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CASE-BASED REVIEW
Systolic Hypertension in Older Patients
Case Study and Commentary, Jason D. Schaechter, BS, and Raymond R. Townsend, MD
Abstract
Hypertension affects more than one half of patients
older than 65 years and remains one of the major modifiable risk factors for cardiovascular disease in this population. Systolic blood pressure is now recommended
as the principal clinical end point for detection, evaluation, and treatment of hypertension. The systolic blood
pressure treatment goal is less than 140 mm Hg in
patients without risk factors such as diabetes. Lifestyle
and dietary modification are recommended for all hypertensive patients, and this includes weight loss, salt
restriction, and smoking cessation. Thiazide diuretics
are the preferred first-line agents for medical therapy,
with β blockers and long-acting calcium channel blockers as other potential first options. Most patients with
systolic hypertension will require 2 to 3 drugs to achieve
goal blood pressure. Care should be taken to maintain
the diastolic blood pressure at 55 mm Hg or higher, as
pressures below this value are associated with an
increase in cardiovascular risk.
N
early 50 million Americans have hypertension, an
important risk factor for many vascular diseases,
including stroke, ischemic heart disease, heart failure, and chronic kidney disease [1]. Hypertension is common
in the elderly in the United States, with prevalence estimates
of 60% in patients aged 65 to 75 years and 70% in patients
older than 75 years [2–5]. Data from the Third National
Health and Nutrition Examination Survey (NHANES III)
shows that only 55% of Americans who are aware of having
hypertension are being treated with medication [2]. Furthermore, blood pressure reduction below 140/90 mm Hg is
achieved in only 29% of all patients with hypertension. The
failure to adequately treat hypertension to goal values once
drug therapy is initiated results in the suboptimal blood pressure control noted in the majority of cases [4] and likely contributes to morbidity and mortality from stroke, coronary
heart disease, heart failure, and end-stage renal disease [3].
The NHANES III data also support the finding that continued systolic blood pressure elevation is the parameter that
most often contributes to poor blood pressure control [2]. In
this article, 2 illustrative cases are presented that underscore
the nuances of treating systolic hypertension. The cases are
representative of the gamut of issues encountered in the
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outpatient management of hypertension. The therapeutic
approach taken in each case represents an amalgam of formal evidence-based treatment recommendations tempered
with changes made as needed based on the physiology of
systolic hypertension and patient quality of life.
CASE STUDY 1
Initial Presentation
A 70-year-old white woman concerned about her
uncontrolled hypertension presents to her primary
care physician.
History
She has a history of uncomplicated hypertension for 35 years,
with the gradual onset of poorer control in the past few years.
Current medications are atenolol 50 mg twice daily, doxazosin 4 mg daily, and hydrochlorothiazide (HCTZ) 25 mg
daily. She does not have diabetes and has no known heart
disease. Her family history shows maternal hypertension,
which was controllable, but the patient cannot recall specific
medications. Her father died from a stroke in his 70s, and her
brother died from heart disease at age 68 years. She does not
have any lipid disorders and is not aware of any in her family. She smoked 1 pack of cigarettes per day for approximately 50 years, although she has now reduced her smoking to
6 or 7 cigarettes per day. She consumes an occasional alcoholic beverage and exercises by walking. She denies the use
of nasal sprays, decongestants, and amphetamines. She is
married and works part-time in a clothing shop.
On review of systems, the patient states that she feels
“OK” and has good appetite. She is not short of breath and
has no chest pain or palpitations. She does not sweat spontaneously. Her bowels are normal. She reports an occasional
episode of nocturia. She denies headaches or dizziness as
well as symptoms of sleep apnea. She describes herself as
somewhat “hyper” and has been told by other physicians
that she may suffer from “white coat” hypertension.
Physical Examination
The patient is 67” tall and weighs 139 lb. Her body mass index
(BMI) is normal at 21.9 kg/m2. Averaged blood pressures
From the Department of Medicine, University of Pennsylvania, Philadelphia, PA.
