Health Centers > Hypertension Health Center > Hypertension: Classification, Epidemiology, Diagnosis, Evaluation and Treatment
Classification and Epidemiology
Results from cross-sectional studies have shown that blood pressure, particularly systolic blood pressure (SBP), increases with increasing age. No age adjustment is made in setting the threshold value that defines high blood pressure. The classification of blood pressure outlined by the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI), shown in Table 40.1, is the same for all adults irrespective of age.
- Classification and Epidemiology
- Diagnosis and Evaluation
L Measurement Issues
L Secondary Causes
L Target Organ Damage and Risk Factor Assessment
L Results from Clinical Trials
L General Approach to Therapy and Monitoring
L Nonpharmacologic Treatment Modalities
- Overview of Pharmacologic Treatments
L Calcium Channel Antagonists
L β-Adrenergic Antagonists
L Angiotensin-Converting Enzyme (ACE) Inhibitors
L α1-Adrenergic Receptor Antagonists
- Patient Adherence and Resistant Hypertension
- Special Clinical Situations
L Hypertensive Urgencies and Emergencies
L Hypertension in Long-Term Care Center Residents
There were several minor modifications made in the JNC-VI revision of blood pressure classification that have major significance with respect to geriatric hypertension. The former category of isolated systolic hypertension [i.e., SBP > 160 mmHg and diastolic blood pressure (DBP) < 90 mmHg] was removed. In addition, the conjunction linking the systolic and diastolic blood pressure columns that define each stage was changed from "and" to "or." As a consequence of this new approach to classification and because isolated diastolic hypertension is so uncommon in older individuals, the correct categorization of blood pressure among those above age 60 may be made by using the level of SBP alone in 99% of cases. Thus, the SBP level matters for the purposes of classification. Finally, as is discussed, treatment recommendations are stratified, based in large part on the classification strategy shown in Table 40.1.
Contrary to a former point of view that held that high blood pressure is an expected normal aspect of aging, it is now evident that hypertension in older individuals defined according to these blood pressure levels should be viewed as a disease state that is associated with an increased risk for adverse outcomes [e.g., coronary heart disease, congestive heart failure (CHF), stroke, peripheral vascular disease, and renal disease) and mortality. Therefore, although common, high blood pressure in older individuals is not benign.
It is also important to note that, for any level of diastolic blood pressure, the risk for these adverse events is progressively greater at higher levels of systolic blood pressure. Thus, systolic blood pressure matters as a risk factor for cardiovascular disease. In addition, it is increasingly being recognized that a major predictor of cardiovascular risk is the pulse pressure-the difference between systolic and diastolic blood pressure. An analysis of data from the Systolic Hypertension in the Elderly Program (SHEP) identified that pulse pressure was a significant predictor of stroke and total mortality independent of the influence of mean arterial blood pressure. Therefore, the age-associated increases in systolic blood pressure and in pulse pressure are important contributors to the morbidity and mortality associated with hypertension in older individuals.
Editor note: [updated at Dec 2, 2007]
Given this information, the recent Joint National Committee (JNC-7) has introduced a new classification system for hypertension.
- PreHypertension - Systolic blood pressure (SBP) 120-139 mm Hg or diastolic blood pressure (DBP) 80-89 mm Hg
- Stage I hypertension - SBP 140-159 mm Hg or DBP 90-99 mm Hg
- Stage II hypertension - SBP >160 mm Hg or DBP > 100 mm Hg *
Often, it is not easy to tell. But there are symptoms people may have.
Epidemiologic studies such as the National Health and Nutrition Examination Surveys have shown that the overall prevalence of hypertension in noninstitutionalized individuals above the age of 65 is between 50% and 70%. The prevalence is highest among African-Americans relative to whites and Mexican-Americans. Unlike the younger hypertensive population in which there is a male predominance, there is no marked gender difference in the overall prevalence of hypertension in the elderly. Moreover, the age-associated increase in the prevalence of isolated systolic hypertension appears to be greater for women than for men.
