Hypertension in the Elderly
Hypertension in the Elderly
Author: Norman M. Kaplan, MD, Professor of Internal Medicine, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Peer Reviewers: Jonathan Abrams, MD, Professor of Medicine, Division of Cardiology, The University of New Mexico, Albuquerque, NM; Michael H. Crawford, MD, Robert S. Flinn Professor, Chief of Cardiology, University of New Mexico, Albuquerque, NM.
Editor’s Note—Hypertension is present in more than 50% of people older than age 65. Almost two-thirds of the hypertension in those older than age 65 is purely or predominantly systolic in nature, reflecting the progressive atherosclerosis of large capacitance vessels, which amplify the pulse wave velocity and produce an early return of pulse wave reflection in systole. Care is needed in making the diagnosis, preferably with multiple out-of-the-office blood pressure (BP) measurements. In addition, postural hypotension frequently accompanies systolic hypertension and, if present, must be managed before treatment of the hypertension.
Treatment of isolated systolic hypertension (ISH) in the elderly provides, in the short term, even greater protection against the various hypertension-induced morbidities and mortalities than does treatment of younger hypertensives. Six major randomized controlled trials have documented the benefits of therapy of the elderly. All but the most recent were diuretic-based, and it should be noted that b-blocker-based therapy has not been shown to benefit the elderly. On the basis of these trials, JNC-6 recommends a diuretic as the preferred treatment of ISH but adds a long-acting dihydropyridine as an appropriate alternative. Other drugs may be useful, including a-blockers for those elderly men with prostatism. In the Swedish Trial in Old Patients-2 study, small doses of an ACE inhibitor provided equal benefit against cardiovascular mortality as did conventional therapy (diuretic, b-blockers or both) or low doses of a calcium channel blocker.
In the enthusiasm to apply these major benefits of therapy to the large population of vulnerable elderly hypertensives, sight should not be lost of the well-described antihypertensive efficacy of multiple lifestyle modifications and of the multiple potential hazards of indiscriminate therapy.
By appropriate use of non-drug and drug therapies, the elderly hypertensive can be protected, sometimes against death but to an even greater degree against debilitating morbidities, surely justifying their therapy.
The Scope of the Problem
The most rapidly expanding part of the population in the United States and other developed societies is the elderly, defined as age 65 or older. Projections estimate that more than 20% of the U.S. population will be older than 65 by the year 2030 with almost 1 million being older than age 100.1 The provision of health care for this large group of elderly people will cost a great amount. From the age of 65 until death, the cumulative cost of health care is estimated to average $150,000 per person who dies at age 75; $250,000 per person dying at age 90; and $400,000 per person dying at age 100.1 Much of the increased costs will be consumed by nursing home care, which as will be noted, could be reduced by effective treatment of hypertension.
The Burden of Hypertension. As the population ages, the incidence of hypertension progressively rises (see Figure 1). By age 65, the majority of people will be hypertensive—the prevalence reaching almost 80% among African-American women. Most of this hypertension is predominantly or purely systolic in nature, reflecting the progressive rise in systolic pressure with age, accompanied by the usual fall in diastolic pressure with age, accompanied by the usual fall in diastolic pressure (see Figure 2). In the Framingham cohort, almost two-thirds of the hypertension seen among those older than age 65 was ISH.2
The Changing Pattern of Blood Pressure
The progressive rise in systolic blood pressure and the usual fall in diastolic pressure noted in Figure 2 is a reflection of the arteriosclerotic and atherosclerotic rigidity of the large capacitance arteries (aorta and major branches) that is almost invariable in people living in developed societies. Thereby the difference between the systolic and diastolic levels, the pulse pressure, progressively widens and, as will be noted, becomes the best prognostic indicator for cardiovascular risk.
As Izzo and colleagues describe:3 "Age-related changes in BP are manifestations of a generalized process of increasing arterial stiffness (or decreasing compliance) that results from the progressive replacement of elastin by collagen in the walls of large arteries. This process of diffuse arteriosclerosis leads to dilation and lengthening of the aorta and its immediate branches through fibrosis and hypertrophy of the arterial muscularis. Arteriosclerosis inevitably accompanies aging in Western societies, but its development is clearly accelerated by the presence of hypertension and the age at which it is expressed varies with the degree of BP elevation.