Vol. 10, No. 1 January 2003 JCOM 47
SYSTOLIC HYPERTENSION
Indicates reflected pulse wave
Shoulder
225
Notch
Pressure, mm Hg
Pressure, mm Hg
150
125
100
75
50
Notch
137
50
0
1.5
Time, s
0
Time, s
1.5
Figure. Two arterial wave contours obtained from the radial artery of a young (left panel) and an older (right panel) subject.
The “notch” indicates aortic valve closure. Note the augmentation of the systolic pressure in the right (older subject) panel
when the pulse wave (depicted as curved arrow) returns to the heart just prior to aortic valve closure. (Reprinted with permission from Malhotra A, Townsend RR. Clinical significance of systolic and pulse pressure. Emerg Med Oct 2000:52–64.)
(2 readings rounded to the nearest even digit in mm Hg) and
heart rate (bpm) are as follows:
Position
Right
Arm
Supine
192/100
Sitting
190/880
Standing
184/980
Left
Arm
Cuff
Size
Heart
Rate
Regular
62
188/100
64
70
Head, eyes, ears, nose, and throat examination shows a
supple neck, no carotid bruits, and no distended veins. Thyroid evaluation is normal. Funduscopic examination shows
vessels with arteriolar narrowing. The chest is clear. The
heart is normal with no gallops noted. Upon abdominal
examination, soft systolic bruits are noted in the midline and
in both upper quadrants. A faint systolic bruit is also noted
in each lower quadrant. All pulses are palpable except for the
dorsalis pedis, which cannot be palpated bilaterally.
On electrocardiogram (ECG), there is no evidence to suggest left ventricular hypertrophy (LVH). Recent testing
showed a creatinine value of 0.7 mg/dL and a potassium
value of 4.1 mEq/L.
• What factors could be contributing to this patient’s elevated systolic values?
Isolated Systolic Hypertension
As defined by JNC-VI, when systolic blood pressure is
140 mm Hg or greater with associated diastolic pressure less
48 JCOM January 2003 Vol. 10, No. 1
than 90 mm Hg, systolic blood pressure elevation is classified
as isolated systolic hypertension, irrespective of age [3].
Systolic hypertension is believed to be an age-related process
involving vascular changes that ultimately result in decreased arterial compliance. The fall in vascular compliance is
the dominant factor in the rise of systolic blood pressure from
age 50 years on [6]. Reduced arterial compliance results from
an imbalance in the quantity of nonelastic collagen (which
increases with aging) and a reduction in the intact elastin in
vascular walls accompanied by a proliferation and subsequent migration of undifferentiated muscle cells of the tunica
media to the intima. These changes cause an increase in arterial stiffness, resulting in vessels without elasticity. As this
arterial stiffening proceeds, the velocity in the reflection of the
pressure waves generated with each heartbeat from the
periphery back to the heart is enhanced, which contributes
further to a disproportionate increase in systolic blood pressure (Figure) [7].
Up to 60% of elderly hypertension patients are believed to
have isolated systolic hypertension [8]. In the Framingham
Study, 57.4% of men and 65.1% of women older than 65 years
were diagnosed with isolated systolic hypertension [9]. The
principal outcome associated with isolated systolic hypertension is cardiovascular disease, including stroke. Although systolic blood pressure traditionally had been considered the less
important metric, its predictive potential for cardiovascular
disease has gained much recent attention. Ameta-analysis conducted by Staessen and colleagues on data from 15,693 patients showed that systolic blood pressure elevations of
10 mm Hg yielded hazard rates of 1.26 for total mortality, 1.22
for stroke, and 1.07 for coronary events [10]. Moreover, the
Multiple Risk Factor Intervention Trial, which evaluated
316,099 men, found that systolic blood pressure was a stronger
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CASE-BASED REVIEW
predictor for assessing risk for cardiovascular disease than was
diastolic blood pressure [11].
