Essential Hypertension
Essential Hypertension
Theory 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Case history 5
Diagnosis 6
Approach 6
History and exam 8
Risk factors 9
Investigations 11
Differentials 13
Criteria 14
Screening 16
Management 17
Approach 17
Treatment algorithm overview 28
Treatment algorithm 31
Emerging 79
Primary prevention 80
Secondary prevention 80
Patient discussions 81
Follow up 82
Monitoring 82
Complications 83
Prognosis 84
Guidelines 85
Diagnostic guidelines 85
Treatment guidelines 86
Online resources 90
Evidence tables 91
References 93
Images 119
Disclaimer 120
Essential hypertension Overview
Summary
Essential hypertension is typically diagnosed by screening of an asymptomatic individual.
Treatment of uncontrolled hypertension reduces the risks of mortality and of cardiac, vascular, renal, and
OVERVIEW
cerebrovascular complications.
Lifestyle changes are recommended for all patients: weight loss, exercise, decreased sodium intake, Dietary
Approaches to Stop Hypertension (DASH) diet, and moderation of alcohol consumption.
Choice of drug therapy is often driven by considerations related to comorbid disease, but achievement of
blood pressure goal may be accomplished with a variety of therapeutic agent(s).
Definition
Essential hypertension is defined as persistently raised blood pressure (BP) with no secondary cause
identified.[1] [2] [3] The main goal of treatment is to decrease the risk of mortality and of cardiovascular and
renal morbidity.[4]
The American College of Cardiology (ACC)/American Heart Association (AHA) guideline defines
hypertension as systolic BP measurement of ≥130 mmHg or diastolic BP measurement of ≥80 mmHg.[3]
The European Society of Cardiology (ESC) and European Society of Hypertension (ESH) guidelines define
hypertension as office (clinic) systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg, which is equivalent to
a 24-hour ambulatory BP measurement average of ≥130/80 mmHg, or a home BP measurement average of
≥135/85 mmHg.[2] [5]
The World Health Organization (WHO) recommends starting pharmacological antihypertensive treatment in
patients with a confirmed diagnosis of hypertension and systolic BP of ≥140 mmHg or diastolic BP of ≥90
mmHg.[6]
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Essential hypertension Theory
Epidemiology
According to a global analysis of trends in hypertension, the number of adults aged 30-79 years with
hypertension increased from 650 million to 1.28 billion in the period 1990-2019.[7] The study also suggested
THEORY
that 53% of women and 62% of men with hypertension were not receiving antihypertensive treatment and
that blood pressure (BP) was controlled (receiving antihypertensive medication and BP <140/90 mmHg) in
fewer than 1 in 4 women and 1 in 5 men with hypertension.[7] The rate of hypertension has decreased in
high-income countries, which now have some of the lowest rates, but has increased in many low- or middle-
income countries.
In the US, surveillance definitions vary widely. Using National Health and Nutrition Examination Surveys
(NHANES) data from 2017 to 2020, the American Heart Association (AHA) estimates that the age-adjusted
prevalence of hypertension (defined as self-reported use of antihypertensive medication, systolic BP ≥130
mmHg, or diastolic BP ≥80 mmHg) among US adults ≥20 years of age is 46.73%, which equates to 122.4
million adults (age ≥20 years) with high BP in the US.[8] Prevalence increases with age: using NHANES
2017 to 2020 data it was 28.5% among 20- to 44-year-olds, 58.6% among those 45-64 years, and 76.5%
among those 65 years of age and over.[8] Prevalence is highest in non-Hispanic black men (57.5%) and
non-Hispanic black women (58.4%).[8] Prevalence is higher in men than in women before 65 years of age,
and higher in women than in men from 65 years of age.[3] [8] The lifetime risk is 90% for men and women
who were normotensive at 55 years of age and survive to 80 years.[9] Studies using data from NHANES has
shown that while control of BP steadily increased over a number of years, it is now declining.[10]
In England, the prevalence of high blood pressure in 2015 was reported as 31% among men and 26%
among women, affecting more than 1 in 4 adults.[11]
Aetiology
A multifactorial and heterogeneous aetiology of essential hypertension has been proposed.[12] However,
some initiating factors may be dampened as the hypertensive state progresses.[13] The following factors
have been shown to disrupt the delicate balance of cardiac output and resistance, ultimately resulting in
hypertension:
Pathophysiology
Blood pressure (BP), the product of cardiac output and peripheral vascular resistance, is affected by
preload, contractility, vessel hypertrophy, and peripheral constriction. The pathology associated with, and
the perpetuation of, the hypertensive state involves structural changes, remodelling, and hypertrophy
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Essential hypertension Theory
in resistance arterioles.[13] These changes have also been associated with the early and progressive
development of small vessel atherosclerosis, which is probably the cause of end-organ damage seen
in advanced hypertension. This occurs through a complex series of interrelated processes including
thrombosis, endothelial injury and dysfunction, the inflammatory cascade, oxidative stress, and autonomic
THEORY
dysregulation in the setting of genetic predisposition.[27]
Trials have demonstrated the importance of systolic BP in the pathophysiology of hypertension and its
associated complications, which differs from older conventional thinking.[28] The rise in systolic BP continues
throughout life, in contrast to diastolic BP, which increases until approximately 50 years of age, tends to level
off over the following decade, and may stabilise or decline subsequently.
Case history
Case history #1
A 64-year-old black man presents for a check-up. He denies past medical problems, but has been told
that his blood pressure was a little high. He has no complaints, takes no medications, tries to adhere to a
healthy diet, and rarely exercises. He reports that over the previous 5 years he has gained 6.8 kg (15 lb).
Review of systems is otherwise non-contributory. Physical examination is notable for obesity and blood
pressure 172/86 mmHg. The remainder of the examination is unremarkable.
Other presentations
Essential hypertension is typically an asymptomatic disease state at its onset and time of diagnosis. It
may be associated with headache or visual changes, but this is rare outside of hypertensive urgency/
emergency situations.
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Essential hypertension Diagnosis
Approach
Most patients diagnosed with hypertension are asymptomatic; therefore, screening is essential. Patients are
usually evaluated through history, physical examination, and routine laboratory tests. The three objectives are
to:
Clinical evaluation
History may elicit family history of hypertension or coronary artery disease risk factors. It is important
to assess overall cardiac risk burden.[2] The age of onset may be of value when considering aetiology,
as the proportion of secondary causes diminishes with increasing age. Patients at increased risk for
essential hypertension include those over 60 years of age, or with diabetes, or of black ancestry.[4] [41]
Excess alcohol intake or lack of exercise should be documented. A thorough medication history should
be taken including screening for use of oral contraceptive pills, non-steroidal anti-inflammatory drugs,
sympathomimetics, or herbal medications. Most patients are asymptomatic, but clinical indications of
hyperthyroidism, hypothyroidism, or catecholamine excess (e.g., tachycardia, weight loss, sweating, or
palpitations), or end-organ damage (e.g., shortness of breath, chest pain, or sensory/motor deficits),
should be sought. Headache or visual changes are unusual.