"Arteriosclerosis can be differentiated pathophysiologically from atherosclerosis, which is primarily related to the effects of abnormal cholesterol oxidation and deposition in the inner layers of large arteries. Atherosclerosis begins as endothelial dysfunction and macrophage uptake of oxidized lipids into the vessel walls and is accelerated by the coexistence of hypertension."
In addition to the higher pressure developing within marrowed capacitance arteries, the arterial rigidity adds another mechanism that Weisfeldt has nicely described:4
"As aging stiffens the central aorta, the left ventricle continues to eject the same amount of blood at the same rate into the aorta. As a result, the velocity of movement of blood down the arterial system accelerates with age. This acceleration in pulse wave velocity extends down the entire arterial tree. When the pulse wave reaches the iliac bifurcation, it is reflected and transmitted back toward the aorta. Moreover, like the forward transmission, the backward transmission wave is also accelerated.
"In the young (20-year-old) aorta, the rate of transmission forward and backward is slow enough so that systole has been completed by the time the reflected wave returns to the heart. This has the effect of raising aortic diastolic pressure after the aortic valve has closed. This does not increase cardiac work and tends to maintain aortic blood pressure during diastoleIn the elderly (80-year-old), the reflected wave returns well before the aortic valve shuts. This elevates systolic left ventricular and arterial blood pressure increasing the work of the left ventricle in ejecting blood. This reflected wave has the additional effect in the elderly of decreasing the diastolic aortic pressure that supports coronary flow. Clearly, this is a potentially important hemodynamic change and may have significant implications for the choice of antihypertensive strategy."
The Implications of Blood Pressure
Since the widening pulse pressure typically seen with aging reflects the arterio- and atherosclerotic changes occurring within the vasculature, it comes as no surprise that this measure is the best predictor of the risk for vascular diseases that are mainly induced by arterio- and atherosclerosis. As Kannel notes, for many years, until the 1970s, most attention was directed to the diastolic blood pressure, both to diagnose hypertension and to monitor therapy.2 Starting in the 1970s and accelerating through the 1980s, there was increasing awareness of the even greater influence of systolic levels. More recently, particularly as more data involved the elderly population, the pulse pressure, reflecting the separate contributions of both the rising systolic and the falling diastolic levels, has been clearly found to be even more accurately predictive of future cardiovascular diseases including coronary, cerebrovascular, and renal diseases as well as congestive heart failure.5 However, as Izzo et al note:3
"Pulse pressure, although slightly more robust than systolic BP as a risk indicator, is considerably less straightforward to use clinically than systolic BP, and it has not yet been validated as a surrogate end point for morbidity or mortality in a prospective randomized clinical trial."
Therefore, systolic BP will remain the major focus of concern in the elderly with the caveat that too low a diastolic pressure may also deserve attention, as will be described.
Postural Hypotension
Often accompanying the vascular rigidity that leads to a rising systolic and falling diastolic pressure, there is with age a progressive loss of sensitivity of the baroreceptor reflexes that are largely responsible for the maintenance of a normal BP despite changes in posture and activity.6 As many as 30% of elderly people with systolic hypertension will have a fall of 20 mm Hg or more in systolic pressure when they stand (i.e., postural hypotension).7 As a consequence, symptoms of cerebral hyperfusion may occur leading to falls and subsequent trauma. The falls in pressure when standing are usually most pronounced upon arising in the morning when syspurthelic nervous activity must immediately rise from the low levels induced by supine sleeping. In some, sylanchnic pooling of blood after meals may also lead to hypotension.