Many age-related changes in physiology contribute to the increase in blood pressure. Lifestyle factors, such as diet, obesity, and physical activity, and the presence of comorbidities are also important contributors. A multitude of pathophysiologic mechanisms interact in the dynamic and complex regulation of arterial blood pressure. The maintenance of blood pressure homeostasis and the provision of adequate cerebral perfusion in the response to such hypotensive stimuli as volume depletion, upright posture, vasodilating medications, or a meal is an important physiologic challenge facing the aging individual.
As is the case in younger individuals, the etiology of essential hypertension in older humans is not known. An increase in peripheral vascular resistance is one pathognomonic feature of hypertension in the elderly. Several mechanisms contribute to the increase in peripheral vascular resistance. Table 40.2 summarizes those mechanisms that appear to be associated with aging and are discussed in detail here. A rational approach to therapy of hypertension in older individuals requires an understanding of this pathophysiologic context. Although not all the following mechanisms have been convincingly proven to be primary age-associated changes (i.e., independent of the effects of disease or lifestyle factors), they may be important contributors to hypertension in the elderly. It is also quite possible that the age-associated increase in blood pressure is secondary to age-related disease or lifestyle factors, because in some populations the increase in blood pressure with aging is either absent or less marked.
An age-associated increase in arterial vascular stiffness has been demonstrated, particularly in the larger arteries. Several alterations in vessel structure contribute to the decrease in distensibility, such as an increase in smooth muscle cell size and number, an increase in medial collagen deposition, and a decrease in elastin content. Arterial compliance and stroke volume are the major determinants of pulse pressure. Because stroke volume does not vary significantly with age, the decline in arterial compliance produces an increase in pulse pressure, which contributes to a disproportionate increase in systolic pressure. This finding may account for the age-associated increase in the prevalence of isolated systolic hypertension, as well as an increase in pulse pressure. Another consequence of the decrease in arterial compliance with aging is an increase in arterial pulse wave velocity. The increase in arterial pulse wave velocity has been shown to lead to an early return of wave reflection, which alters the aortic pressure wave contour, increasing the pressure in late systole. The wave reflection further accentuates the increase in pulse pressure between central and peripheral arteries.
- Primary (Essential) Hypertension
L Sympathetic nervous system hyperactivity
L Abnormal cardiovascular development
L Renin-angiotensin system activity
L Defect in natriuresis
L Intracellular sodium and calcium
L Exacerbating factors
- Secondary Hypertension
L Renal disease
L Genetic causes
L Renal vascular hypertension
L Primary hyperaldosteronism
L Cushing's syndrome
L Coarctation of the aorta
L Hypertension associated with pregnancy
L Estrogen use
L Other causes of secondary hypertension
In addition to changes in vascular structure, the dynamic regulation of vascular tone by the autonomic nervous system, as well as by the vascular endothelium, is an important determinant of peripheral vascular resistance. A decrease in baroreceptor sensitivity with age has been described, perhaps as a manifestation of the decrease in arterial distensibility already discussed.
The decline in baroreceptor sensitivity alters the central nervous system (CNS) control of sympathetic nervous system (SNS) outflow, resulting in two important manifestations. First, having an insensitive baroreceptor means that a larger change in blood pressure is needed to activate the baroreceptor and produce the appropriate compensatory response. Attenuated baroreceptor sensitivity is believed to contribute to the greater blood pressure variability in older individuals.
Second, attenuated baroreceptor sensitivity results in enhanced SNS activity for a given level of arterial blood pressure. Many studies have demonstrated an age-associated increase in the activity of the SNS measured by an increase in plasma norepinephrine levels, rates of norepinephrine release determined from tracer kinetics studies, and muscle sympathetic nerve activity.
The increase in the rate of norepinephrine release would be expected to result in increased cardiovascular adrenergic responses if it were not for the corresponding downregulation of adrenergic receptor function. Indeed, there is evidence to suggest an age-associated decrease in adrenergic responsiveness for β-adrenergic receptor chronotropic, inotropic, and vascular responses, as well as for α-adrenergic vasoconstrictor responses.