• Office blood pressure (BP) measurement: the patient should be seated quietly for at least 5
minutes, with feet on the floor and arm supported at heart level. Caffeine, smoking, and exercise
should be avoided for 30 minutes prior to examination. An appropriately sized cuff should be used
and the patient's arm should be supported (e.g., resting on a desk). The bladder should encircle at
least 80% of the arm. At the first visit, BP should be recorded in both arms, using the arm that gives
DIAGNOSIS
the higher reading for subsequent visits. Two or more measurements should be made on two or
more occasions and the average recorded. Verification should be obtained in the contralateral arm.
The American College of Cardiology (ACC)/American Heart Association (AHA) guideline defines
hypertension as any systolic BP measurement of ≥130 mmHg or any diastolic BP measurement of
≥80 mmHg.[3] The European Society of Cardiology (ESC) and European Society of Hypertension
(ESH) guidelines define hypertension as office (clinic) systolic BP ≥140 mmHg and/or diastolic BP
≥90 mmHg.[2] [5]
• Examination of optic fundi
• Calculation of BMI from height and weight
• Auscultation for possible carotid, abdominal, or femoral bruits
• Palpation of the thyroid gland
• Examination of the heart and lungs
• Examination of the abdomen for enlarged kidneys, masses, distended urinary bladder, or abnormal
aortic pulsation
• Palpation of the lower extremities for oedema and pulses
• Neurological assessment.
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Essential hypertension Diagnosis
Physical examination may reveal end-organ damage associated with untreated hypertension: for example,
retinopathy, vascular bruits, signs of congestive heart failure, evidence of aortic aneurysm (pulsatile
mass/bruit), left ventricular hypertrophy (displaced point of maximal impact), or neurological deficit(s).
Absence of femoral pulses suggests coarctation of the aorta. An abdominal bruit may suggest aortic
aneurysm or renal artery stenosis. Occasionally, patients may have stigmata of endocrinopathy such
as Cushing's disease (moon face, centripetal obesity, striae), acromegaly (acral enlargement), Graves'
disease (goitre, exophthalmos, pretibial myxoedema), or hypothyroidism (dry skin, delayed return of deep
tendon reflexes), indicating a secondary cause of hypertension.
US and European guidelines recommend the use of out-of-office BP measurement in addition to office
BP measurement prior to diagnosis of hypertension, using ambulatory blood pressure monitoring (ABPM)
or home blood pressure monitoring (HBPM), or both.[3] [5][59][60] With ABPM, patients go about their
normal daily activities wearing a monitor, and measurements are taken periodically to provide a mean
BP during the monitoring period. With HBPM, the patient takes BP measurements in the morning and
evening while seated and resting, and this is repeated over a period of days to provide a mean BP.
Thresholds for elevated BP measured by ABPM and HBPM differ to thresholds used in the office;
guidelines provide corresponding values.[2] [3] [5][60] For example, according to ACC/AHA guidelines,
an office BP measurement of 130/80 mmHg corresponds to home BP 130/80 mmHg, daytime ABPM
130/80 mmHg, night-time ABPM 110/65 mmHg, and 24-hour ABPM 125/75 mmHg.[3] In ESH guidelines,
hypertension is defined as an office BP measurement of ≥140 mmHg (systolic) and/or ≥90 mmHg
(diastolic), which corresponds to mean awake ABPM ≥135 mmHg and/or ≥85 mmHg, mean asleep ABPM
≥120 mmHg and/or ≥70 mmHg, mean 24-hour ABPM ≥130 mmHg and/or ≥80 mmHg, and mean HBPM
≥135 mmHg and/or ≥85 mmHg.[5]
Auscultatory devices (e.g., mercury, anaeroid) are not generally useful for HBPM because patients rarely
master the required technique for BP measurement using these devices. Automated validated devices
should be used instead. European guidelines also now recommend that automatic electronic devices are
used for office measurement, rather than manual devices.[5]
Unattended automated office blood pressure (AOBP) is another option that has been designed to more
accurately measure BP.[57] Multiple measurements are taken while the patient is alone in a quiet room,
DIAGNOSIS
sitting with legs uncrossed, back supported, and arm supported at heart level. Depending on the device
used, 3 to 6 measurements are taken over a short time period and the mean BP is calculated.[61] AOBP
measures about 5 mmHg lower than research-quality BPs, and 10 to 15 mmHg lower than routine office
BP measurements.[62] [63] When using AOBP, hypertension is defined as ≥135/85 mmHg.
White-coat hypertension is suspected when BP readings in the office exceed those outside of the clinical
setting. Masked hypertension is suspected when out-of-office BP measurements exceed those taken in
the clinical setting. ABPM or HBPM can be used to identify these patients.[3] [5]
Tests
Routine metabolic panel and lipid levels are required. Glomerular filtration rate is calculated according to
the Modification of Diet in Renal Disease (MDRD) formula or the Chronic Kidney Disease Epidemiology
Collaboration (CKD-EPI) equation.[64] In particular, features of the metabolic syndrome (hyperglycaemia,
dyslipidaemia) or hyperuricaemia should be noted. Haemoglobin and routine urinalysis with albumin
excretion are also recommended for possible identification of causes of hypertension. An ECG should be
obtained.
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Essential hypertension Diagnosis
More extensive testing for secondary causes of hypertension is generally not indicated, unless BP is
difficult to control or clinical or routine lab data suggest identifiable secondary causes such as signs
of unprovoked hypokalaemia or renal insufficiency.[2] [3] Echocardiogram and carotid Dopplers may
have prognostic implications, but they are not routinely recommended except as recommended by
guidelines. There was increased risk of mortality and cardiovascular events in patients with increased
left ventricular mass and abnormal geometric left ventricular hypertrophy on echocardiogram.[65] [66]
Increased cardiovascular events were associated with higher intima media thickness values on carotid
Dopplers.[67]
Sleep study may be considered in cases of resistant hypertension and also for patients with signs or
symptoms of obstructive sleep apnoea.[42]
If secondary hypertension is suggested by history, or physical or routine laboratory testing, further testing
can be performed.[2]
systolic blood pressure (BP) ≥130 mmHg or diastolic BP ≥80 mmHg (common)
• The American College of Cardiology (ACC)/American Heart Association (AHA) guideline defines
hypertension as systolic BP measurement of ≥130 mmHg or diastolic BP measurement of ≥80
mmHg.[3] The European Society of Cardiology (ESC) and European Society of Hypertension (ESH)
guidelines define hypertension as office (clinic) systolic BP ≥140 mmHg and/or diastolic BP ≥90
mmHg.[2] [5]
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Essential hypertension Diagnosis
retinopathy (common)
• Retinal vascular changes are seen commonly in long-standing hypertension.
dyspnoea (uncommon)
• Suggests possible congestive heart failure or coronary artery disease. Dyspnoea may be an anginal
equivalent, particularly in the setting of diabetes.