Recognition of the Problem. All elderly and diabetic patients should be asked about symptoms that could connote postural and post-proudial hypotension. Their examination should always include careful measurement of, first, BP after five minutes supine and then repeated measurements immediately and after two minutes of standing. If necessary, the patient can hold on to the table but must bear their weight on their upright body. If a reading is not taken immediately upon standing, a rapid and significant postural fall may be missed since the reflex may still be active but slow.8
Management. If the systolic falls more than 20 mm Hg, corrective measures should be taken before treatment of the seated/supine hypertension is attempted; otherwise, the postural symptoms will likely be aggravated by whatever antihypertensive therapy that is used. The helpful maneuvers are listed in Table 1. Since the greatest fall in BP usually occurs upon arising, it is helpful to raise the head of the bed by 12-15°, maintaining sympathetic nervous system activity through the night so the change upon arising is not so abrupt. Before standing, the patient should do 3-5 isometric exercises such as tightly squeezing a tennis ball—raising the BP by 30-40 mm Hg. If these maneuvers aren’t enough, drinking 16 oz of water before standing has been found to raise systolic BP by 30-40 mm Hg in patients with significant autonomic insufficiency.9
| Table 1. Nonpharmacological and Pharmacological Measures in the Management of Postural Hypotension Due to Neurogenic Failure |
| Nonpharmacological Measures |
| To Be Avoided |
| Sudden head-up postural change (especially on walking) |
| Prolonged recumbency |
| Straining during micturition and defecation |
| High environmental temperature (including hot baths) |
| Large meals (especially with refined carbohydrates) |
| Alcohol |
| Drugs with vasodepressor properties |
| To Be Introduced |
| Arise slowly |
| Head-up tilt during sleep |
| Small, frequent meals |
| 16 oz of water before arising |
| Isometric exercise before arising |
| To Be Considered |
| Elastic stockings |
| Abdominal binders |
| Pharmacological Measures |
| Starter drug—Fludrocortisone |
| Sympathomimetics—Ephedrine, Midodrine |
| Specific targeting—Octreotide, Desmopressin, Erythropoietin |
| Adapted from: Mathias C, Kimber J. Annu Rev Med 1999;50:317-336. |
Lifestyle Modifications
Once postural hypotension, if present, is managed, the systolic hypertension should be treated, first with lifestyle changes and then, if needed, with one or more antihypertensive drugs.
The lifestyle changes universally recommended are listed in Table 2. Some of these are even more useful in the elderly: The response to sodium reduction is greater, and the effect of smoking cessation may be profound with an immediate decrease in BP and improvement to cerebral blood flow.
| Table 2. Lifestyle Modifications for Hypertension Prevention and Management |
| • Lose weight if overweight |
| • Limit alcohol intake |
| • Increase aerobic physical activity (30-45 minutes most days of the week) |
| • Reduce sodium intake to no more than 100 mmoL/d (2.4 g of sodium or 6 g of sodium chloride) |
| • Maintain adequate intake of dietary calcium and magnesium |
| • Stop smoking and reduce intake of dietary saturated fat and cholesterol |
The best documentation of the benefits of both sodium reduction and weight loss in the elderly comes from the large and long Trial of Nonpharmacologic Interventions in the Elderly (TONE).10 In this trial, 975 elderly hypertensives who were being well controlled on medication had their medications stopped. They were then randomly placed on one of four regimens: sodium reduced diet; weight loss by caloric restriction and exercise; both sodium reduction and weight loss; or no change in either (i.e., usual care). They were then carefully monitored for the return of hypertension while remaining on no antihypertensive medication for 30 months.
As seen in Figure 3, the results were impressive. Even though the average amount of sodium reduction (40 mm/d) and weight loss (10 lbs) was relatively small, their effect was significant. Whereas only 16% of those on usual care remained normotensive on no drugs over 30 months, twice as many of those on either lifestyle regimen and three times as many on both remained normotensive.