As a result of the decrease in arterial α-adrenergic receptor response, it appears that overall arterial α-adrenergic tone is similar in older normotensive compared with younger normotensive subjects and that an increase in peripheral vascular resistance cannot be accounted for solely by age-associated changes in SNS function. Hypertensive older individuals, however, have been characterized by having greater arterial α-adrenergic receptor responsiveness relative to their level of SNS activity in comparison to older normotensive subjects.
Another important modulator of vascular tone is the vascular endothelium, which synthesizes a number of vasoactive substances. Endothelial-derived relaxing factor (EDRF) is a potent vasodilator that has been extensively investigated since being identified as nitric oxide. Several studies have demonstrated that there is an age-associated decrease in EDRF-mediated vasocilation, and there may also be endothelial dysfunction with hypertension. Impaired function of this important regulator of vasodilator tone could lead to an increase in peripheral vascular resistance if not met by appropriate compensatory alterations in other vasoactive systems. The extent to which impaired endothelial function contributes to an increase in blood pressure in aging remains to be defined.
Several age-associated changes in renal function (e.g., decreased renal blood flow and glomerular filtration rate) combine to result in an age-associated inability to rapidly excrete a sodium load. The net result of these alterations is a tendency for sodium retention by the aging kidney and an increase in total body sodium. It has been observed that a greater proportion of older hypertensives demonstrate an increase in mean arterial blood pressure in response to challenge with a sodium load or demonstrate sodium sensitivity. These renal changes in sodium balance may contribute to the increased prevalence for sodium sensitivity among older individuals.
The renin-angiotensin system represents another blood pressure regulatory system that may be altered with advancing age. The evidence in this instance is for an age-associated decline in plasma renin activity. There is a corresponding low prevalence of older hypertensives with high renin levels. The decrease in plasma renin activity may be related to a decrease in the number of glomeruli, as well as an increased delivery of sodium to the macula densa.
Several studies have identified an age-associated impairment in glucose tolerance. Decreased sensitivity to the peripheral effects of insulin on carbohydrate metabolism, or insulin resistance, with aging may contribute to the decline in glucose tolerance. Insulin resistance and an associated increase in fasting insulin levels have been shown to be a characteristic of some hypertensive groups, including older hypertensives. Although a mechanistic causal link between insulin resistance and hypertension has not yet been identified, if such a mechanism exists, an age-associated decline in insulin sensitivity could contribute to hypertension. However, based on the results of a study performed to determine predictors of insulin sensitivity, it appears that age is not an independent predictor of insulin sensitivity after accounting for the confounding effects of higher body mass index and blood pressure. Thus, although there is a clear association between blood pressure and insulin resistance and many older hypertensives are insulin resistant, there are no data to indicate that an age-associated decline in insulin sensitivity independently contributes to hypertension in older adults.
1. Kannel WB, Gordon T. Evaluation of cardiac risk in the elderly. Bull N Y Acad Med. 1978;54:573-591.
2. Sheps SG. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. NIH Pub. 1997;98:4080.
3. Lloyd-Jones DM, Evans JC, Larson MG, O'Donnell CJ, Levy D. Differential impact of systolic and diastolic blood pressure level on JNC-VI staging. hypertension. 1999;34:381-385.
4. Kannel WB, Cupples LA, Vokonas PS. Epidemiology and risk of hypertension in the elderly: the Framingham study. J Hypertens. 1986;6(suppl 1):S3-S9.
5. Alli C, Avanzini F, Betelli G, Colombo F, Torri V, Tognoni G. The long-term prognostic significance of repeated blood pressure measurements in the elderly: SPAA (Studio sulla Pressione Arteriosa nell' Anziano) 10-year follow-up. Arch Intern Med. 1999;159:1205-1212.
6. Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. hypertension. 1998;32:560-564.
7. Domanski MJ, Davis BR, Pfeffer MA, Kastantin M, Mitchell GF. Isolated systolic hypertension: prognostic information by pulse pressure. hypertension. 1999;34:375- 380.