Risk factors
Strong
obesity
• Data from the Nurses' Health Study showed that a gain of 5 kg above weight at 18 years of age was
associated with 60% higher risk of development of hypertension in middle age.[29] A 4.5 mmHg
increase in blood pressure has been associated with each 4.5 kg (10 lb) gain in weight.[30] One
DIAGNOSIS
systematic review found that risk of hypertension increased continuously with increasing body mass
index (BMI), waist circumference, weight gain, and waist-to-hip and waist-to-height ratio.[31] One study
found that younger age at onset of overweight across adulthood was associated with significantly
increased risk of hypertension, with the highest relative risk with onset of overweight at 18-39 years of
age.[32]
• It has been postulated that the link between obesity and hypertension is driven by increased
circulating volume, leading to increased cardiac output and persistently elevated peripheral vascular
resistance.[26]
• Obesity is associated with metabolic syndrome, insulin resistance, and type 2 diabetes.
• Bariatric treatment of class III obesity (BMI 40 or above) can reduce or eliminate risk factors for
cardiovascular disease, with an effect on hypertension, diabetes, and dyslipidaemia.[33] [34] [35]
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Essential hypertension Diagnosis
moderate/high alcohol intake
• Chronic alcohol consumption of more than 1 drink per day in women and more than 2 drinks per day
in men has been shown to be associated with an increased risk of blood pressure (BP) elevation.[3]
[37] One Cochrane review of the effect of alcohol on BP found that high-dose alcohol (>30 g) has a
biphasic effect, decreasing BP up to 12 hours after consumption and increasing BP after 13 hours.[38]
Another systematic review and meta-analysis in healthy adults found a direct linear relationship
between alcohol consumption and BP, with no suggestion of a threshold, particularly for systolic
BP.[39]
metabolic syndrome
• Abdominal obesity has been specifically associated with an increased risk of hypertension, as
compared with generalised obesity.[40]
• Insulin resistance and hyperinsulinaemia are thought to contribute to the development of hypertension
through a variety of inflammatory mechanisms.[13]
diabetes mellitus
• Hyperglycaemia, hyperinsulinaemia, and insulin resistance lead to endothelial damage and oxidative
stress, and are independently associated with the development of hypertension.[41]
black ancestry
• Highest incidence of hypertension is seen in black non-Hispanic people, at all age levels.[4]
sleep apnoea
DIAGNOSIS
• Obstructive sleep apnoea is a risk factor for several cardiovascular diseases, including
hypertension.[3] [42] In addition, there is a possible dose-response relationship between the severity of
obstructive sleep apnoea and the risk of essential hypertension.[43]
• Obstructive sleep apnoea is also associated with an increased risk of resistant hypertension.[44]
Weak
sodium intake >1.5 g/day
• Individuals show a varied tolerance for sodium intake, and reduced sodium intake has modest effect
on blood pressure (BP) lowering.[15] [16] Meta-analyses have shown the amount of BP lowering
achieved with sodium reduction has a dose-response relation and is greater for older populations, non-
white populations, and those with higher baseline systolic BP.[45] [46]
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Essential hypertension Diagnosis
dyslipidaemia
• Risk of hypertension is increased in the setting of the metabolic syndrome.
Investigations
1st test to order
Test Result
ECG may show evidence of left
ventricular hypertrophy or
• Normal result does not rule out coronary artery disease.
old infarction
DIAGNOSIS
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Essential hypertension Diagnosis
Test Result
plasma renin activity low renin suggests
hyperaldosteronism
• Indicated when unprovoked hypokalaemia present.
plasma aldosterone high aldosterone or
failure to suppress with
• Indicated in the following situations: BP is sustained above
salt loading suggests
150/100 mmHg on 3 measurements over different days, with
hyperaldosteronism
hypertension resistant to 3 conventional antihypertensive drugs
(including a diuretic), or controlled BP (140/90 mmHg) on 4 or more
antihypertensive drugs; hypertension and spontaneous or diuretic-
induced hypokalaemia; hypertension and adrenal incidentaloma;
hypertension and sleep apnoea; hypertension and a family history of
early-onset hypertension or cerebrovascular accident at a young age
(40 years); hypertensive first-degree relatives of patients with primary
aldosteronism.[68]
renal duplex ultrasound/MRA renal arteries/CT angiography may show renal artery
stenosis, renal scarring,
• Young patients (age <40 years) with severe hypertension or renal
or lesions
artery bruits.
• Ultrasound provides haemodynamic information and magnetic
resonance angiogram (MRA) provides anatomical information, in lieu
of renal angiogram. CT angiography is accurate in atherosclerotic
disease.
24-hour urine phaeochromocytoma screen elevated catecholamines
if phaeochromocytoma
• Indicated with symptoms/signs of catecholamine excess.
plasma fractionated metanephrines elevated metanephrines if
phaeochromocytoma
• Indicated with signs/symptoms of catecholamine excess. This test is
easier to perform than 24-hour urine screen, but has a higher rate of
false positives.
24-hour urine free cortisol elevated in Cushing's
disease
DIAGNOSIS
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Essential hypertension Diagnosis
Differentials
DIAGNOSIS
Renal artery stenosis • Typically younger • Renal duplex ultrasound,
patients with difficult-to- magnetic resonance
control hypertension or angiogram, or CT angiogram
older patients at risk of of renal arteries confirms
atherosclerotic disease. diagnosis.
• Renal artery bruits may be
present.
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Essential hypertension Diagnosis
Criteria
2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/
PCNA guideline for the prevention, detection, evaluation, and
management of high blood pressure in adults[3]
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Essential hypertension Diagnosis
Blood pressure (BP) is categorised in four levels based on an average of two or more properly taken BP
measurements on two or more occasions in a healthcare setting (office [clinic] setting):
Office (clinic) BP
DIAGNOSIS
• Systolic BP ≥120 mmHg and/or diastolic BP ≥70 mmHg for night-time BP
• Automated office (clinic) BP: a displayed mean systolic BP ≥135 mmHg or diastolic BP ≥85 mmHg is
high.
• Non-automated office BP: a mean systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg is high, and
a systolic BP between 130 and 139 mmHg and/or a diastolic BP between 85 and 89 mmHg is high-
normal.
• Ambulatory BP monitoring: patients can be diagnosed as hypertensive if the mean awake systolic BP
is ≥135 mmHg or the diastolic BP is ≥85 mmHg, or if the mean 24-hour systolic BP is ≥130 mmHg or
the diastolic BP is ≥80 mmHg.
• Home BP monitoring: patients can be diagnosed as hypertensive if the mean systolic BP is ≥135
mmHg or the diastolic BP is ≥85 mmHg. If the office BP measurement is high and the mean home
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Essential hypertension Diagnosis
BP is <135/85 mmHg, it is advisable to either repeat home monitoring to confirm that the home BP
is <135/85 mmHg or perform 24-hour ambulatory BP monitoring to confirm that the mean 24-hour
ambulatory BP monitoring is <130/80 mmHg and the mean awake ambulatory BP monitoring is
<135/85 mmHg before diagnosing white-coat hypertension.