White Coat Hypertension
JNC-VI defines white coat hypertension as blood pressure
elevated in the clinical setting but normal at other times [3].
Self-measurement outside of the physician’s office or ambulatory blood pressure monitoring may be useful in determining if the clinical setting is indeed responsible for the
blood pressure elevation. White coat hypertension is seen
more often in elderly women [12]. Disagreement exists regarding exact mm Hg values that constitute “normal” at
home and “high” in the health care setting. We generally use
values of less than 130 mm Hg for systolic (< 85 mm Hg diastolic) at home and greater than 140 mm Hg for systolic
(> 90 mm Hg diastolic) in the office. In making a diagnosis of
white coat hypertension, it is important to ensure that the
patient is using an accurate device and performing the measurement correctly [13].
In some cases of white coat hypertension, particularly
with systolic values greater than 160 mm Hg in the office, an
echocardiogram may be useful to rule out the possibility of
diastolic dysfunction or LVH since drug treatment for hypertension is sometimes withheld in these patients. If the echocardiogram shows impaired left ventricular diastolic function or LVH, initiation of antihypertensive drug therapy
would be reasonable. If the health care setting is causing a
blood pressure elevation because of a heightened sympathetic nervous system response, it is conceivable that other
perceived stressful environments could elevate blood pressure as well. If such circumstances exist, it may be prudent to
treat the augmented blood pressure, although debate persists on this issue [14]. Moreover, it is also possible that some
patients, particularly older patients with predominantly systolic hypertension, have greater lability in blood pressure
readings that is most pronounced in the systolic blood pressure readings and is evident at home as well as in the office
setting [15]. White coat hypertension does affect patients
with hypertension and should be considered in patients
with “drug-resistant” hypertension [16].
Pseudohypertension
Due to age-related increases in arterial wall rigidity from
medial sclerosis and calcification, falsely augmented sphygmomanometer readings (pseudohypertension) occasionally
occur in the elderly population. A higher cuff pressure is
required to occlude these rigid arteries, and an augmented
systolic pressure reflects the pressure necessary to collapse the
sclerotic calcified wall, not the true intra-arterial pressure.
Although verification of pseudohypertension requires an
intra-arterial pressure measurement, the clinician may suspect
it when the brachial or radial artery is clearly palpable after
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inflation of the blood pressure cuff to values that render the
artery pulseless. In some cases, the patient may report symptoms of severe dizziness and even syncope with “good” blood
pressure control on medication; therefore, great care should be
taken when measuring blood pressure [17].
• What is the significance of the abdominal bruits?
Abdominal bruits auscultated in the epigastric region in conjunction with hypertension may be a sign of renal vascular
hypertension. Studies suggest that between 75% and 85% of
patients with renal artery stenosis demonstrated by angiography have abdominal bruits [18]. It is beyond the scope of
this review to fully discuss renovascular disease and renovascular hypertension, but recent studies suggest that it is
worthwhile to attempt medical therapy in many patients
with hypertension and renal artery stenosis [19].
• Are laboratory tests recommended in this patient?
The findings from the history and physical examination
indicate a significant elevation in systolic blood pressure,
which requires consideration of further diagnostic and pharmacologic intervention. Routine laboratory tests are recommended to further assess any target organ damage or other
confounding factors prior to drug intervention when the
presenting hypertension is below a systolic pressure of
180 mm Hg and below a diastolic pressure of 110 mm Hg, or
coincident with medication changes when the hypertension
is more severe [3]. Tests include urinalysis, complete blood
cell count, and blood chemistry, including measurement of
potassium, creatinine, glucose, and lipid levels. Secondary
hypertension etiologies such as pheochromocytoma, primary aldosterone excess, and renovascular diseases are all worthy of consideration in patients who present with refractory
hypertension. Some authorities suggest measuring plasma
renin activity and serum aldosterone concentration to screen
for aldosterone excess [20]. There is nothing to suggest catecholamine excess in this patient.