8. Wilking SVB, Belanger A, Kannel WB, D'Agostino RB, Steel K. Determinants of isolated systolic hypertension. JAMA. 1988;260(23):3451-3455.
9. Lakatta E. Mechanisms of hypertension in the elderly. J Am Geriatr Soc. 1989;37:780-790.
10. Hallock P, Benson I. Studies on the elastic properties of human isolated aorta. J Clin Investig. 1937;16:595-602.
11. Cooper LT, Cooke JP, Dzau VJ. Minireview: The vasculopathy of aging. J Gerontol Biol Sci. 1994;49(5):B191- B196.
12. Nichols W, O'Rourke M, Avolio A, et al. Effects of age on ventricular-vascular coupling. Am J Cardiol. 1985;55:11789-11184.
13. O'Rourke MF, Kelly RP. Wave reflection in the systemic circulation and its implications in ventricular function. J Hypertens. 1993;11:327-337.
14. Gribbin B, Pickering TG, Sleight P. Effect of age and high blood pressure on baroreflex sensitivity in man. Circ Res. 1971;29:424-420.
15. Shimada K, Kitazumi T, Sadakane N, Ogura H, Ozawa T. Age-related changes of baroreflex function, plasma norepinephrine, and blood pressure. hypertension. 1985;7:113-117.
16. Lipsitz LA. Minireview: Altered blood pressure homeo-stasis in advanced age: clinical and research implications. J Gerontol Med Sci. 1989;44(6):M179-M183.
17. Hajduczok G, Chapleau MW, Johnson SL, Abboud FM. Increase in sympathetic activity with age. I. Role of impairment of arterial baroreflexes. Am J Physiol. 1991;260:H1113-H1120.
18. Pfeifer MA, Weinberg CR, Cook D, Best JD, Reenan A, Halter JB. Differential changes of autonomic nervous system function with age in man. Am J Med. 1983;75:248- 258.
19. Linares OA, Halter JB. Sympathochromaffin system activity in the elderly. J Am Geriatr Soc. 1987;35:448-453.
20. Ziegler MG, Lake CR, Kopin IJ. Plasma noradrenaline increases with age. Nature. 1976;261:333-335.
21. Supiano MA, Linares OA, Smith MJ, Halter JB. Age-related differences in norepinephrine kinetics: effect of posture and sodium-restricted diet. Am J Physiol. 1990;259:E422-E431.
22. Hogikyan RV, Supiano MA. Arterial ?-adrenergic responsiveness is decreased and sympathetic nervous system activity is increased in older humans. Am J Physiol. 1994;266:E717-E724.
23. Iwase S, Mano T, Watanabe T, Saito M, Kobayashi F. Age-related changes of sympathetic outflow to muscles in humans. J Gerontol. 1991;46:M1-M5.
24. Vestal RE, Wood AJJ, Shand DG. Reduced beta- adrenoreceptor sensitivity in the elderly. Clin Pharmacol Ther. 1979;26:181-186.
25. Guarnieri T, Filburn CR, Zitnik G, Roth GS, Lakatta EG. Contractile and biochemical correlates of beta-adrenergic stimulation of the aged heart. Am J Physiol. 1980;239:H501-H508.
26. Hoffman BB, Blaschke TF, Ford GA. Beta adrenergically medicated cardiac chronotropic and vascular smooth muscle responses during propranolol therapy and withdrawal in young and elderly persons. J Gerontol. 1992;47(1):M22-M26.
27. Supiano MA, Hogikyan RV, Stoltz AM, Orstan N, Halter JB. Regulation of venous ?-adrenergic responses in older humans. Am J Physiol. 1991;260:E599-E607.
28. Supiano MA, Hogikyan RV, Sidani MA, Galecki AT, Krueger JL. Sympathetic nervous system activity and ?-adrenergic responsiveness in older hypertensive humans. Am J Physiol. 1999;276:E519-E528.