• Stage 1 hypertension: clinic BP ranging from 140/90 mmHg to 159/99 mmHg and subsequent
ambulatory blood pressure monitoring (ABPM) daytime average or home blood pressure monitoring
(HBPM) average ranging from 135/85 mmHg to 149/94 mmHg
• Stage 2 hypertension: clinic BP ranging from 160/100 mmHg to 179/119 mmHg and subsequent
ABPM daytime average or HBPM average is 150/95 mmHg or higher
• Stage 3 or severe hypertension: clinic systolic BP is 180 mmHg or higher or clinic diastolic BP is 120
mmHg or higher.
Screening
The vast majority of hypertensive patients will be detected during an asymptomatic screening during some
contact with the medical system. The US Preventive Services Task Force (USPSTF) has recommended
annual screening for adults aged ≥40 years or for those at increased risk for high blood pressure (BP) (high-
normal BP, overweight or obese, or African-American). Adults aged 18-39 years with normal BP without other
risk factors were advised to be re-screened every 3-5 years.[59] The American College of Cardiology (ACC)/
American Heart Association (AHA) guideline, however, recommends annual screening in all patients with
normal BP.[3] Measurements should be obtained outside of the clinical setting (ambulatory blood pressure
monitoring [ABPM] or home blood pressure monitoring [HBPM]) to confirm the diagnosis.[3] [59] If a patient
has an untreated systolic BP >130 mmHg but <160 mmHg or diastolic BP >80 mmHg but <100 mmHg, it is
reasonable to screen for the presence of white-coat hypertension by using either daytime ABPM or HBPM
before diagnosis of hypertension.[3] In adults with elevated clinic BP (120-129/<80 mmHg) but not meeting
DIAGNOSIS
the criteria for hypertension, screening for masked hypertension with daytime ABPM or HBPM is reasonable.
Guidelines for other countries may recommend different screening intervals. The European Society of
Cardiology (ESC)/European Society of Hypertension (ESH) guideline recommends annual screening for
patients with high-normal BP 130 to 139/85 to 89 mmHg, at least every 3 years for patients with normal BP
120 to 129/80 to 84 mmHg, and at least every 5 years for patients with optimal BP <120/80 mmHg.[2]
These screening guidelines are often exceeded, as BP measurement is standard for each encounter in
many practice settings. Elevated readings should always be confirmed on a second visit prior to diagnosing
hypertension.
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Essential hypertension Management
Approach
The main goal of treatment is to decrease the risk of mortality and of cardiovascular and renal morbidity.[4]
[72] [Evidence A] Treatment options include lifestyle modifications and antihypertensive drugs.
The American College of Cardiology (ACC)/American Heart Association (AHA) guideline recommends a
blood pressure (BP) target of <130/80 mmHg for adults, regardless of age, with confirmed hypertension
and known cardiovascular disease (CVD), or a 10-year atherosclerotic CVD risk (using the atherosclerotic
CVD [ASCVD] risk estimator) of 10% or more.[3] [American College of Cardiology: ASCVD risk estimator
plus] (https://tools.acc.org/ASCVD-Risk-Estimator-Plus/#!/calculate/estimate) For adults with confirmed
hypertension without additional markers of increased CVD risk, a BP target of <130/80 mmHg may be
reasonable.
The European Society of Cardiology (ESC) and European Society of Hypertension (ESH) guidelines
recommend an initial treatment target of <140/90 mmHg in all patients (<140/80 mmHg in the 2023 ESH
guideline). If treatment is well tolerated, the BP can then be targeted to 130/80 mmHg or lower in most
patients.[2] [5]
The World Health Organization (WHO) recommends a target BP of <140/90 mmHg in all patients with
hypertension without comorbidities. In those with hypertension and known CVD or at high CVD risk, with
diabetes, or with chronic kidney disease, the WHO recommends a target systolic BP <130mmHg.[6]
MANAGEMENT
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Essential hypertension Management
target of 110 to <130 mmHg had a lower incidence of cardiovascular events (composite of stroke, acute
coronary syndrome, acute decompensated heart failure, coronary revascularisation, atrial fibrillation, or
death from cardiovascular causes) than those treated to a target of 130 to <150 mmHg.[79] In the STEP
trial, clinic BP was measured by trained staff, with home BP measurements also used as an adjunct.
Patients with diabetes were included; patients with prior stroke were not. In the STEP trial, intensive
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Essential hypertension Management
treatment did not have a significant effect on cardiovascular or all-cause mortality.[79] Longer-term follow-
up of the SPRINT trial found that after the trial ended, the beneficial effect on cardiovascular and all-
cause mortality did not persist, noting the importance of consistent long-term control of hypertension
beyond the trial protocols.[80]
Because of differences in the general health of older patients, the decision to treat should be on an
individual basis, and BP lowering should be gradual and carefully monitored by the physician.[2] [81]
The SPRINT trial results showed equal benefit in people aged >75 years, regardless of frailty or walking
speed.[82] Patients with orthostasis at enrolment, patients with dementia, and those resident in a
nursing home were excluded from the trial. One systematic review found insufficient evidence regarding
the benefits of hypertension treatment for frail people >80 years of age taking multiple medications,
concluding that treatment should be individualised.[83] Older patients >80 years should not be denied
treatment or have treatment withdrawn solely on the basis of age.[2]
One Cochrane review of treatment goals in people with hypertension and a history of cardiovascular
disease (myocardial infarction, angina, stroke, peripheral vascular occlusive disease) concluded that
there was no benefit in treating to lower BP targets (≤135/85 mmHg) compared with standard BP targets
(≤140 mmHg to 160mmHg/90 mmHg to 100 mmHg) in terms of total and cardiovascular mortality or
cardiovascular events.[84]
Regarding patients with concomitant diabetes mellitus, there is good-quality evidence from the ACCORD
trial that very intensive BP lowering (targeting a systolic pressure <120 mmHg, as compared with
targeting <140 mmHg) does not lessen risk (composite outcome: non-fatal myocardial infarction, non-fatal
stroke, or death from cardiovascular cause) and may increase risk of adverse events.[85] One systematic
review and meta-analysis found that intensive BP lowering (systolic BP <130 mmHg) was associated with
reduced risk of major cardiovascular diseases in patients with type 2 diabetes; a target systolic BP <140
mmHg was associated with reduced all-cause death, though further reduction did not result in further
benefits.[86] The American Diabetes Association (ADA) recommends that BP targets in people with
diabetes and hypertension are individualised by assessing cardiovascular risk, potential adverse effects,
and patient preference.[87] The ACC/AHA and the ADA both recommend a BP goal of <130/80 mmHg for
patients with diabetes.[3] [87]
Lifestyle modification
The initial approach to a newly diagnosed patient should include a thorough explanation of the risks
associated with hypertension and the need for adequate control and adherence to therapy. Initial
therapeutic measure should be lifelong lifestyle modification including:[2] [3] [5][47] [88] [89] [90]
• Sodium reduction (optimal goal ≤1.5 g/day). Use of salt substitutes has demonstrated BP-mediated
protective effects for major cardiovascular events and mortality.[53] [54] [91] [92]
• Potassium supplementation (3.5 to 5.0 g/day): preferably by consumption of a potassium-rich diet
unless contraindicated.