Management
Routine laboratory tests are ordered. Because of the
patient’s “white coat” history, the physician recommends that she obtain a home blood pressure kit, and she is
asked to bring data from her home monitoring to the next
visit. Plasma renin activity and serum aldosterone concentration tests are discussed with the patient, and an appointment
is made to perform these tests before her next visit. Pursuit of
Vol. 10, No. 1 January 2003 JCOM 49
SYSTOLIC HYPERTENSION
renovascular disease is discussed, but the patient is reluctant
to undergo further evaluation unless “absolutely necessary.”
It is agreed to try medication adjustment first, assuming reasonable renal function can be maintained.
• What is the recommended treatment for systolic hypertension?
nel blockers consideration as therapy for systolic hypertension [3]. It is important to remember that if dihydropyridine
calcium channel blockers are used, the short-acting (immediate) forms should be avoided because they increase cardiovascular risk [29].
The recent STOP hypertension trials suggest that even
patients at the extremes of older age derive benefit from systolic and diastolic blood pressure control [30]. Drawbacks to
pharmacologic intervention exist, however. Elderly patients
commonly suffer from glucose intolerance, a condition that
may be worsened by diuretics and β blockers. Therefore,
medication choice should include consideration of existing
risk factors.
An important point regarding hypertension treatment is
the need to discard the myth of monotherapy. Using a single
agent to control systolic blood pressure is effective in less
than half of patients, and achieving the currently recommended systolic blood pressure goals will usually require 2
or 3 drugs. Of these, at least 1 is usually a diuretic, and another will often be a dihydropyridine calcium channel blocker.
Lifestyle Changes
For all forms of hypertension, lifestyle and dietary modification are helpful in blood pressure reduction. Lifestyle modifications prevent or delay normotensive patients from developing hypertension later in life [21,22]. Patients should be
encouraged to increase their amount of physical activity, for
example, by trying to walk 1 mile a day. Sodium intake
should be reduced to less than 2.4 g per day [3], and a “sodium counter” type of handout should be provided. Use of
tobacco should be discouraged. Those who continue to
smoke during the course of antihypertensive therapy may
fail to benefit from medication as much as nonsmokers [23].
Lifestyle modifications become even more vital for the
treatment regimen when patients have additional cardiovascular disease risk factors such as dyslipidemia or diabetes
mellitus. In the DASH diet study, a diet rich in fruits and vegetables and low in fats, especially saturated fats, significantly lowered blood pressure [24]. For patients who are currently overweight with a BMI of 27.5 kg/m2 or more, a
weight reduction of as little as 10 lb may result in reduced
blood pressure [25]. Evidence suggests that although lifestyle modifications alone are often not sufficient to control
elevated blood pressure, they reduce the number of antihypertensive medications required to ultimately achieve blood
pressure control [26].
• Why was a potassium-sparing diuretic selected?
Drug Therapy
In untreated hypertensives with blood pressures less than
160 mm Hg systolic, if the blood pressure goal is not
achieved by lifestyle modification alone after approximately
3 to 6 months, then drug therapy is indicated. Thiazide
diuretics or β blockers are considered first option medications, with diuretics being the preferred first-line intervention [3]. The Systolic Hypertension in the Elderly Program
(SHEP) treated patients with isolated systolic hypertension
with chlorthalidone 12.5 mg to 25 mg, and atenolol 25 to
50 mg was added in patients with more stubborn hypertension; the results showed significant reductions in stroke,
myocardial infarction, and left ventricular failure [27]. In the
Systolic Hypertension in Europe trial, the dihydropyridine
calcium antagonist nitrendipine decreased the incidence of
stroke by 42% [28], earning dihydropyridine calcium chan-
The amiloride choice was based on the finding that many
older patients have low plasma renin activity, and manipulation of the diuretic regimen is often effective in such circumstances [31,32]. If the patient is already on a thiazide diuretic,
as the case patient is, consideration of spironolactone or amiloride is reasonable [33]. By binding to and blocking luminal
sodium channels, amiloride inhibits sodium reabsorption
from the late distal tubule and collecting duct. Minimizing
sodium retention is often the key to improvement in lowrenin hypertension patients. Because of the potassiumsparing nature of amiloride (and spironolactone), it is important to periodically monitor serum potassium and to be
cautious in the use of angiotension-converting enzyme (ACE)
inhibitors, angiotensin receptor blockers, and nonsteroidal
anti-inflammatory drugs, all of which may potentiate the
50 JCOM January 2003 Vol. 10, No. 1
Adjustment of Antihypertensive Regimen
At the initial visit, the patient is prescribed amiloride
5 mg daily (titrating to 10 mg daily in 2 weeks), and
she remains on her other medications. In addition, the physician discusses with the patient the issue of salt restriction
and encourages her to participate in physical activity. He
strongly recommends that she stop smoking and discusses
available options such as nicotine replacement and behavioral therapies. A follow-up visit is scheduled in 6 weeks to
assess the effectiveness of the medication change and for the
presence of any adverse side effects.