These data are strong affirmations of the major benefits to be derived from even relatively small degrees of sodium reduction and weight loss. Though not separately evaluated, regular aerobic and resistance exercise can be equally effective, not only in lowering BP but also in reducing glucose intolerance and dyslipidemia.11
Moderation of alcohol consumption is also important. Those who drink more than two portions per day (a portion equals 1.5 oz of spirits, 4 oz of wine, or 12 oz of beer) should be strongly advised to cut back to no more than two per day both to reduce BP and to remove other dangers of excess alcohol. However, regular daily drinking of as little as one-half to two portions per day clearly provides protection against myocardial infarction, stroke, and overall mortality.12
Consumption of a diet rich in fresh fruits and vegetables and low in saturated fat can also lower BP while reducing other cardiovascular risks.13 The DASH diet is also relatively low in sodium (130 mm/d), and further benefit has been noted when additional sodium reduction is added to this diet (see Table 3).
| Table 3. The DASH Diet | ||||
| Food Group | Daily Servings | Serving Sizes | Examples and Notes | Significance of Each Food Group to the DASH Diet Program |
| Grains and grain potatoes |
7-8 | 1 slice bread 1/2 C dry cereal 1/2 C cooked rice,pasta, or cereal |
whole wheat bread, English muffin, pita bread, bagel, cereals, grits, oatmeal |
major sources of energy and fiber |
| Vegetables | 4-5 | 1 C raw leafy vegetable 1/2 C cooked vegetable 6 oz vegetable juice |
tomatoes, potatoes, carrots, peas, squash, broccoli, turnip greens, collards, kale, spinach, artichokes, beans, sweet potatoes |
rich sources of potassium, magnesium, and fiber |
| Fruits | 4-5 | 6 oz fruit juice 1 medium fruit 1/4 C dried fruit 1/4 C fresh, frozen, or canned fruit |
apricots, bananas, dates, grapes, oranges, orange juice, grapefruit, grapefruit juice, mangoes, melons, peaches, pineapples, prunes, raisins, strawberries, tangerines |
important source of potassium, magnesium, and fiber |
| Low-fat or nonfat dairy foods |
2-3 | 8 oz milk 1 C yogurt 1.5 oz cheese |
skim or 1% milk, skim or lowfat buttermilk, nonfat or lowfat yogurt, part-skim mozzarella cheese, nonfat cheese |
major sources of protein |
| Meats, poultry, and fish |
2 or less | 3 oz cooked meats, poultry, or fish |
select only lean; trim away visible fats; broil, roast, or boil, instead of frying; remove skin from poultry |
rich sources of protein and magnesium |
| Nuts, seeds, and legumes |
4-5 per week | 1/5 oz or 1/3 C nuts 1/2 oz or 2 Tbsp seeds 1/2 C cooked legumes |
almonds, filbers, mixed nuts, peanuts, walnuts, sunflower seeds, kidney beans, lentils |
rich sources of energy, magnesium, potassium, protein, and fiber |
Antihypertensive Drug Therapy
If lifestyle changes are not enough to lower systolic BP to below 160 mm Hg, antihypertensive drug therapy should be given. Whether to give drugs to the large group of elderly people with "borderline" systolic hypertension (i.e., levels between 140 and 160 mm Hg), remains an open issue. Most recent guidelines from expert committees recommend drug therapy for those with systolic levels above 140 mm Hg if they are at high risk because of the coexistence of diabetes, renal insufficiency, or congestive heart failure.14-17 However, absent data from randomized controlled trials (RCTs) in relatively low-risk elderly patients with systolic levels below 160 mm Hg, there is generally hesitation in treating such patients. Trials now in progress should soon provide evidence of the wisdom of treating such patients.
