(Circulation. 2000;101:446.)
© 2000 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
Essential Hypertension
Part II: Treatment
From the Hypertension and Vascular Research Division, Heart and Vascular Institute, Henry Ford Hospital, Detroit, Mich (O.A.C.), and the Division of Cardiovascular Disease, Vascular Biology and Hypertension Program, University of Alabama School of Medicine, Birmingham (S.O.).
Correspondence to Oscar A. Carretero, MD, Hypertension and Vascular Research Division, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202. E-mail ocarret1{at}hfhs.org
Key Words: hypertension • pathology • diagnosis
The goal of antihypertensive treatment is to reduce overall CVD risk and thus its morbidity and mortality rates. In any given patient, the decision to begin treatment is governed by the risk of CVD, which is determined by the magnitude of the BP elevation and the presence or absence of target organ disease and/or additional CVD risk factors. Recent consensus committees, including JNC VI and the World Health Organization–International Society of Hypertension (WHO-ISH) Guidelines Subcommittee, have modified traditional treatment recommendations in several important ways3,35 : (1) Criteria for initiation of treatment now take into consideration total cardiovascular risk rather than BP alone, such that treatment is now recommended for persons whose BP is in the normal range but still bear a heavy burden of CVD risk factors or established CVD. (2) Systolic BP is recognized as an important target for treatment, particularly in older persons, because it is an even more important determinant of CVD risk than diastolic BP. (3) More aggressive BP goals are recommended for hypertensive patients with comorbid conditions such as diabetes mellitus or renal insufficiency. (4) The importance of tailoring the choice of antihypertensive drug treatment to the patient’s individual profile of concomitant CVD risk factors/comorbid conditions is emphasized. (5) The role of simultaneous reduction of multiple CVD risk factors in improving prognosis in hypertensive patients is stressed. (6) Home and ambulatory BP measurement has been recommended because of its value in guiding therapy and enhancing adherence to treatment. (7) Greater reliance on evidence-based medicine (ie, results of randomized controlled trials with CVD outcomes) in making treatment decisions has been endorsed.
JNC VI has arrived at an empirical classification that stratifies
hypertensive patients into risk groups for therapeutic decisions (Table 4
). Risk group A includes patients who do
not have clinical CVD, target organ damage, or other CVD risk factors.
Persons with stage 1 hypertension in risk group A are candidates for a
trial (up to 1 year) of vigorous lifestyle modification with BP
monitoring. If goal BP is not achieved, pharmacological therapy should
be added. For persons with stage 2 or 3 hypertension, immediate drug
therapy is warranted. Risk group B includes patients who do not have
clinical CVD or target organ damage but do have 1 or more major
CVD risk factors other than diabetes. The large majority of
hypertensive patients are among this group. If multiple CVD risk
factors are present, immediate drug therapy should be considered
and lifestyle modification should be used as adjunctive treatment. Risk
group C includes patients who have clinically manifest CVD or target
organ damage. JNC VI recommends that patients who have high normal BP
accompanied by renal insufficiency, heart failure, or diabetes mellitus
should receive immediate pharmacological therapy accompanied by
appropriate lifestyle modifications. The WHO-ISH Guidelines
Subcommittee has adopted a similar scheme of risk stratification to
quantify prognosis (Table 5).
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The initial goal of antihypertensive therapy for most patients is to
lower diastolic BP to <90 mm Hg and systolic
BP to <140 mm Hg with minimal adverse effects. More aggressive
BP goals (
130/85 mm Hg) are recommended for patients with
concomitant diabetes mellitus or renal insufficiency. When
self-measurement of BP or automated ambulatory BP measurements are used
to guide therapy, a reasonable goal is <135/85 mm Hg.
The ultimate theoretical goal of treatment is to achieve optimal BP
levels with respect to cardiovascular risk, for
example, <120/80 mm Hg. The rationale for this approach is
related to early reports that a major determinant of the risk reduction
conferred by antihypertensive therapy is the level of BP
achieved.36 37 However, such aggressive BP lowering is
often poorly tolerated and therefore impractical for the general
hypertensive population. Furthermore, concerns have been raised that
reducing diastolic BP levels to <85 mm Hg may
increase the risk of ischemic events (presumably secondary to
coronary hypoperfusion) in hypertensive patients with
preexisting coronary artery disease and those with a pulse
pressure >60 mm Hg, the so-called J-curve hypothesis. Large
prospective clinical trials, particularly the recent Hypertension
Optimal Treatment (HOT) study, have failed to substantiate the J-curve
hypothesis.38 Comparison of outcomes among the 3
randomized BP target groups in the HOT study (diastolic BP
90, 85 or 80 mm Hg) was unable to detect significant
differences in the risk of CVD between adjacent target groups. There
was no increase in CVD risk in patients randomly assigned to the lowest
target group (diastolic BP 80 mm Hg). Furthermore,
data from studies of patients with isolated systolic
hypertension have shown no increase in cardiovascular
morbidity and mortality rates in response to reductions in
diastolic BP to <90 mm Hg.