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CASE-BASED REVIEW
retention of potassium. Diabetics and patients with impaired
renal function are at greater risk of hyperkalemia.
Alternatively, a long-acting dihydropyridine calcium
channel blocker such as amlodipine, felodipine, isradipine, or
nisoldipine could have been used in this patient, as reviewed
above. In addition, an ACE inhibitor [34] or an angiotensin
receptor blocker [35] is also effective in systolic hypertension
when used with a diuretic. Recently, the LIFE study compared
an angiotensin receptor blocker with a β-blocker–based regimen for treatment of isolated systolic hypertension. Although
similar blood pressure reduction and virtually identical blood
pressure control were achieved with each therapy, cardiovascular events were significantly reduced in the angiotensinreceptor blocker group compared with the β-blocker group,
suggesting that in some cases specific mechanisms of antihypertensive therapy may provide greater cardiovascular benefit [35]. In the case patient, we were reluctant to use an ACE
inhibitor or an angiotensin receptor blocker because of the
bilateral bruits [36].
Follow-up at 6 Weeks
The patient returns for her follow-up visit. Blood
testing results show a plasma renin activity of 0.4 ng
A-1/mL/h. This value is somewhat on the low side for an
average salt intake, but measurement of urine sodium was
not done with which this could be verified. β-Blocker therapy suppresses plasma renin and may be a contributing factor in this case. The serum aldosterone concentration is
19 ng/dL, which is within the laboratory limits of normal
when the sample for the tests is drawn with the patient in the
seated position (the sample was drawn in the seated position, at midday, without any specific preparation such as
high salt intake). The physician interprets these results as
indicative of low renin activity, even if the β blocker is a factor, with evidence of some aldosterone effect. These findings
support the use of a potassium-sparing diuretic approach.
Blood pressures taken in the left arm (which had a higher
diastolic value compared with the right arm) with the patient
sitting were as follows: 164/72 mm Hg, 172/74 mm Hg, and
154/70 mm Hg. Heart rate is 56 bpm. The patient has responded to the amiloride. Her potassium level is measured
again at 4.3 mEq/L. As such, the amiloride is titrated to the
maximal dosage, 20 mg daily taken as 10 mg twice daily.
Her home blood pressures have ranged around
150 mm Hg systolic and have been as low as 134/69 mm Hg.
She has brought her Omron HEM 711 device with her, and
the physician checks it against the office readings by having
the patient measure her own (supervised) blood pressure
during the visit. The instrument is judged to be accurate
(within 4 mm Hg systolic) and the patient’s technique appears to be good. A follow-up visit is scheduled.
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At 10 Weeks
The patient’s record of at-home blood pressures shows that
her readings have usually been below 140 mm Hg systolic.