• Dietary Approaches to Stop Hypertension (DASH) diet (8-10 servings of fruit and vegetables daily,
whole grains, low sodium, low-fat proteins).
MANAGEMENT
• Waist circumference <102 cm (<40 inches) for men and <88 cm (<35 inches) for women; weight
loss to a BMI of about 25 kg/m².
• Increased physical activity: at least 30 minutes of moderate-intensity, dynamic aerobic exercise
(walking, jogging, cycling, or swimming) 5 days per week to total 150 minutes per week, as
tolerated or recommended by physician.
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• Limited alcohol consumption: ≤2 standard drinks (<20-30 g alcohol) per day in hypertensive
men; ≤1 standard drink (<10-20 g alcohol) per day in hypertensive women. Total weekly alcohol
consumption should not exceed 14 standard drinks (140 g) for men and 8 standard drinks (80 g) for
women.
Advice about lifestyle modification should be given upon diagnosis and should continue concurrently with
all other therapeutic measures. Prior to initiation of an exercise programme, patients should discuss a
plan with their healthcare provider.
Obesity is a major cause of hypertension. In addition to lifestyle modifications for weight loss, anti-obesity
pharmacotherapy and metabolic surgery may be considered in select patients to treat obesity and prevent
or attenuate hypertension.[93]
Smoking cessation should always be encouraged as well, to promote general vascular health, though
smoking cessation has not been associated with decreased BP.
Antihypertensive drugs
The main classes of antihypertensives include:[2] [3]
• Diuretics:
Calcium-channel blockers may cause peripheral oedema that can lead to a diuretic being prescribed;
however, diuretics are generally not indicated in this situation.[96]
The Diuretic Comparison Project compared hydrochlorothiazide with chlortalidone in patients aged
65 years or older; patients were already receiving hydrochlorothiazide and were randomised to either
continue or switch to chlortalidone. At a median follow-up of 2.4 years, there was no difference between
the groups in the primary composite outcome of non-fatal myocardial infarction, stroke, heart failure
resulting in hospitalisation, urgent coronary revascularisation for unstable angina, and non-cancer-related
death.[97]
MANAGEMENT
Studies confirm that patients with COVID-19 should continue to take ACE inhibitors and angiotensin-
II receptor antagonists as prescribed.[98] [99] For more information, see Management of coexisting
conditions in the context of COVID-19 .
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Initiating therapy for stage 1 hypertension
The ACC/AHA guideline defines stage 1 hypertension as BP 130-139/80-89 mmHg.[3] The ESC/ESH
guideline defines this as high-normal BP.[2]
CVD risk assessment tools are used to guide initial approach to therapy and whether the patient should
receive antihypertensive medication or can be managed with lifestyle modifications.[2] [3] [6] The ACC/
AHA guideline recommends using the Pooled Cohort Equations to assess 10-year atherosclerotic CVD
risk. [American College of Cardiology: ASCVD risk estimator plus] (https://tools.acc.org/ASCVD-Risk-
Estimator-Plus/#!/calculate/estimate)
The ACC/AHA guideline recommends that patients with stage 1 hypertension and assessed as at low risk
of CVD (<10% 10-year atherosclerotic CVD risk) may initially be managed with lifestyle modifications and
re-assessment in 3-6 months to determine if pharmacological therapy is necessary.[3] [100] Most patients
will require drug therapy to achieve target BP control.
For stage 1 hypertension, combination therapy or monotherapy where appropriate can be initiated.[3]
[101] The choice of antihypertensive agent is driven by efficacy, adverse-effect profile, and cost. The
ACC/AHA guideline recommends initiating a single antihypertensive agent for patients with a 10-year
atherosclerotic CVD risk ≥10% or known cardiovascular disease, diabetes, or chronic kidney disease
(CKD).[3] [American College of Cardiology: ASCVD risk estimator plus] (https://tools.acc.org/ASCVD-
Risk-Estimator-Plus/#!/calculate/estimate)
The ESC/ESH guideline states that adults with documented CVD, including asymptomatic atheromatous
disease on imaging, type 1 or 2 diabetes mellitus, very high levels of individual CVD risk factors, or
CKD are automatically considered to be at high or very high CVD risk (10-year CVD mortality of 5%
to 10% and ≥10%, respectively) and do not need formal risk assessment.[2] For all other patients with
hypertension, the ESC guideline recommends that 10-year CVD mortality risk is estimated using the
SCORE system. [ESC: SCORE2 and SCORE2-OP] (https://www.escardio.org/Education/Practice-
Tools/CVD-prevention-toolbox/SCORE-Risk-Charts) European guidelines recommend initiating
antihypertensive treatment with a two-drug combination, preferably a single pill combination, with the
exception of patients with high-normal BP and a high cardiovascular risk or in frail older patients in whom
initiating treatment with monotherapy may be appropriate.[2] [5] In patients with high-normal BP and a
high cardiovascular risk only a small reduction in BP may be required to achieve the BP target, and in frail
older patients baroreflex sensitivity is frequently impaired and the risk of hypotension is greater.[2] For
lower-risk patients with grade 1 hypertension, European guidelines advise that antihypertensive treatment
should be initiated after 3-6 months if BP is not controlled by lifestyle interventions alone.[2] [5]
Many people with stage 1 hypertension have a constellation of other cardiovascular risk factors such as
smoking or mild dyslipidaemia that increase the importance of BP lowering.
If BP cannot be controlled with a single agent, a drug from a different class of antihypertensives is added.
A choice among four preferred classes of drugs is recommended for initial therapy.[2] [3] [102] [103]
Thiazide (or thiazide-like) diuretics have been shown to be safe and efficacious first-line therapy.[104]
They also decrease renal calcium excretion, so may be a good choice for women with osteoporosis.
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Initial dose of antihypertensive medications depends on clinical situation; medications are titrated for a
therapeutic effect, while observing for potential adverse effects.
Alternative first-line choices include ACE inhibitors, angiotensin-II receptor antagonists, or calcium-
channel blockers, or a combination of two different drugs from these classes (excluding the combination
of ACE inhibitors and angiotensin-II receptor antagonists; generally, when an ACE inhibitor would usually
be chosen but is not tolerated, an angiotensin-II receptor antagonist can be substituted). Aliskiren, a
direct renin inhibitor, is also available; however, its place in the treatment pathway is not yet clear due to
concerns about risks in combination with ACE inhibitors or angiotensin-II receptor antagonists, and in the
settings of diabetes or renal impairment, and it is not considered to be a preferred option.