Among diabetic patients in the HOT study, there was a significantly lower risk of CVD in those assigned to the lowest BP target. Recent data support the value of lowering BP even farther in the prevention of renal disease and CVD in diabetes. For example, the results of the United Kingdom Prospective Diabetes Study Group trial demonstrated that tight BP control (an average achieved BP of 144/82 mm Hg) substantially reduced the risk of major CVD events compared with less tight BP control (an average achieved BP of 154/87 mm Hg).39
On the basis of these findings, WHO-ISH guidelines recommend achieving optimal or normal BPs in young, middle-aged, or diabetic subjects (<130/85 mm Hg; Table 1) and at least high normal BPs in elderly patients (<140/90 mm Hg; Table 1). JNC VI guidelines recommend similar BP goals, with even more aggressive targets (125/75 mm Hg) for patients with renal disease and heavy proteinuria (>1 g/24 h).
Antihypertensive treatment is indicated in isolated systolic hypertension because, especially among older persons, systolic BP is a better predictor of events (coronary heart disease, CVD, heart failure, stroke, end-stage renal disease, and mortality from all causes) than diastolic BP. Elevated pulse pressure, an indicator of reduced compliance in large vessels, is a better marker of increased CVD risk than either systolic or diastolic BP alone, particularly in elderly individuals with isolated systolic hypertension.40 41 Pharmacological therapy is well tolerated and effective in lowering BP and reducing CVD morbidity and mortality rates (particularly by reducing stroke) in patients with isolated systolic hypertension. Patients with systolic BP >160 mm Hg are generally considered to require treatment, with the goal of lowering systolic BP to <140 mm Hg, though an interim goal of systolic BP <160 mm Hg may be necessary in patients with marked elevations in pretreatment systolic BP.
Lifestyle Modification
Overall Recommendations
Lifestyle modifications are generally beneficial in reducing a
variety of CVD risk factors (including high BP) and promoting good
health and should therefore be used in all hypertensive patients,
either as definitive treatment or as an adjunct to drug
therapy.42 Although sustained modifications in diet and
lifestyle are difficult to achieve and have never been shown to reduce
CVD morbidity or mortality rates in controlled trials, they may lower
BP and obviate the need for drug treatment or reduce the dosages of
antihypertensive drugs needed to control BP. Therapy should be tailored
to the individual characteristics of each patient, such as weight
reduction and exercise for the overweight patient and moderate alcohol
consumption for the heavy drinker. A reasonable generalized approach
for all patients includes (1) weight loss for the overweight patient;
(2) regular physical activity; (3) moderation of alcohol consumption;
(4) dietary modification to reduce sodium and fat and increase calcium,
potassium, magnesium, vitamins, and fiber from food sources; and
(5) cessation of smoking. Such an approach has been shown to produce
significant sustained reductions in BP while reducing overall
cardiovascular risk. In well-motivated patients with
stage 1 or 2 hypertension, modifying lifestyle effectively lowers BP
and may be more important than the initial choice of antihypertensive
drug. The same lifestyle modifications that are effective in treating
hypertensive patients may be useful in the primary prevention of
essential hypertension.
Weight Reduction
Weight loss is closely correlated with reduction in BP and appears
to be the most effective of all nonpharmacological measures used to
treat hypertension. Weight loss also enhances the efficacy of
antihypertensive drugs. This effect is independent of dietary sodium
restriction and is seen in both obese and nonobese hypertensive
individuals. Weight reduction of as little as 10 lb reduces BP in a
large proportion of overweight hypertensive persons and has a
beneficial effect on associated coronary artery disease risk
factors such as insulin resistance, diabetes,
hyperlipidemia, and left ventricular
hypertrophy, as well as the patient’s self-image and sense
of well-being.