Office blood pressures (not averaged this time) in the left arm
with the patient seated are 156/70 mm Hg, 146/72 mm Hg,
and 138/74 mm Hg. The heart rate is 54 bpm. The patient
has maintained her response to the amiloride. Her heart
rates are low, and in the future it may be possible to reduce
her β-blocker dosage; however, this remains a long-term
goal. The patient is asked to return for a follow-up visit in
3 months.
• How does diastolic blood pressure respond to treatment for systolic hypertension?
During the course of treatment for systolic hypertension, antihypertensive medications may inadvertently lower an already
controlled diastolic blood pressure. Data from the SHEP study
showed that diastolic pressures that fell below 55 mm Hg in
elderly patients were associated with a modest rebound increase in the risk for stroke [37]. In younger patients, the usual
blood pressure reduction is in the range of 3 mm Hg systolic
for each 2 mm Hg diastolic, and reduction of 12/8 mm Hg is
common. In older patients with systolic hypertension, it is
common to see reductions of 3 or even 4 mm Hg systolic for
each 1 mm Hg diastolic pressure reduction.
One caveat in treating hypertension has to do with “overtreatment” in which the degree of blood pressure lowering
results in a loss of antihypertensive benefit and an actual
increase in cardiovascular risk. This tends to occur principally when the diastolic blood pressure is excessively lowered
and is known as the J-point phenomenon. This issue was
partially addressed in the HOT study but not laid to rest [38].
In HOT it appeared that the subjects achieving the lowest
diastolic blood pressure values had confidence intervals for
cardiovascular risk that suggested an increase in risk at the
extremes of achieved diastolic values. At present, it is generally recommended to maintain the diastolic blood pressure
at or above 55 mm Hg to minimize risk from the J-point phenomenon [37].
Follow-up at 28 Weeks
At this visit, the blood pressures (not averaged) in the
left arm with the patient seated are 148/72 mm Hg
and 148/72 mm Hg. Heart rate is 58 bpm. Her creatinine level
is 0.9 mg/dL and glucose (fasting) is 80 mg/dL. When the
physician questions the patient about side effects from her
therapy, she states that she has been feeling tired since starting the atenolol and is a little more tired now; however, it is
Vol. 10, No. 1 January 2003 JCOM 51
SYSTOLIC HYPERTENSION
not restricting daily activities, and she agrees to bear with it
for a while longer. At this time there are no plans to pursue
the renovascular disease further, but it remains an option for
the future.
• How can the patient’s complaint of fatigue be addressed?
Blood pressure control in this patient is now reasonable, and
her creatinine has not changed in the course of therapy. In
some patients, step-down therapy can be undertaken to address side effects, but we usually reserve this maneuver until
after approximately 8 to 12 months of prolonged blood pressure control has been in place. If fatigue on therapy is not so
profound as to interfere with daytime activity, we encourage
patients with refractory hypertension who have responded
well to therapy to stay with the regimen. We specify an interval such as “another 3 months” since an exact period is usually more likely to be accepted by the patient. In some patients,
the fatigue lessens as the adaptation to either the drug, the
lower blood pressure, or both improves. In others, a change in
therapy becomes necessary when fatigue persists or worsens.
CASE STUDY 2
Initial Presentation and History
A 60-year-old woman concerned about her uncontrolled hypertension presents to her primary care physician. Antihypertensive therapy was started about 9 years
ago, but blood pressure control has become increasingly difficult recently. Current medications include verapamil-long acting 240 mg daily and metoprolol-XL 50 mg daily. The patient
is not diabetic and has no known heart disease and no known
drug allergies. Her past medical history is remarkable for a
stress/anxiety disorder diagnosed at age 34 years. Her family
history shows an absence of any known hypertension in her
parents. No information regarding dyslipidema or renal disease is known. Social history shows that she smoked briefly
when younger. She also drank alcohol, sometimes “excessively” when younger, but not in the past 10 years. She had exercised daily in the past, but recently her physical activity has
been curtailed due to back discomfort. She states that she is
under significant family-related stress.
On review of systems, the patient shows a stable weight.