29. Lowenstein CJ, Dinerman JL, Snyder SH. Nitric oxide: a physiologic messenger. Ann Intern Med. 1994;120:227- 237.
30. Vallance P, Collier J, Moncada S. Effects of endothelium-derived nitric oxide on peripheral arteriolar tone in man. Lancet. 1989;2:997-1000.
31. Egashira K, Inou T, Hirooka Y, et al. Effects of age on endothelium-dependent vasodilation of resistance coronary artery by acetylcholine in humans. Circulation. 1993;88:77-81.
32. Panza JA, Casino PR, Kilcoyne CM, Quyyumi AA. Role of endothelium-derived nitric oxide in the abnormal endothelium-dependent vascular relaxation of patients with essential hypertension. Circulation. 1993;87:1468- 1474.
33. Meyer BR. Renal function in aging. J Am Geriatr Soc. 1989;37:791-800.
34. Lever AF, Berretta-Piccoli C, Brown JJ, Davies DL, Fraser R, Robertson JIS. Sodium and potassium in essential hypertension. Br Med J. 1981;283:1-15.
35. Luft FC, Weinberger MH, Fineberg NS, Miller JZ, Grim CE. Effects of age on renal sodium homeostasis and its relevance to sodium sensitivity. Am J Med. 1987;82(suppl 1B):9-15.
36. Dengel DR, Hogikyan RV, Brown MD, Glickman SG, Supiano MA. Insulin sensitivity is associated with blood pressure response to sodium in older hypertensives. Am J Physiol. 1998;274:E403-E409.
37. Hall JE, Coleman TG, Guyton AC. The renin-angiotensin system: normal physiology and changes in older hypertensives. J Am Geriatr Soc. 1989;37:801-813.
38. Shimokata H, Muller DC, Fleg JL, Sorkin J, Ziemba AW, Andres R. Age as independent determinant of glucose tolerance. Diabetes. 1991;40:44-51.
39. Reaven GM, Chen N, Hollenbeck C, Chen Y-DI. Effect of age on glucose tolerance and glucose uptake in healthy individuals. J Am Geriatr Soc. 1989;37:735-740.
40. Rowe JW, Minaker KL, Pallotta JA, Flier JS. Characterization of the insulin resistance of aging. J Clin Investig. 1983;71:1581-1587.
41. Chen M, Bergman R, Pacini G, Porte D. Pathogenesis of aging-related glucose intolerance in man: insulin resistance and decreased ?-cell function. J Clin Endocrinol Metab. 1984;60:13-20.
42. Fink RI, Kolterman OG, Griffin J, Olefsky JM. Mechanisms of insulin resistance in aging. J Clin Investig. 1983;71:1523-1535.
43. Ferrannini E, Buzzigoli G, Bonadonna R, et al. Insulin resistance in essential hypertension. N Engl J Med. 1987;317:350-357.
44. Swislocki ALM, Hoffman BB, Reaven GM. Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension. Am J Hypertens. 1989;2:419-423.
45. Supiano MA, Hogikyan RV, Morrow LA, et al. hypertension and insulin resistance: role of sympathetic nervous system activity. Am J Physiol. 1992;263:E935-E948.
46. Supiano MA, Morrow LA, Hogikyan RV, et al. Aging and insulin resistance: role of sympathetic activity and blood pressure. J Gerontol Med Sci. 1993;48:M237-M243.
47. Applegate W. High blood pressure treatment in the elderly. Clin Geriatr Med. 1992;8(1):103-117.
48. O'Callaghan WG, Fitzgerald DJ, O'Malley K, O'Brien E. Accuracy of indirect blood pressure measurement in the elderly. BMJ. 1983;286:1545-1546.
49. Vardan S, Mookherjee S, Warner R, Smulyan H. Systolic hypertension: direct and indirect BP measurements. Arch Intern Med. 1983;143:935-938.