Selection of Initial Therapy. All of these expert committee guidelines agree on the choices of initial drug therapy for elderly patients with ISH: a low dose of a long reacting diuretic or dihydropyridine calcium channel blocker (DHP-CCB) (see Table 4). The "compelling" indications shown in the World Health Organization-International Society of Hypertension (WHO-ISH) guideline15 shown in Table 4 are in agreement with those from the U.S. Joint National Committee14 and other recent guidelines.16,17
| Table 4. Guidelines for Selecting Drug Treatment of Hypertension | ||||
| Class of Drug | Compelling Indications | Possible Indications | Compelling Contraindications | Possible Contraindications |
| Diuretics | Heart failure Elderly patients Systolic hypertension |
Diabetes | Gout | Dyslipidemia Sexually active males |
| b-blockers | Angina After myocardial infarct Tachyarrhythmias |
Heart failure Pregnancy Diabetes |
Asthma, COPD Heart block* |
Dyslipidemia Athletes and physically active patients Peripheral vascular disease |
| ACE inhibitors | Heart failure Left venticular dysfunction After myocardial infarct Diabetic nephropathy |
Pregnancy Hyperkalaemia Bilateral renal artery stenosis |
||
| Calcium antagonists | Angina Elderly patients Systolic hypertension |
Peripheral vascular disease |
Heart block | Congestive heart failure |
| a-blockers | Prostatic hypertrophy | Glucose intolerance Dyslipidemia |
Orthostatic hypotension | |
| Angiotensin II antagonists |
ACE inhibitor cough | Heart failure | Pregnancy Bilateral renal artery stenosis Hyperkalemia |
|
| * Grade 2 or 3 atrioventricular block | ||||
| Grade 2 or 3 atrioventricular block with verapamil or diltiazem | ||||
| Verapamil or diltiazem. Angiotensin converting enzyme (ACE) | ||||
The choice of a low-dose diuretic or a DHP-CCB is based on data from the RCTs that have been nicely summarized by Staessen et al18 (see Figure 4). In this meta-analysis of all eight published outcome trials in the elderly with ISH, involving 15,693 patients who were followed up for an average of 3.8 years, active treatment (either diuretic-based or DHP-CCB based) reduced total mortality by 13%, cardiovascular mortality by 18%, all cardiovascular events by 26%, stroke by 30%, and coronary events by 23%. Staessen et al calculated the number of elderly ISH patients who would need to be treated for five years to prevent a fatal or nonfatal event: 26 for any cardiovascular event, 48 for a stroke, and 64 for a heart attack. The number needed to treat was lower in men older than age 70 and in those who had survived a previous cardiovascular complication.
Patients Older Than Age 80. The benefits of antihypertensive drug therapy have been shown to extend to those older than age 80. In a subgroup meta-analysis of the 1670 participants in the RCTs who were 80 years or older, treatment was shown to prevent 34% of strokes, 22% of major cardiovascular events, and 39% of heart failure.19 As noted in Figure 4, in all RCTs of patients older than age 60 with ISH, total mortality was reduced much less than was morbidity—not surprising since it is likely that no medical intervention can prolong the duration of life to a significant degree in older people. However, the reduction of morbidity that makes life so difficult for the elderly provides more than enough rationale for the use of appropriate antihypertensive therapy.
In the Syst-Eur trial involving active treatment with the DHP-CCB nitrendipine, the incidence of dementia was reduced by 50%, from 7.7 in those on placebo to 3.8 cases per 1000 patient-years in those on treatment.20 Whether such protection can accompany other forms of antihypertensive therapy is not known since no other published data on the incidence of dementia have appeared.
Other Drugs. As noted in Table 4, elderly patients with other coexisting diseases should be provided appropriate therapy. Examples include: b-blockers for those with coronary disease, particularly if they have survived a myocardial infarction; ACE inhibitors for those with heart failure or diabetic nephropathy; a-blockers for those with prostatism.
On the other hand, b-blockers alone have not provided primary protection against coronary disease in the elderly.21 Moreover, in the patients enrolled in the Antihypertensive and Lipid Lowering (ALLHAT) trial, the a-blocker doxazosin did not protect against the development of heart failure as well as did the diuretic chlorthalidone, leading to discontinuation of that portion of the ALLHAT trial.22 Nonetheless, both b-blockers and a-blockers should be used if they are otherwise indicated, but not as primary choices for the broader range of ISH patients.
The Place for ACE Inhibitors. ACE inhibitors may turn out to be an appropriate choice for more elderly patients than those shown in Table 4. In a large, nonplacebo RCT of three different drug therapies in 6614 patients aged 70-84 years with combined systolic and diastolic hypertension (BP > 180/105 mm Hg), those on an ACE inhibitor did as well as those on conventional therapy (diuretic + beta-blocker or a DHP-CCB).23 The ACE inhibitor-treated third had fewer heart attacks and episodes of heart failure than the CCB-treated third.