In the general black population, including those with diabetes, a thiazide (or thiazide-like) diuretic or a
calcium-channel blocker is recommended as initial pharmacological therapy.[2] [3] The recommendation
is derived from a pre-specified subgroup analysis of black patients, 46% of whom had diabetes, in the
Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).[105] [106]
In patients with diabetes who have increased albumin excretion, ACE inhibitors or angiotensin-II receptor
antagonists are recommended. The ALLHAT study showed that chlortalidone, amlodipine, or lisinopril
were co-equal for mild hypertension in type 2 diabetes.[105] ACE inhibitors are renoprotective, decreasing
the progression of proteinuria in patients with diabetes.[107] Sleep-time BP is the most significant
independent prognostic marker of cardiovascular events in diabetes.
Sodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated BP-lowering effects and may be
considered in patients with type 2 diabetes.[108] In trials, the SGLT2 inhibitors empaglifozin, dapagliflozin,
and canagliflozin have been found to lower systolic and diastolic BP and cardiovascular risk in people
with type 2 diabetes compared with placebo.[109] [110] [111] [112] [113] [114] [115] The glucagon-like
peptide 1 (GLP-1) receptor antagonists liraglutide and semaglutide have also shown a beneficial effect on
BP.[116] [117] For more information, see Diabetic cardiovascular disease .
ACE inhibitors have been shown in some trials to decrease cardiovascular events, while other studies
have not demonstrated a benefit for ACE inhibitors in the setting of stable CAD with normal left ventricular
function.[123] [124] [125] Beta-blockers, ACE inhibitors, or angiotensin-II receptor antagonists can be
used as first-line for compelling indications (e.g., previous myocardial infarction, stable angina).[2] [3]
Other drugs such as dihydropyridine calcium-channel blockers, thiazide diuretics, and/or mineralocorticoid
receptor antagonists are added as required to further control hypertension.
Many patients with CAD also take nitrates, which act as an exogenous nitric oxide donor. Modest
reductions in systolic BP can be observed, but the US Food and Drug Administration has not approved
MANAGEMENT
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Comorbid heart failure (HF)
Recommended medications for HF also lower BP; however, HF guidelines note that clinical trials
assessing the impact of BP reduction on outcomes in patients with hypertension and HF are lacking and
that the optimal BP goal and antihypertensive regimen are not known.[126] [127]
Treatment of HFrEF (left ventricular EF <40%) is similar in hypertensive and normotensive patients. For
most patients with HFrEF, a combination of drugs from the following four medication classes should be
started initially and continued long-term:[127]
Additionally, the combination of hydralazine and a nitrate (e.g., isosorbide dinitrate/hydralazine) has been
shown to be of benefit for black patients who have persistent symptoms despite receiving optimal medical
therapy, as well as in all patients with HF who cannot receive ACE inhibitors, angiotensin-II receptor
antagonists, or ARNi because of intolerance or contraindications.[126] [127]
Non-dihydropyridine calcium-channel blockers are not recommended for the treatment of hypertension in
adults with HFrEF.[3]
For more information, see Heart failure with reduced ejection fraction .
HFpEF is defined as symptoms and signs of HF, with left ventricular EF ≥50%.[128]
Diuretics should be used to control hypertension in patients with comorbid HFpEF who present with
symptoms of volume overload.[3]
While optimal BP goal and antihypertensive regimens are not known for patients with HFpEF, the
American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Failure Society of
America (HFSA) guideline for management of HF advises that ACE inhibitors, angiotensin-II receptor
antagonists, aldosterone antagonists, and possibly ARNi could be first-line agents to control BP, given
experience with their use in HFpEF trials.[126] Similarly, a 2023 expert consensus document from the
ACC suggests that, in addition to diuretics, patients with hypertension and HFpEF can be treated with
ARNis, angiotensin-II receptor antagonists, and aldosterone antagonists.[129]
SGLT2 inhibitors (which have demonstrated BP-lowering effects) are also now recommended in the US
and European guidelines for all patients with HFpEF.[126] [129] [130] For more information, see Heart
MANAGEMENT
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comorbid LVH. Angiotensin-II receptor antagonists have been shown to decrease morbidity and mortality
in patients with hypertension and LVH.[131]
Continuing ACE inhibitor or angiotensin-II receptor antagonist therapy may be associated with
cardiovascular benefit as kidney function declines.[133]
Second-choice options are a calcium-channel blocker or a thiazide diuretic. In the CLICK trial, in patients
with advanced CKD and poorly controlled hypertension, chlortalidone therapy improved BP control at 12
weeks compared with placebo.[134] [135] A non-dihydropyridine calcium-channel blocker (i.e., diltiazem,
verapamil) may be indicated if there is proteinuria.[136]
Spironolactone may further reduce proteinuria when added to an ACE inhibitor or angiotensin-II receptor
antagonist, but also raises the risk of hyperkalaemia.[137] [138] Spironolactone is usually added to an
ACE inhibitor or angiotensin-II receptor antagonist, after a thiazide diuretic has been added to minimise
hyperkalaemia.
The 2021 Kidney Disease: Improving Global Outcomes (KDIGO) guideline for management of BP in
CKD recommends that patients with CKD are treated to a target systolic BP <120 mmHg, specifying
that this should be measured using standardised office (clinic) BP measurement, preferably automated
office BP.[132] The ACC/AHA guideline recommends treating patients with CKD to a target of <130/80
mmHg.[3]
SGLT2 inhibitors have demonstrated renal benefits, and dapagliflozin may be considered in patients
with CKD (stages 2-4) with and without diabetes.[139] [140] [141] [142] Use of SGLT2 inhibitors is
contraindicated in patients with an estimated glomerular filtration rate (eGFR) of <30 mL/minute/1.73 m².
Finerenone, a non-steroidal mineralocorticoid receptor antagonist, is approved for use in diabetic CKD
and has also been shown to have BP-lowering effects.[143] [144] SGLT2 inhibitors and finerenone should
be used according to their approval for CKD treatment in addition to antihypertensive drug therapy.[5] For
more information, see Chronic kidney disease . Data on combining finerenone and SGLT2-inhibitors are
limited.
Evidence from post-hoc analyses suggests that angiotensin-II receptor antagonists and ACE inhibitors
do not prevent the occurrence or the recurrence of atrial fibrillation.[145] [146] [147] [148] However, more
recent guidelines note that use of ACE inhibitors and angiotensin-II receptor antagonists may be effective
in the prevention of atrial fibrillation.[3] [149] More investigation is needed.
The ALLHAT study conclusively demonstrated that alpha-blockers should not be a first-line
antihypertensive therapy for patients with symptomatic benign prostatic hypertrophy (BPH). In these
patients, the preferred first-line antihypertensive options are the same as for most other groups (i.e.,
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thiazide [or thiazide-like] diuretics, ACE inhibitors, angiotensin-II receptor antagonists, and calcium-
channel blockers), and the alpha-blocker indication is simply to treat the BPH symptoms.