50. Zweifler AJ, Shahab ST. Pseudohypertension: a new assessment. J Hypertens. 1993;11(1):1-6.
51. Messerli FH. Osler's maneuver, pseudohypertension, and true hypertension in the elderly. Am J Med. 1986;80:906- 910.
52. Taapatsatis NP, Napolitana GT, Rothchild J. Osler's maneuver in an outpatient clinic setting. Arch Intern Med. 1991;151:2209-2211.
53. Oliner CM, Elliott WJ, Gretler DD, Murphy MB. Low predictive value of positive Osler manoeuvre for diagnosing pseudohypertension. J Hum Hypertens. 1993;7:65-70.
54. Staessen JA, Thijs L, Fagard R, et al. Predicting cardiovascular risk using conventional vs. ambulatory blood pressure in older patients with systolic hypertension. JAMA. 1999;282:539-546.
55. Streeten DHP, Anderson GH, Richardson R, Thomas FD. Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: evidence for excessive venous pooling. J Lab Clin Med. 1988;111(3):326-335.
56. Mader SL. Aging and postural hypotension: an update. J Am Geriatr Soc. 1989;37:129-137.
57. Mader SL, Josephson KR, Rubenstein LZ. Low prevalence of postural hypotension among community-dwelling elderly. JAMA. 1987;258(11):1511-1514.
58. Harris T, Lewis A, Kleinman JC, Cornoni-Huntley J. Postural change in blood pressure associated with age and systolic blood pressure. J Gerontol Med Sci. 1991;46(5):M159-M163.
59. Lipsitz LA, Storch HA, Minaker KL, Rowe JW. Intra- individual variability in postural blood pressure in the elderly. Clin Sci. 1985;69:337-341.
60. Stenstrom G, Svardsudd K. Pheochromocytoma in Sweden 1959-1981: an analysis of the national cancer registry data. Acta Med Scand. 1986;220:225-232.
61. Staessen JA, Gasowski JG, Thijs L, et al. Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials. Lancet. 2000;355:865-872.
62. 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;265(24):3255-3264.
63. European Working Party. Mortality and morbidity results from the European Working Party on high blood pressure in the elderly trial. Lancet. 1985;i:1349-1354.
64. MRC Working Party. Medical research council trial of treatment of hypertension in older adults: principal results. Br Med J. 1992;304:405-412.
65. National Heart Foundation of Australia. Treatment of mild hypertension in the elderly. Med J Aust. 1981;2:398- 402.
66. Veterans Administration Cooperative Study Group on Antihypertensive Agents. Effects of treatment on morbidity in hypertension. Circulation. 1972;45:991-1004.
67. Dahlof B, Lindholm LH, Hannson L, Schersten B, Ekbom T, Wester P-O. Morbidity and mortality in the Swedish trial in old patients with hypertension (STOP-hypertension). Lancet. 1991;338:1281-1285.
68. Sprackling ME, Mitchell JR, Short AH, Watt G. Blood pressure reduction in the elderly: a randomised controlled trial of methyldopa. Br Med J (Clin Res Ed). 1981;283:1151- 1153.
69. Coope J, Warrender TS. Randomized trial of treatment of hypertension in the elderly patients in primary care. Br Med J (Clin Res Ed). 1986;293:1145-1148.
70. Maxwell MH, Ford CE. Cardiovascular morbidity and mortality in HDFP patients 50-69 years old at entry. J Cardiovasc Pharmacol. 1985;7(suppl 2):S5-S9.
71. Insua JT, Sacks HS, Lau T-S, et al. Drug treatment of hypertension in the elderly: a meta-analysis. Ann Intern Med. 1994;121:355-362.
72. Ogden LG, He J, Lydick E, Whelton PK. Long-term absolute benefit of lowering blood pressure in hypertensive patients according to the JNC VI risk stratification. hypertension. 2000;35:539-543.
73. Kostis JB, Davis BR, Cutler J, et al. Prevention of heart failure by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA. 1997;278:212-216.
74. Forette F, Seux ML, Staessen JA, for the Syst-Eur Investigators. Prevention of dementia in randomised double-blind placebo-controlled Systolic hypertension in Europe (Syst-Eur) trial. Lancet. 1998;352:1347-1351.