Moreover, half of the 9297 high-risk patients older than age 55 with vascular disease or diabetes plus one other cardiovascular risk factor who were enrolled in the Heart Outcomes Prevention Evaluation (HOPE) study and received the ACE inhibitor ramipril did significantly better than the half who did not receive the ACE inhibitor.24 These patients, most with hypertension, many with diabetes, had little additional fall in BP (2-3 mm Hg) beyond that provided by their other therapies to which the ACE inhibitor was added. Therefore, the significant additional benefits of the ACE inhibitor have been attributed to additional effects beyond the antihypertensive effect.
These additional benefits of ACE inhibitors may or may not apply to the rapidly expanding group of angiotensen II—receptor blockers (ARBs). All of the expert committee guidelines14-17 recommend that they be used only in those in whom an ACE inhibitor is needed but who cannot tolerate that drug, usually because of cough, since there are no outcome data on their use in hypertension. The only currently available head-to-head comparison of an ACE inhibitor (captopril) against an ARB (losartan), performed in 3152 patients aged 60 years or older with class II-IV heart failure, confirms the wisdom of this recommendation: Those on the ACE inhibitor did better than did those on the ARB.25
Effects on Pulse Pressure. As previously noted, cardiovascular risk in the elderly reflects both the rise in systolic pressure and the fall in diastolic pressure—both reflections of atherosclerotic rigidity of large arteries. Therefore, not surprisingly, the wide pulse pressure that combines the two altered levels of BP adds even more prognostic certainty than either BP level alone.26 In the last few years, as the importance of wide pulse pressure has been recognized, interest has risen on the effects of various antihypertensive therapies on pulse pressure in addition to their effects on systolic hypertension alone.
In all of the studies of elderly patients with ISH, a greater antihypertensive effect has been noted on the elevated systolic levels than on the already low diastolic levels. For example, in the Systolic Hypertension in the Elderly Program (SHEP) trial, the average reductions provided by the diuretic-based therapy were 25 mm Hg and 9 mm Hg, respectively: 170 mm Hg systolic reduced to 145, 77 mm Hg diastolic reduced to 68.27 In the Syst-Eur trial wherein the average pretreatment BPs were 174/85 mm Hg, the effects of CCB-based therapy were on average a 23 mm Hg fall in systolic and a 7 mm Hg fall in diastolic levels.28
In the only currently completed comparative trial of representative drug from each major class, the VA Cooperative Study involving 1292 men with an average pretreatment BP of 152/99, only those given a diuretic had a reduction in pulse pressure after one year of therapy, whereas the pulse pressure rose in those on the other classes of antihypertensive agents.29 These data, though suggestive, are not definitive and may not even apply to the elderly with ISH.
On the other hand, limited experience with nitrate therapy, specifically isosobide mononitrate, has shown a somewhat more selective fall in systolic levels than in diastolic levels, presumably reflecting a greater reduction in arterial rigidity than that provided by other drugs.30 No large-scale trials are currently available but one or another agent that reduces vascular rigidity by providing nitric oxide may turn out to be particularly useful in the elderly.
The Potential Danger of Reductions in Diastolic Pressure. The desire to reduce only the elevated systolic pressures and not to reduce the already low diastolic pressures further comes both from observational data on the additional risks seen with naturally low diastolics3,4 and from data in patients whose diastolics were lowered by antihypertensive therapy.27,31 Among the patients enrolled in the SHEP trial who received diuretic-based therapy, a higher rate of cardiovascular events (mainly strokes) was seen in those whose diastolics were lowered by 5 mm Hg or more than in those whose diastolics were lowered less.27 In a prospective population cohort study of 2351 elderly hypertensives (average BP of 157/80 mm Hg), there was a significant increase in the risk of stroke in those whose diastolic pressure was reduced to below 65 mm Hg by antihypertensive therapy.31
Therefore, caution is advised in the treatment of ISH in the elderly: If the already low diastolic pressures are inadvertently reduced to below 65 mm Hg, therapy should be slowed or reduced. It should be noted that even with the apparent added risk of those whose diastolics fell in the SHEP trial, those treated did better than did those whose systolic hypertension was not treated (i.e., left on placebo). The need for treatment of ISH remains unequivocal. However, caution is advised not to lower diastolic levels too much to avoid the "J-curve" seen with significant reductions in pressure.