Weight reduction of at least 10 lb (with further increments depending on the initial response and the patient’s baseline weight) through a combination of dietary caloric restriction and increased physical activity is recommended for all overweight hypertensive individuals.35 These patients should avoid appetite suppressants, which contain sympathomimetics such as phenylpropanolamine that can elevate BP. The appetite suppressant drugs fenfluramine and phentermine have been withdrawn from the market because of cardiovascular toxicity, including serious mitral, aortic, and tricuspid regurgitant lesions and, rarely, pulmonary hypertension. Because sustained weight reduction is so difficult to achieve, more emphasis should be placed on prevention of weight gain, particularly in younger individuals with high normal BP and in families with a high prevalence of hypertension.
Increased Physical Activity
At least 30 minutes of moderately intense physical activity, such
as brisk walking, swimming, bicycling, or yard work, at least 3 times
per week (preferably once per day) can lower BP in both normotensive
and hypertensive individuals. Studies suggest that such moderate
activity may lower systolic BP by 
4 to 8 mm Hg and is
more effective than more strenuous forms of exercise such as running
and jogging.43 Additional benefits of regular physical
activity include weight loss, enhanced sense of well-being, improved
functional health status, and reduced risk of CVD and mortality from
all causes. Accordingly, regular aerobic physical activity is
recommended for all hypertensive individuals, including those with
target organ damage. Patients with advanced or unstable CVD may require
a medical evaluation before initiation of exercise or a medically
supervised exercise program. Isometric exercise such as heavy weight
lifting can have a pressor effect and should be avoided.
Moderation of Alcohol Intake
Alcohol consumption elevates BP both acutely and chronically. In
cross-sectional and prospective studies involving all kinds of
populations, the relationship between alcohol consumption, BP levels,
and the prevalence of hypertension has been remarkably
consistent.8 The relationship is linear, but some
studies show a threshold effect of 2 to 3 drinks a day. The effect
increases with age, is independent of the type of alcoholic beverage,
and is additive but independent of the effects of obesity, oral
contraceptives, and high salt intake.44 Clinical studies
show that BP falls 4 to 5 mm Hg in days or weeks with abstinence
from alcohol.45 However, moderate alcohol consumption (<3
standard drinks a day) reduces overall CVD risk in the general
population.46 Whether this risk reduction also occurs in
the hypertensive population needs to be studied further. Those having
more than 2 standard alcohol drinks per day show an increase in both
mortality rates and hypertension.47 It is estimated that
in men, the contribution of alcohol to the prevalence of hypertension
is 11%.47 In nonobese heavy drinkers, systolic BP
was 4 to 5 mm Hg higher than in nondrinkers.44
The mechanism by which alcohol raises BP is not known. Excessive
alcohol intake also appears to cause resistance to antihypertensive
therapy. For unrelated health reasons, alcohol consumption is not
recommended for nondrinkers; for drinkers, intake should be limited to
1 oz of alcohol per day (2 oz of 100-proof whiskey, 8 oz of wine, or 24
oz of beer) in most men and half that amount in women and small
men.
Dietary Modification
Two clinical trials, one with a comprehensive food plan that
supplied the recommended dietary allowances of all major
nutrients48 and the other with a diet rich in fruits,
vegetables, and low-fat dairy products and reduced in saturated and
total fat,9,49 produced reductions in BP comparable to or
greater than those usually seen with monotherapy for stage 1
hypertension. The Dietary Approaches to Stop Hypertension (DASH) trial
showed overall reductions in BP of 11.4/5.5 mm Hg in hypertensive
persons on a diet rich in fruits, vegetables, and low-fat dairy
products, compared with control subjects on a so-called "usual
American diet," while dietary sodium intake and weight were held
constant. The DASH "combination diet" also produced reductions in
BP of 3.5/2.1 mm Hg in subjects without hypertension. Remarkably,
subgroup analysis of the DASH trial indicated that the
combination diet lowered BP effectively in all participating groups
examined, independent of race, sex, age, BMI, level of education,
income, physical activity, family history of hypertension, and
geographic location of the study site.49 African American
participants, who were intentionally overrepresented in the
trial (60% of the cohort), realized greater benefit from the DASH
combination diet (mean BP decrease 6.9/3.7 mm Hg;
P<0.001) than whites (mean BP decrease 3.7/2.4 mm Hg;
P<0.01). Among African Americans with hypertension, the
DASH combination diet reduced BP by 13.2/6.1 mm Hg and among
normotensive African Americans by 4.3/2.6 mm Hg (Figure 3). Among whites, BP decreased by
6.3/4.4 mm Hg in hypertensive participants and 2.0/1.2
mm Hg in normotensive participants.