75. Mattila K, Haavisto M, Rajala S, Heikinheimo R. Blood pressure and five year survival in the very old. Br Med J. 1988;296:887-889.
76. Heikinheimo RJ, Haavisto MV, Kaarela RH, Kanto AJ, Koivunen MJ, Rajala SA. Blood pressure in the very old. J Hypertens. 1990;8:361-367.
77. Satish S, Freeman DH, Ray L, Goodwin JS. The relationship between blood pressure and mortality in the oldest old. J Am Geriatr Soc. 2001;49:367-374.
78. Gueyffier F, Bulpitt C, Boissel J-P, et al. Antihypertensive drugs in very old people: a subgroup meta-analysis of randomised controlled trials. Lancet. 1999;353:793-796.
79. Somes GW, Pahor M, Short RI, Cushman WC, Applegate WB. The role of diastolic blood pressure when treating isolated systolic hypertension. Arch Intern Med. 1999;159:2004-2009.
80. Whelton PK, Appel LJ, Espeland MA, et al. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomized controlled trial of nonpharmacologic interventions in the elderly (TONE). JAMA. 1998;279:839-846.
81. Midgley JP, Matthew AG, Greenwood CM, et al. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA. 1996;275:1590-1597.
82. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336:1117-1123.
83. Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, for the DASH-Sodium Collaborative Research Group. Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. N Engl J Med. 2001;344:3-10.
84. Plan and operation of the second National Health and Nutrition Examination Survey, 1976-1980. Vital and Health Statistics, Series 1, No. 15. Hyattsville, MD; National Center for Health Statistics; 1981.
85. Landsberg L. Pathophysiology of obesity-related hypertension: role of insulin and the sympathetic nervous system. J Cardiovasc Pharm. 1994;23(suppl 1):S1-S8.
86. The Trials of hypertension Prevention Collaborative Research Group. Reducing blood pressure by nonpharmacologic interventions. JAMA. 1992;267:1213-1220.
87. Cutler JAK. Combinations of lifestyle modification and drug treatment in management of mild-moderate hypertension: a review of randomized clinical trials. Clin Exp Hypertens. 1993;15(6):1193-1204.
88. Schotte DE, Stunkard AJ. The effects of weight reduction on blood pressure in 301 obese patients. Arch Intern Med. 1990;150:1701-1704.
89. Kelley G, McClellan P. Antihypertensive effects of aerobic exercise: a brief meta-analytic review of randomized controlled trials. Am J Hypertens. 1994;7:115-119.
90. Hagberg JM, Montain SJ, Martin WHI, Ehsani AA. Effect of exercise training in 60- to 69-year-old persons with essential hypertension. Am J Cardiol. 1989;64:348-353.
91. Wright JM, Lee C-H, Chambers GK. Systematic review of antihypertensive therapies: does the evidence assist in choosing a first-line drug?Can Med Assoc J (CMAJ). 1999;161:25-32.
92. Ekbom T, Dahlof B, Hansson L, Lindholm LH, Schersten B, Wester P-O. Antihypertensive efficacy and side effects of three beta-blockers and a diuretic in elderly hypertensives: a report from the STOP-hypertension study. J Hypertens. 1992;10:1525-1530.
93. Espeland MA, Kumanyika S, Kostis JB, et al. Antihypertensive medication use among recruits for the trial of nonpharmacologic interventions in the elderly (TONE). J Am Geriatr Soc. 1996;44:1183-1189.
94. Moser M. Why are physicians not prescribing diuretics more frequently in the management of hypertension? JAMA. 1998;279:1813-1816.
95. Vidt DG, Borazanian RA. Calcium channel blockers in geriatric hypertension. Geriatrics. 1991;46:28-38.
96. Materson BJ, Reda DJ, Cushman WC, et al. Single-drug therapy for hypertension in men. N Engl J Med. 1993;328:914-921.