The Special Needs of Diabetic Hypertensives. At any age, the coexistence of diabetes with hypertension markedly increases cardiovascular risk. The elderly, including those with ISH, share this increased risk. Therefore, there is a need to treat them more intensively to levels of BP considerably lower (i.e., to below 130/80), than recommended for nondiabetic patients.14 The need for this more intensive therapy was shown in the massive Hypertension Optimal Treatment (HOT) trial.32 Among the 1501 diabetic hypertensives, those whose diastolic pressures were reduced the most (average, 81 mm Hg) had half as many major cardiovascular events as did those whose pressures were reduced the least (average, 85 mm Hg).
The HOT trial used the DHP-CCB felodipine as baseline therapy, but many patients also needed additional therapies of an ACE inhibitor (41%), b-blocker (28%), or diuretic (22%). On the basis of considerable data documenting the special benefits of ACE inhibitors in diabetics along with the strong evidence of the benefits of ramapril in the 3577 diabetics enrolled in the HOPE trial,33 an ACE inhibitor ought to almost always be the initial drug used in a diabetic hypertensive. If, as is likely, more therapy is needed, a diuretic and then a DHP-CCB would be logical additions since they provided excellent protection in the SHEP and Syst-Eur trials.34 Beta-blockers may also be considered since in the United Kingdom Prospective Diabetes Study (UKPDS), atenolol did somewhat better than did captopril in reducing cardiovascular events in 1200 diabetic hypertensives over a nine-year follow-up.35
However the BP is lowered, a goal of well below 140/90 mm Hg should be sought in diabetic hypertensives, particularly if diabetic nephropathy is present. When more intensive antihypertensive therapy, along with more intensive control of diabetes and dyslipidemia, was provided to such patients, the incidences of progressive renal, neurological, and retinal disease were markedly reduced.36 Therefore, as difficult and costly as it may be, intensive management of these high-risk patients is clearly needed.
Summary
Table 5 lists appropriate guidelines for the treatment of hypertension in the elderly. Such patients may pose multiple barriers to effective control but, with caution and persistence, they should benefit from currently available management.
| Table 5. Guidelines in Treating Hypertension in the Elderly | ||||
| • Check for postural and postprandial hypotension before starting | ||||
| • Choose drugs that will help other concomitant conditions | ||||
| • Start with small doses, titrating gradually | ||||
| • Use longer acting, once-daily formulations | ||||
| • Avoid drug interactions, particularly from over-the-counter medications (e.g., NSAIDs) | ||||
| • Look for subtle drug-induced adverse effects (e.g., weakness, dizziness, depression, confusion) | ||||
| • Monitor home BPs to avoid over and under treatment | ||||
| • Aim for the goal of SBP = 140-145, DBP = 80-85 | ||||
References
1. Spillman B, Lubitz J. The effect of longevity on spending for acute and long-term care. N Engl J Med 2000;342:1409-1415.
2. Kannel W. Elevated systolic blood pressure as a cardiovascular risk factor. Am J Cardiol 2000;85:251-255.
3. Izzo J, Levy D, Black H. Importance of systolic blood pressure in older Americans. Hypertension 2000;35:1021-1024.
4. Weisfeldt Myron. Aging, changes in the cardiovascular system, and responses to stress. Am J Hypertens 1988;11:41S-45S.
5. Franklin S. Is there a preferred antihypertensive therapy for isolated systolic hypertension and reduced arterial compliance? Curr Hypertens Reports 2000;2:253-259.
6. Mathias C, Kimber J. Postural hypotension: Causes, clinical features, investigation, and management. Annu Rev Med 1999; 50:317-336.
7. Kaplan NM. Primary hypertension: Natural history, special populations, and evaluation. In: Clinical Hypertension. 7th ed. Baltimore, Md: Williams & Wilkins; 1998.
8. Caine S, Alsop K, Mahon M. Overlooking orthostatic hypotension with routine blood-pressure equipment. Lancet 1998;352:458.