She is not short of breath and has no chest pain. She has noted
a fluttering sensation in the chest in the past. She does not
sweat spontaneously. Her bowels are constipated. She denies
headaches or dizziness. She denies symptoms of sleep apnea.
Physical Examination
On physical examination, the patient is 60” tall and weighs
112 lb. Her BMI is normal at 21.9 kg/m2. The blood pressures
52 JCOM January 2003 Vol. 10, No. 1
(average of 2 readings, rounded to an even digit) are as follows:
Position
Right
Arm
Supine
196/90
Sitting
192/88
Standing
192/92
Left
Arm
186/84
Cuff
Size
Heart
Rate
Regular
72
72
76
Head, eyes, ears, nose, and throat examination show a
supple neck, no carotid bruits, unremarkable fundi, and no
jugular venous distension when upright. The chest is clear to
auscultation with symmetric sounds. The heart examination
is normal. Extremities are without edema, and the pedal
pulses are intact. There are no abdominal bruits.
The patient has brought with her records of a recent ECG
and results from laboratory testing done within the last
6 months. These are unremarkable.
Management
The physician discusses performing renin activity and serum
aldosterone tests with her, but she declines these unless they
are “absolutely necessary.” The physician also discusses the
nature of primary/essential hypertension versus secondary
forms with the patient, explaining that systolic hypertension
is a disorder of vascular stiffness and indicating that his
approach to therapy for predominantly systolic hypertension
is to incorporate a diuretic into the regimen. She has been
reluctant in the past to take a diuretic because of concerns
regarding excessive voiding. The physician explains that
urine volume is more dependent on fluid intake and less on
the diuretic after the first 2 or 3 weeks of therapy. This
assuages her concerns sufficiently for her to try diuretic therapy. The physician prescribes 12.5 mg HCTZ daily (one-half
25 mg tablet daily), with plans to titrate the dosage to 25 mg
daily in 4 to 6 weeks. Because of the constipation, the verapamil is discontinued. The physician also recommends that
the patient monitor her blood pressure at home and record
her measurements in a log book. He asks her to bring the
book to her next visit.
• What is the goal systolic blood pressure when treating
older patients?
The goals for systolic blood pressure control in older patients
remain the same as goals for blood pressure treatment in
younger patients. For patients with severe systolic elevations,
the National High Blood Pressure Education Program
suggests a temporary systolic goal of 160 mm Hg [21]. In most
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CASE-BASED REVIEW
patients the systolic blood pressure treatment goal is less than
140 mm Hg. In higher risk patients, such as those with diabetes or proteinuria (greater than 500 mg daily), a systolic
blood pressure goal of less than 130 mm Hg (diabetes) or less
than 125 mm Hg (proteinuria) is recommended to reduce further the risk for cardiovascular and renal disease [3].
An additional consideration to keep in mind is that current blood pressure goals may need further revision when
target organ damage is present. This was supported by the
recent PROGRESS study, which showed that the combination of an ACE inhibitor with diuretic therapy reduced the
likelihood of a second stroke when a first stroke had already
occurred, even in normotensive individuals [39].
• What is an acceptable degree of systolic blood pressure
control?
Systolic blood pressure control is unlikely to reach 100% of
guideline recommendations. The recent CONVINCE data
suggest that achieving a blood pressure of less than 140 mm
Hg in 60% of patients is a realistic level of systolic control
[40]. In our experience, we are usually able to decrease an
elevated systolic pressure to less than 160 mm Hg about 85%
of the time and to below 140 mm Hg about 60% of the time
[31]. The measures we have found most useful are to initiate
or manipulate a diuretic regimen, add or adjust a dihydropyridine calcium channel blocker, and add or adjust an
angiotensin receptor blocker [41].