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The success of the DASH diet in lowering BP cannot be attributed solely to its micronutrient content (high in calcium, potassium, and magnesium) because the foods included in the DASH trial contain complex combinations of minerals, mac-ronutrients, fiber, phytochemicals, vitamins, and other factors that alone or in combination could lower BP.50 Translation of the results of the DASH trial to advice for the general public or the universe of hypertensive patients is more easily accomplished by recommending 4 servings of fruit, 4 servings of vegetables, and 3 servings of low-fat dairy products per day than by prescribing a specific daily intake of calcium, potassium, and magnesium. The paradigm shift toward recognition of the powerful role of total diet (rather than individual nutrients) in the prevention and treatment of hypertension in particular and CVD in general deserves emphasis.
Sodium Reduction
High sodium intake has generally been related to BP elevation,
particularly in hypertensive individuals, and this effect appears to be
augmented by concomitant low potassium intake. On the basis of these
observations and the small but consistent BP-lowering effects
observed in clinical trials of dietary sodium reduction in hypertensive
subjects, particularly obese patients, older patients, blacks, and
women, avoiding excessive sodium intake is recommended for all
hypertensive individuals. Additional benefits of sodium reduction
include reduced diuretic-induced hypokalemia and greater ease
of BP control with diuretic therapy, protection from
osteoporosis and fractures by reducing urinary calcium excretion, and
favorable effects on left ventricular
hypertrophy. A number of agencies have codified this
recommendation as a reduction in daily consumption of sodium chloride
to 6 g and of sodium to 2400 mg.3,35 51 52 This can be
achieved by avoiding obviously salty foods, not adding salt at the
table, and eating more meals cooked directly from natural ingredients.
Whether this level of sodium reduction is helpful for the general
population in preventing hypertension and related CVD morbidity and
mortality is a matter of debate, considering the minimal effect of
dietary sodium reduction on BP in normotensive subjects and possible
adverse effects of reduced sodium intake on the
cardiovascular system over time.53 54
Furthermore, the impressive results of the DASH diet (which is rich in
fruits, vegetables, and low-fat dairy foods) in lowering BP in
hypertensive subjects may diminish the role of modifying intake of
single nutrients, including sodium, in hypertension control and
prevention.
Potassium Repletion
Maintenance of adequate potassium intake (>100
mmol/d), preferably from dietary sources, is recommended for
hypertensive individuals and those with high normal BP. A diet rich in
fruits and vegetables (DASH diet) is better than pills or other
supplements as a source of potassium because these foods contain other
nutrients, for example, calcium, magnesium, and vitamins, which may
also have beneficial effects on BP. Moreover, it is clear that
potassium supplements can be harmful and should be avoided or used only
with extreme caution in patients with renal insufficiency, diabetics,
and those receiving potassium-sparing diuretics, ACE
inhibitors, or angiotensin II receptor
blockers.55
Calcium Repletion
Although there is insufficient evidence to recommend high calcium
intake for prevention or treatment of hypertension, calcium deficiency
should be avoided. Importantly, 75% to 90% of adults in the United
States fail to consume the recommended daily allowance of calcium (1200
to 1500 mg for adolescents/young adults and pregnant/nursing women;
1000 mg for mature adults younger than 65 years of age; 1500 mg for
adults older than 65 years of age). Inadequate calcium intake is
particularly common in populations at high risk of developing
hypertension, including the elderly and African Americans. Maintaining
the recommended daily allowance for calcium, preferably from food
sources, is beneficial for a variety of reasons, such as preventing
osteoporosis. Furthermore, the DASH trial showed that a diet rich in
low-fat dairy foods is associated with major reductions in BP in both
normotensive and hypertensive persons.9,48 49 50
Macronutrient Alteration
A variety of macronutrients, including fiber, fish oils rich in
-3 fatty acids, garlic, fat, carbohydrates, and protein have been
related to BP, mainly on the basis of observations that populations
that consume unusually large amounts of these nutrients have low BP and
a low prevalence of hypertension. Careful observational studies in this
area are few and have tended not to confirm the hypothesized
relationships between macronutrient intake and BP. Similarly, clinical
trial data are sparse. Further study is needed before a judgment can be
made regarding the value of these interventions in the prevention or
treatment of hypertension.