9. Jordan J, Shannon J, Black B, et al. The pressor response to water drinking in humans: A sympathetic reflex? Circulation 2000; 101:504-509.
10. Whelton P, Appel L, Espeland M, et al. Sodium reduction and weight loss in the treatment of hypertension in older persons. JAMA 1998;279:839-846.
11. Kelley G, Kelley K. Progressive resistance exercise and resting blood pressure: A meta-analysis of randomized controlled trials. Hypertension 2000;35:838-843.
12. Gaziano J, Gaziano T, Glynn R, et al. Light-to-moderate alcohol consumption and mortality in the physicians’ health study enrollment cohort. J Am Coll Cardiol 2000;35:96-105.
13. Appel L, Moore T, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997; 336:1117-1124.
14. Joint National Committee. The sixth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;360:757-764.
15. Guidelines Subcommittee. 1999 World Health Organization-international society of hypertension guidelines for the management of hypertension. J Hypertension 1999;17:151-183.
16. Ramsay LE, Williams B, Johnston GD, et al. Guidelines for management of hypertension: Report of the third working party of the British hypertension Society. J Hum Hypertens 1999;13:569-592.
17. Feldman R, Campbell N, Larochelle P, et al. 1999 Canadian recommendations for the management of hypertension. CMAJ 1999;161:S1-S22.
18. Staessen JA, Gasowski J, Wang JG, et al. Risks of untreated and treated isolated systolic hypertension in the elderly: Meta-analysis of outcome trials. Lancet 2000;355:865-872.
19. 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.
20. Forette F, Seux M-L, Staessen JA, et al. Prevention of dementia in randomised double-blind placebo-controlled Sys-Eur trial. Lancet 1998;352:1347-1351.
21. Messerli F, Grodzicki T. Antihypertensive therapy in the elderly: Evidence-based guidelines and reality. Arch Intern Med 1999;159:1621-1622.
22. The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone. JAMA 2000;283:1967-1975.
23. Hansson L, Lindholm LH, Ekbom T, et al. Randomised trial of old and new antihypertensive drugs in elderly patients: Cardiovascular morbidity and mortality in the Swedish Trial in Old Patients with hypertension-2 study. Lancet 1999;354:1751-1756.
24. The Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med 2000;342:145-153.
25. Pitt B, Poole-Wilson P, Segal R, et al. Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: Randomised trial—The Losartan Heart Failure Survival Study ELITE II. Lancet 2000;355:1582-1587.
26. Blacher J, Staessen J, Girerd X. Pulse pressure not mean pressure determines cardiovascular risk in older hypertensive patients. Arch Intern Med 2000;160:1085-1089.
27. Somes G, Pahor M, Shorr R, et al. The role of diastolic blood pressure when treating isolated systolic hypertension. Arch Intern Med 1999;159:2004-2009.
28. Staessen J, 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.
29. Cushman W, Materson B, Reda D, et al. Pulse pressure changes with six classes of antihypertensive agents and placebo. Am J Hypertens 2000;13:22A.
30. Stokes G, Ryan M, Brnabic A. A controlled study of the effects of isosorbide mononitrate on arterial blood pressure and pulse wave form in systolic hypertension. J Hypertens 1999;17:1767-1773.
31. Voko Z, Bots M, Hofman A, et al. J-shaped relation between blood pressure and stroke in treated hypertensives. Hypertension 1999;34:1181-1185.
32. Hansson L, Zanchetti A, Carruthers G, et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: Principal results of the hypertension optimal treatment (HOT) randomised trial. Lancet 1998;351:1755-1762.
33. Heart Outcomes Prevention Evaluation (HOPE) Study Investigators. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: Results of the HOPE study and MICRO-HOPE substudy. Lancet 2000;355:253-259.
34. Tuomilehto J, Rastenyte D, Birkenhager W, et al. Effects of calcium-channel blockade in older patients with diabetes and systolic hypertension. N Engl J Med 1999;340:677-684.
35. UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ 1998;317:713-720.
36. Gaede P, Vedel P, Parving H-H, et al. Intensified multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: The Steno type 2 randomised study. Lancet 1999;353: 617-622.
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