Follow-up at 4 Weeks
Blood pressures (not averaged) in the right arm with
the patient in a seated position are 156/72 and
158/72 mm Hg. Her home blood pressure values also reflect
improvement. The physician verifies the accuracy of her
home UA AND 767 monitor and her technique. However,
she relates significant dismay over how she feels on the
diuretic, and has read the package insert prepared by the
pharmacist for her. She produces the package insert, which
has multiple areas highlighted in yellow marker. She also
feels she is “going to the bathroom too often.” The physician
reviews these issues with her, and although satisfied with
the answers, she is still reluctant to continue the HCTZ.
Felodipine 5 mg daily is substituted. A careful review of calcium channel blocker side effects is undertaken with her
prior to her leaving the office.
At 10 Weeks
Blood pressures (not averaged) in the right arm with the
patient in a seated position are 168/84 and 160/82 mm Hg.
Heart rate is 64 bpm. At-home readings average approxiwww.turner-white.com
mately 150 mm Hg. The felodipine dosage is increased to
10 mg daily. The physician informs her that it is likely that
an additional agent will be necessary to supplement the
felodipine and metoprolol-XL and instructs her to call in her
blood pressures in 2 weeks after the increase to 10 mg of
felodipine. He also tells her that he would likely choose an
angiotensin receptor blocker such as losartan or valsartan
and reviews the side effect profiles of these agents with her.
An appointment is scheduled for another 4 weeks.
She calls with interval blood pressure values after 2 weeks,
which though slightly better, are still short of goal, and valsartan 80 mg daily is added.
At 14 Weeks
Blood pressure readings and heart rate are as follows:
Position
Right Arm
Heart Rate
Sitting
132/60
64
Sitting
130/60
Standing
136/66
62
Blood pressure control is reasonable with the combination of felodipine 10 mg daily, valsartan 80 mg daily, and
metoprolol-XL 50 mg daily. No further changes are made in
her regimen. An appointment is scheduled for 3 months to
assess maintenance of blood pressure control.
• What are the interesting points of this case?
Several issues in this case are worth reviewing. First, a longacting dihydropyridine calcium channel blocker (felodipine)
was substituted for a phenylalkylamine calcium channel
blocker (verapamil). Although this change would seem unlikely to result in a significant reduction in blood pressure,
the combination of β blocker with a dihydropyridine calcium channel blocker in our experience has been generally
more effective than the combination of nondihydropyridine
calcium channel blocker therapy with β blockade.
It was frustrating to abandon HCTZ therapy in this patient, but it was clear that she had serious concerns about
side effects, and the package inserts summarizing 40 years of
experience with thiazide therapy in literally millions of patients treated can be quite daunting. Because there were
acceptable alternative therapies, however, stopping HCTZ
therapy seemed the wiser choice.
The patient’s ability to measure blood pressure was verified in the office, and her therapy was altered outside the
office because we trusted her readings and had discussed the
option before hand and she agreed to this approach.
Vol. 10, No. 1 January 2003 JCOM 53
SYSTOLIC HYPERTENSION
Growing support for home monitoring is evident by the frequency with which hypertensive patients perform home
blood pressure measurements. When done properly, such
measurements can add to patient compliance and understanding [42]. An ongoing study is evaluating the benefit of
home- versus office-based blood pressure management [43].
Conclusion
Hypertension remains one of the most treatable risk factors
for cardiovascular disease. In the elderly especially, when the
lifetime accumulation of risk factors for cerebral and cardiac
disease become increasingly troubling, antihypertensive
therapy is critically important. The risks from high blood
pressure are offset, in part, by the fact that older patients are
more likely to derive benefit from blood pressure treatment
than younger patients [44].
Corresponding author: Raymond R. Townsend, MD, University of
Pennsylvania, 210 White Building, 3400 Spruce St., Philadelphia, PA
19104.
Financial disclosures: None.
Funding/support: The research in this work was supported by NIH
grant K24-DK-02684.
Author contributions: conception and design, RRT; drafting of the
article, JDS; critical revision of the article for important intellectual
content, RRT; final approval of the article, RRT; collection and assembly of data, JDS.
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Vol. 10, No. 1 January 2003 JCOM 55