Smoking Avoidance/Cessation
Although cessation of smoking does not alter BP, it is important
for the prevention of both CVD and non-CVD morbidity and mortality. All
hypertensive patients who smoke should be counseled to stop, and
nicotine replacement therapy should be considered. Measures to avoid or
minimize weight gain after one stops smoking may be needed.
Pharmacological Treatment
General Considerations
Reducing BP by pharmacological means clearly reduces CVD morbidity
and mortality rates. Benefits include protection from stroke,
coronary events, heart failure, progression of renal disease,
progression to more severe hypertension, and, most importantly,
mortality from all causes. The benefits of antihypertensive treatment
in the elderly and in persons with isolated systolic
hypertension are greater than in younger persons. However, keeping
patients on treatment and treating to a goal BP are difficult in
practice, and <25% of hypertensive patients in the United States are
controlled (BP <140/90 mm Hg).3,56 A major problem
is the very high rate of discontinuance or change in medications by
hypertensive patients: 50% to 70% of new treatments are changed or
discontinued within the first 6 months in most
practices.42 These high discontinuance rates probably
reflect a combination of adverse drug effects, cost of drugs, poor
efficacy, changes in provider, dissatisfaction with other aspects of
care, and lack of understanding of the risks of target organ damage.
Dealing with these barriers to adherence to prescribed therapy is the
key to the successful treatment of hypertensive patients. Maximizing
adherence is clearly more important than choosing a specific drug or
regimen in achieving the desired outcome.
Given these practical considerations, it is reasonable to individualize antihypertensive treatment on the basis of each patient’s personal needs with respect to tolerability, convenience, and quality of life. Initiation of treatment with a drug that is expected to be well tolerated and therefore likely to be effective in lowering BP over time is prudent. Long-acting agents are preferable because adherence to therapy and consistency of BP control are superior when the drug is taken once a day. Low-dose, fixed-dose combination therapy can be used in place of monotherapy as initial treatment or as an alternative to adding a second agent of a different therapeutic class to unsuccessful monotherapy. The advantage of this approach is that low doses of drugs that act by different mechanisms may have additive or synergistic effects on BP with minimal dose-dependent adverse effects. Giving the patient a single tablet provides an additional benefit.
The treatment algorithm outlined in Figure 4 has been put forth by JNC VI. Treatment
should always include lifestyle modifications. For the minority of
hypertensive patients without comorbid conditions, target organ damage,
or concomitant CVD risk factors, JNC VI recommends starting drug
therapy with a diuretic or ß-blocker because (1) these are
the only antihypertensive drugs shown to reduce CVD morbidity and
mortality rates in randomized controlled trials, and (2) they are
less costly than the newer classes of drugs. Long-term, controlled
clinical trials are needed to clarify the benefits and risks of CVD
outcomes associated with BP reduction with the newer classes of
antihypertensive agents, particularly in patients with multiple CVD
risk factors. Randomized trials in progress around the world, with a
projected patient enrollment of 200 000, are addressing this
issue. These randomized trials, which are free of treatment assignment
bias, are needed to settle controversies raised by uncontrolled
observational studies about the potential adverse effects of some
classes of antihypertensive drugs on CVD outcomes, such as the recent
calcium channel blocker controversy. Three to 5 years of follow-up will
be required to determine whether there are significant differences in
CVD outcomes in response to treatment with different classes of
antihypertensive drugs.
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Comorbid Conditions
Comorbid conditions that influence the choice of antihypertensive
therapy, principally target organ damage and major CVD risk factors,
have been demonstrated in 50% to 70% of patients with essential
hypertension, particularly the elderly (Table 6). Antihypertensive drugs that have
added benefit for patients with these conditions should be included as
part of the treatment program, although additional drugs may be needed
to bring BP under control. Agents that have adverse effects on these
comorbid conditions should not be selected as first- or second-line
therapy but may be needed to control BP in patients with
resistant hypertension who also have one of these comorbid
conditions.
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Compelling indications for initial drug choices from specific classes are based on randomized clinical trials. ACE inhibitors, used alone or in combination with diuretics and digoxin, both prevent congestive heart failure and reduce morbid and mortal events in patients with established failure and therefore are recommended as first-line agents for treating hypertensive patients with this condition. Recent clinical trials have also shown benefit from appropriately dosed ß-blockers in the setting of heart failure.57 58 Clinical trials in progress are focused on the question of whether angiotensin II receptor blockers (ARBs) will prove useful in the treatment of heart failure, either in substitution for or as an adjunct to ACE inhibitors. Alternative therapies include hydralazine and isosorbide dinitrate as well as the dihydropyridine calcium channel blockers amlodipine and felodipine, which have been shown to be safe in patients with heart failure.