Stage 2 hypertension
The ACC/AHA guideline defines stage 2 hypertension as BP ≥140/90 mmHg.[3] The ESC/ESH guidelines
define this category of BP in 3 grades:[2] [5]
Representative agents of the main treatment class options, including ACE inhibitors, angiotensin-II
receptor antagonists, and calcium-channel blockers, should be maximised. ACE inhibitors, angiotensin-
II receptor antagonists, and/or direct renin inhibitors should not be used together due to the risk of
acute renal failure. An optimally dosed thiazide-like diuretic, such as chlortalidone or indapamide,
should be used over hydrochlorothiazide.[152] In the CLICK trial, in patients with advanced CKD and
poorly controlled hypertension, chlortalidone therapy improved BP control at 12 weeks compared with
placebo.[134] [135]
The fourth-line drug option is generally spironolactone. Eplerenone can be used as an alternative.
Spironolactone and eplerenone are contraindicated in patients with hyperkalaemia. Caution should be
used in patients with renal impairment; either a dose adjustment may be required, or the drug may be
contraindicated depending on the severity of renal impairment, indication for use (i.e., hypertension
versus heart failure), and local guidance. Concomitant administration with potassium-sparing diuretics is
MANAGEMENT
contraindicated.
Otherwise, a safe fourth- or fifth-line option is a peripheral adrenergic blocker. Hydralazine is a less-
preferred option due to its twice-daily dose requirement and increased risk of oedema with simultaneous
calcium-channel blocker treatment. Minoxidil is rarely required in patients with advanced CKD, and its
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use requires some expertise in anticipating and managing adverse effects of fluid retention. Combined
alpha- and beta-blockers (e.g., carvedilol, labetalol) are considerations. Additionally, physicians with
expertise in managing difficult-to-control hypertension have had niche success using a combination of
a dihydropyridine calcium-channel blocker plus a non-dihydropyridine calcium-channel blocker (e.g.,
amlodipine plus diltiazem). Clonidine is generally avoided because of its adverse effect profile.
1. Promotion of medication adherence using the principle of pill reduction (i.e., use of single pill, fixed-
dose combination formulations or avoidance of twice-daily dose regimens when possible)
2. Maximising the dose of the diuretic (thiazide or thiazide-like)
3. Use of spironolactone or eplerenone as a fourth drug when possible.[153]
It is also important to question the patient's alcohol use and offer lifestyle counselling; structured diet and
exercise programmes can lower BP in patients with resistant hypertension.[154] [155]
Older adults
In the oldest adult patients, many physicians are reluctant to treat hypertension in accordance with usual
BP goals, for a number of reasons, including concerns about fall risk, drug interactions, adverse effects,
and lack of benefit in mortality reduction. Previous literature reviews and meta-analysis demonstrated
reductions in stroke, heart failure, and cardiovascular events in much older adults without reaching
mortality benefit.[156] [157] However, the SPRINT trial found that treating ambulatory adults aged 75
years or older to a systolic BP target of <120 mmHg (as measured by AOBP) resulted in significantly
lower rates of fatal and non-fatal major cardiovascular events and death from any cause, compared with
a systolic BP target of <140 mmHg.[82] The STEP trial found that treating patients aged 60-80 years to a
systolic BP target of 110 to <130 mmHg (measured by trained staff in clinic, with home BP measurements
also used as an adjunct) had a lower incidence of cardiovascular events than those treated to a target of
130 to <150 mmHg, but intensive treatment did not have a significant effect on cardiovascular or all-cause
mortality.[79] The SPRINT trial also found that intensive BP control did not result in any adverse effects
on cognition: the risk of mild cognitive impairment and the combined rate of mild cognitive impairment or
probable dementia was reduced in patients treated to a systolic BP target of <120 mmHg; however, the
incidence of probable dementia was not reduced.[158] Patients with orthostasis at enrolment, patients
with dementia, and those resident in a nursing home were excluded from the trial. One meta-analysis of
randomised controlled trials (including SPRINT) found that pharmacological treatment of hypertension in
adults aged over 60 does not worsen cognition, and may reduce cognitive decline.[159] One Cochrane
review assessing whether pharmacological treatment of hypertension can prevent cognitive impairment
or dementia in people who have no history of cerebrovascular disease found insufficient evidence.[160]
Another meta-analysis found that BP reduction in patients in late-mid and later life reduced the risk of
incident dementia compared with placebo.[161] One meta-analysis looking at the effects of intensive
BP-lowering treatment on orthostatic hypotension found that intensive treatment of BP lowers the risk
of orthostatic hypotension (not raises it), and this finding was consistent regardless of age.[162] One
meta-analysis comparing the effects of BP-lowering treatment on the risk of major cardiovascular events
MANAGEMENT
in groups of patients stratified by age and BP at baseline found that pharmacological BP reduction was
effective in older adults.[163]
One secondary analysis of randomised controlled trials (including SPRINT, STEP, and ACCORD) found
that the benefit of intensive BP control in adults aged 60 years and over may be most appropriate in those
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Essential hypertension Management
with a life expectancy of more than 3 years, and that harms may outweigh benefits in those with a life
expectancy of less than 1 year.[164]
The 2017 ACC/AHA guideline recommends a systolic BP goal of <130 mmHg for non-institutionalised
ambulatory community-dwelling adults. For older adults ≥65 years of age with hypertension and a high
burden of comorbidity and limited life expectancy, clinical judgement, patient preference, and a team-
based approach to assess risk/benefit is reasonable for decisions regarding intensity of BP lowering and
choice of antihypertensive drugs.[3]
European guidelines recommend a BP target of <140/90 mmHg in all patients including independent
older patients and, if treatment is tolerated, a BP target of ≤130/80 mmHg in most patients.[2] UK
guidelines from the National Institute for Health and Care Excellence recommend a BP target of <150/90
mmHg for patients aged 80 years and over.[60]
Pregnancy
Treatment described in this topic is for non-pregnant patients. Management in pregnancy should be
referred to an obstetrician specialising in high-risk patients.
