgins M, Horan MJ, Labarthe D. Prevalence of hypertension in the US adult population. Hypertension. 1995;25:305-313.
[Abstract/Free Full Text] - Rowland M, Roberts J. Blood Pressure Levels and Hypertension in Persons Aged 6-74 Years. United States, 1976-1980. Washington, DC: US Department of Health and Human Services; 1982. NCHS advance data, No. 84, Vital and Health Statistics of the National Center for Health Statistics.
- Safar ME. Pulse pressure in essential hypertension: clinical and therapeutical implications. J Hypertens. 1989;7:769-776.[Medline] [Order article via Infotrieve]
-
James MA, Watt PAC, Potter JF, Thurston H, Swales JD. Pulse pressure and resistance artery structure in the elderly. Hypertension. 1995;26:301-306.
[Abstract/Free Full Text] -
Madhavan S, Ooi W, Cohen H, Alderman MH. Relation of pulse pressure and blood pressure reduction to the incidence of myocardial infarction. Hypertension. 1994;23:395-401.
[Abstract/Free Full Text] -
Sutton-Tyrell K, Alcorn HG, Wolfson SK Jr, Kelsey SF, Kuller LH. Predictors of carotid stenosis in older adults with and without isolated systolic hypertension. Stroke. 1993;24:355-361.
[Abstract/Free Full Text] - Perry HM, Miller PP, Fornoff JR, Baty JD, Sambhi MP, Rutan G, Moskowitz DW, Carmody SE. Early predictors of 15-year end-stage renal disease in hypertensive patients. Hypertension. 1995;25(part 1):587-594.
-
Setaro JF, Saddler MC, Chen CC, Hoffer PB, Roer DA, Markowitz DM, Meier GH, Gusberg RJ, Black HR. Simplified captopril renography in diagnosis and treatment of renal artery stenosis. Hypertension. 1991;18:289-298.
[Abstract/Free Full Text] - Folkow B. Pathophysiology of hypertension: differences between young and elderly. J Hypertens. 1993;11(suppl 4):S21-S24.
- Cavallini MC, Roman MJ, Pini R, Pickering TG, Devereux RB. Relation of pulse pressure to target organ damage in hypertensive patients. J Am Coll Cardiol. 1995;25:299A. Abstract.
- Pannier B, Brunei P, Aroussy WE, Lacolley P, Safar ME. Pulse pressure and echocardiographic findings in essential hypertension. J Hypertens. 1989;7:127-132.[Medline] [Order article via Infotrieve]
- Ekpo EB, White AD, Fernando MU, Shah IU. Is isolated systolic hypertension in the elderly more associated with left ventricular hypertrophy and significant carotid artery stenosis than mixed hypertension and isolated diastolic hypertension? J Hum Hypertens. 1995;9:809-813.[Medline] [Order article via Infotrieve]
-
Darne B, Girerd X, Safar M, Cambien F, Guize L. Pulsatile versus steady component of blood pressure: a cross-sectional analysis and a prospective analysis on cardiovascular mortality. Hypertension. 1989;13:392-400.
[Abstract/Free Full Text] - Stewart IMG. Relation of reduction in pressure to first myocardial infarction in patients receiving treatment for severe hypertension. Lancet. 1979;1:861-865.[Medline] [Order article via Infotrieve]
- Cruickshank JM, Throp JM, Zacharias FJ. Benefits and potential harm of lowering blood pressure. Lancet. 1987;1:581-584.[Medline] [Order article via Infotrieve]
- Farnett L, Mulrow CD, Linn WD, Lucey CR, Tuley MR. The J-curve phenomenon and the treatment of hypertension: is there a point beyond which pressure reduction is dangerous? JAMA. 1991;265:489-495.[Abstract]
- Glynn RJ, Field TS, Rosner B, Hebert PR, Taylor JO, Hennekens CH. Evidence for a positive linear relation between blood pressure and mortality in elderly people. Lancet. 1995;345:825-829.[Medline] [Order article via Infotrieve]
-
Flack JM, Neaton J, Grimm R, Shih J, Cutler J, Ensrud K, MacMahon S. Blood pressure and mortality among men with prior myocardial infarction. Circulation. 1995;92:2437-2445.
[Abstract/Free Full Text] - D'Agostino RB, Belanger AJ, Kannel WB, Cruickshank JM. Relation of low diastolic blood pressure to coronary heart disease death in presence of myocardial infarction: the Framingham Study. Br Med J. 1991;303:385-389.
- Sleight P. Blood pressure, heart, and U-shaped curves. Lancet. 1988;1:235.[Medline] [Order article via Infotrieve]
- SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension: final results of the Systolic Hypertension in the Elderly Program (SHEP). JAMA. 1991;266:3255-3264.[Medline] [Order article via Infotrieve]
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Burt VL, Culter JA, Higgins M, Horan MJ, Labarthe D, Whelton P, Brown C, Roccella EJ. Trends in the prevalence, awareness, treatment and control of hypertension in the adult US population: data from the health examination surveys, 1960 to 1991. Hypertension. 1995;26:60-69.
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