ACE inhibitors are recommended as first-line agents for treating hypertension in diabetic patients, particularly patients with type 1 diabetes and/or diabetic nephropathy, because they reduce proteinuria and slow the rate of deterioration in renal function. Ongoing clinical trials are testing whether ARBs have similar benefits. Other classes of antihypertensive drugs can be used and indeed are needed in diabetics. Because of the aggressive nature of target organ damage in diabetics, a lower BP goal (<130/85 mm Hg) is recommended, usually necessitating a multidrug regimen.
Hypertensive patients with renal dysfunction should be evaluated
thoroughly to rule out reversible causes of hypertension and/or
end-stage renal failure. These patients should be treated aggressively
(goal BP <130/85 or 125/75 mm Hg) in the presence of
proteinuria (>1 g/24 h) to prevent both progression of renal disease
and CVD events. As in diabetes (which often accompanies hypertension in
these patients), multidrug therapy is usually needed to accomplish this
goal. An ACE inhibitor should be included in the regimen
unless contraindicated. Loop diuretics are needed for BP
control in patients with serum creatinine levels 
2.5
mg/dL. Potassium-sparing diuretics should be avoided.
Patients with coronary heart disease clearly have target organ damage and deserve aggressive antihypertensive treatment. However, they are exceptionally vulnerable to rapid fluctuations in BP, which may be associated with catecholamine surges and concomitant arrhythmias and myocardial ischemia/infarction. Short-acting drugs that cover the hours after waking, the peak time for CVD events, are clearly preferable in coronary patients. ß-Blockers and some long-acting calcium channel blockers have antiangina properties, whereas ß-blockers are useful in the secondary prevention of acute myocardial infarction and sudden cardiac death. In randomized controlled trials, ACE inhibitors have been shown to prevent myocardial remodeling, heart failure, and death in patients with myocardial infarction and left ventricular systolic dysfunction. ß-Blockers and more recently spironolactone have also been shown to decrease morbidity and mortality rates in patients with heart failure.57 59 The utility of ARBs in these patients is currently being tested in clinical trials.
Conclusions
Recognition of the genetic and environmental factors that elevate
BP and lead to target organ damage and death from CVD may pave the way
for nonpharmacological methods of prevention, treatment, and even cure
of hypertension. There is now clear evidence that changes in lifestyle,
including dietary modifications that reduce body weight, fat, and
alcohol intake and increase potassium and calcium intake, as well as
exercise, can reduce or normalize BP in many people. Identification of
the constellation of genes responsible for inherited essential
hypertension will likely yield even more targeted and effective
preventive and therapeutic strategies. This may occur through specific
lifestyle modifications directed toward persons at high risk for CVD
because of their genotype, made possible by more selective,
genotype-targeted "pharmacogenomic" treatments or even gene
therapy.
Results of controlled clinical trials and observational studies have led to important modifications in traditional guidelines for antihypertensive treatment. The threshold for initiating treatment is now based on total risk for CVD rather than BP alone. Treatment is now recommended for those persons with high normal BP who have multiple CVD risk factors or established CVD. Simultaneous reduction of multiple CVD risk factors rather than isolated treatment of hypertension is now recommended, as is tailoring the choice of antihypertensive treatment to the patient’s unique profile of concomitant CVD risk factors and/or comorbid conditions. Systolic BP has emerged as an important therapeutic target because it is a more important determinant of CVD risk than diastolic BP. Home and ambulatory BP measurement is recommended for its value in guiding therapy and enhancing adherence to treatment. More aggressive BP goals are appropriate for hypertensive patients with comorbid conditions such as diabetes and renal insufficiency, and greater reliance on evidence-based medicine in making treatment decisions has been endorsed. Implementation of these contemporary treatment recommendations, coupled with future advances that will accompany our more complete understanding of the pathophysiology of hypertension, holds the promise for improved BP control and prevention of CVD in the general population.
Acknowledgments
This work was supported by National Institutes of Health grant HL-28982.
Note: References 1 through 34 appear in Part I of this article, which was published in Circulation. 2000;101:329–335.
Footnotes
This is Part II of a 2-part article. Part I of this article was published in Circulation. 2000;101:329–335. Note: Figures 1 and 2 and Tables 1 through 3 were published in Part I (Circulation. 2000;101:329–335).
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