97. Applegate WB, Phillips HL, Schnaper H, et al. A randomized controlled trial of the effects of three antihypertensive agents on blood pressure control and quality of life in older women. Arch Intern Med. 1991;151:1817-1823.
98. Donnelly R, Reid JL, Meredith PA, Ahmed JH, Elliott HL. Factors determining the response to calcium antagonists in hypertension. J Cardiovasc Pharmacol. 1988;12(suppl 6):S109-S113.
99. Oesterling JE. Benign prostatic hyperplasia: medical and minimally invasive treatment options. N Engl J Med. 1995;332:99-109.
100. Staessen JA, Fagard R, Thijs L, et al. Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. Lancet. 1997;350:757-764.
101. Staessen JA, Fagard R, Thijs L, et al. Subgroup and per-protocol analysis of the randomized European trial on isolated systolic hypertension in the elderly. Arch Intern Med. 1999;158:1681-1691.
102. Tuomilehto J, Rastenyte D, Birkenhager WH, et al. Effects of calcium-channel blockade in older patients with diabetes and systolic hypertension. N Engl J Med. 1999;340:677-684.
103. National Intervention Cooperative Study in Elderly Hypertensives Study Group. Randomized double-blind comparison of a calcium antagonist and a diuretic in elderly hypertensives. hypertension. 1999;34:1129-1133.
104. Messerli HF, Grossman E, Goldbourt U. Are beta- blockers efficacious as first-line therapy for hypertension in the elderly? a systematic review. JAMA. 1998;279:1903- 1907.
105. Weder AB. The renally compromised older hypertensive: therapeutic considerations. Geriatrics. 1991;46:36-48.
106. Eisalo A, Virta P. Treatment of hypertension in the elderly with labetalol. Acta Med Scand. 1984;65(suppl 6):129-133.
107. Neaton JD, Grimm RHJr, Prineas RJ, et al. Treatment of mild hypertension study; final results. JAMA. 1993;270:713-724.
108. Thacker HL, Jahnigen DW. Managing hypertensive emergencies and urgencies in the geriatric patient. Geriatrics. 1991;46:26-37.
109. Joint National Committee on Detection Evaluation, and Treatment of High Blood Pressure. The Fifth Report of The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1993;153:154-183.
110. Zeller KR, Kuhnert LV, Matthews C. Rapid reduction of severe asymptomatic hypertension: a prospective, controlled trial. Arch Intern Med. 1989;149:2186-2189.
111. Auseon A, Ooi WL, Hossain M, Lipsitz LA. Blood pressure behavior in the nursing home: implications for diagnosis and treatment of hypertension. J Am Geriatr Soc. 1999;47:285-290.
112. Gambassi G, Lapane K, Sgadari A, et al. Prevalence, clinical correlates, and treatment of hypertension in elderly nursing home residents. Arch Intern Med. 1998;158:2377- 2385.
113. Stoneking HT, Hla KM, Samsa GP, Feussner JR. Blood pressure measurements in the nursing home: are they accurate. Gerontologist. 1992;32(4):536-540.
114. Jansen RWMM, Lipsitz LA. Postprandial hypotension: epidemiology, pathophysiology, and clinical management. Ann Intern Med. 1995;122:286-295.
115. Vaitkevicius PV, Esservein DM, Maynard AK, O'Connor FC, Fleg JL. Frequency and importance of postprandial blood pressure reduction in elderly nursing-home patients. Ann Intern Med. 1991;115(11):865-870.
116. Myers AH, Baker SP, Van Natta ML, Abbey H, Robinson EG. Risk factors associated with falls and injuries among elderly institutionalized persons. Am J Epidemiol. 1991;133(11):1179-1190.
117. Granek E, Baker SP, Abbey H, et al. Medications and diagnoses in relation to falls in a long-term care facility. J Am Geriatr Soc. 1987;35:503-511.
118. Lipsitz LA, Jonsson PV, Kelley MM, Koestner JS. Causes and correlates of recurrent falls in ambulatory frail elderly. J Gerontol Med Sci. 1991;46(4):M114-M122. * Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-52. [Medline].