Implementation success
High levels of hypertension control in large multi-ethnic populations has been demonstrated using basic
principles of implementation science.[165] [166] [167] Core principles include:
The patient should be considered a hypertension team member. The TASMINH4 trial has shown that
self-monitoring, with or without telemonitoring, used by general practitioners to titrate antihypertensive
medication in patients with poorly controlled BP, leads to significantly lower BP compared with titration
guided by clinic readings.[171]
An important goal is to continue to make efforts to improve disparities in BP control among people of
different ancestries.[172]
MANAGEMENT
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Acute ( summary )
without chronic renal disease or
cardiovascular disease (CVD)-related
comorbidity: lower CVD risk and
without diabetes
stage 1 not at goal with 1st thia zide diuretic + ACE inhibitor or
monotherapy or stage 2 angiotensin-II receptor antagonist
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Acute ( summary )
stage 1 not at goal with 1st beta-blocker + calcium-channel blocker
monotherapy or stage 2
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Acute ( summary )
plus lifestyle modification
1st beta-blocker
Ongoing ( summary )
refractory/resistant to optimised
triple therapy at any stage: without
congestive heart failure
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Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Acute
without chronic renal disease or
cardiovascular disease (CVD)-related
comorbidity: lower CVD risk and
without diabetes
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Acute
comorbidity: higher CVD risk or with
diabetes
OR
OR
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Acute
were co-equal for mild hypertension in type 2
diabetes.[105]
maximum 40 mg/day
OR
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Essential hypertension Management
Acute
» enalapril: 5 mg orally once daily initially,
increase gradually according to response,
maximum 40 mg/day as a single dose or in 2
divided doses
OR
OR
OR
OR
OR
OR
OR
OR
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Essential hypertension Management
Acute
OR
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Essential hypertension Management
Acute
plus lifestyle modification
Treatment recommended for ALL patients in
selected patient group
» All patients should be given a thorough
explanation of the risks associated with
hypertension and the need for adequate control
and adherence to therapy.
OR
OR
OR
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Essential hypertension Management
Acute
» diltiazem: 120-180 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 480 mg/day
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Essential hypertension Management
Acute
contraindicated; Dietary Approaches to Stop
Hypertension (DASH) diet (8-10 servings of
fruit and vegetables daily, whole grains, low
sodium, low-fat proteins); maintaining waist
circumference of <102 cm (<40 inches) for
men and <88 cm (<35 inches) for women and
weight loss to a body mass index of about 25
kg/m²; increased physical activity consisting
of at least 30 minutes of moderate-intensity,
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
1st ACE inhibitor or angiotensin-II receptor
antagonist + thia zide diuretic or calcium-
channel blocker
Primary options
maximum 32 mg/day
-or-
» irbesartan: 75 mg orally once daily initially,
increase gradually according to response,
maximum 300 mg/day
-or-
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Essential hypertension Management
Acute
» losartan: 25-50 mg orally once daily initially,
increase gradually according to response,
maximum 100 mg/day as a single dose or in
2 divided doses
-or-
» azilsartan: 40-80 mg orally once daily
-or-
» telmisartan: 40 mg orally once daily initially,
increase gradually according to response,
maximum 80 mg/day
-or-
» valsartan: 40-80 mg orally once daily
initially, increase gradually according to
response, maximum 320 mg/day
--AND--
» hydrochlorothiazide: 12.5 to 25 mg orally
once daily initially, increase gradually
according to response, maximum 50 mg/day
-or-
» chlortalidone: 12.5 mg orally once daily
initially, increase gradually according to
response, maximum 25 mg/day
-or-
» indapamide: 1.25 mg orally once daily
initially, increase gradually according to
response, maximum 2.5 mg/day
-or-
» amlodipine: 2.5 mg orally once daily initially,
increase gradually according to response,
maximum 10 mg/day
-or-
» felodipine: 2.5 mg orally once daily initially,
increase gradually according to response,
maximum 10 mg/day
-or-
» nifedipine: 30-60 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 90 mg/day
-or-
» diltiazem: 120-180 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 480 mg/day
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Essential hypertension Management
Acute
» Combination, low-dose therapy with an ACE
inhibitor or angiotensin-II receptor antagonist
plus a thiazide (or thiazide-like) diuretic or
calcium-channel blocker is an alternative first-
line option to monotherapy.
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Essential hypertension Management
Acute
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
stage 1 not at goal with 1st thia zide diuretic + ACE inhibitor or
monotherapy or stage 2 angiotensin-II receptor antagonist
Primary options
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Essential hypertension Management
Acute
» azilsartan: 40-80 mg orally once daily
-or-
» telmisartan: 40 mg orally once daily initially,
increase gradually according to response,
maximum 80 mg/day
-or-
» valsartan: 40-80 mg orally once daily
initially, increase gradually according to
response, maximum 320 mg/day
42 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Oct 17, 2023.
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Essential hypertension Management
Acute
kg/m²; increased physical activity consisting
of at least 30 minutes of moderate-intensity,
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
1st ACE inhibitor or angiotensin-II receptor
antagonist + calcium-channel blocker
Primary options
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Essential hypertension Management
Acute
» telmisartan: 40 mg orally once daily initially,
increase gradually according to response,
maximum 80 mg/day
-or-
» valsartan: 40-80 mg orally once daily
initially, increase gradually according to
response, maximum 320 mg/day
--AND--
» amlodipine: 2.5 mg orally once daily initially,
increase gradually according to response,
maximum 10 mg/day
-or-
» felodipine: 2.5 mg orally once daily initially,
increase gradually according to response,
maximum 10 mg/day
-or-
» nifedipine: 30-60 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 90 mg/day
-or-
» diltiazem: 120-180 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 480 mg/day
44 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Oct 17, 2023.
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Essential hypertension Management
Acute
» All patients should be given a thorough
explanation of the risks associated with
hypertension and the need for adequate control
and adherence to therapy.
OR
OR
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Essential hypertension Management
Acute
American College of Cardiology (ACC)/American
Heart Association (AHA) defines stage 1
hypertension as BP 130-139/80-89 mmHg.[3]
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Essential hypertension Management
Acute
weight loss to a body mass index of about 25
kg/m²; increased physical activity consisting
of at least 30 minutes of moderate-intensity,
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
2nd calcium-channel blocker
Primary options
OR
OR
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Essential hypertension Management
Acute
hypertension and the need for adequate control
and adherence to therapy.
maximum 10 mg/day
-or-
» nifedipine: 30-60 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 90 mg/day
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Essential hypertension Management
Acute
» The classification of blood pressure (BP)
differs between guidelines.[2] [3] [6] The
American College of Cardiology (ACC)/American
Heart Association (AHA) defines stage 2
hypertension as BP ≥140/90 mmHg.[3]
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Essential hypertension Management
Acute
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
2nd beta-blocker + ACE inhibitor or
angiotensin-II receptor antagonist
Primary options
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Essential hypertension Management
Acute
» irbesartan: 75 mg orally once daily initially,
increase gradually according to response,
maximum 300 mg/day
-or-
» losartan: 25-50 mg orally once daily initially,
increase gradually according to response,
maximum 100 mg/day as a single dose or in
2 divided doses
-or-
» azilsartan: 40-80 mg orally once daily
-or-
» telmisartan: 40 mg orally once daily initially,
increase gradually according to response,
maximum 80 mg/day
-or-
» valsartan: 40-80 mg orally once daily
initially, increase gradually according to
response, maximum 320 mg/day
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Essential hypertension Management
Acute
» All patients should be given a thorough
explanation of the risks associated with
hypertension and the need for adequate control
and adherence to therapy.
52 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Oct 17, 2023.
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Essential hypertension Management
Acute
» indapamide: 1.25 mg orally once daily
initially, increase gradually according to
response, maximum 2.5 mg/day
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Essential hypertension Management
Acute
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
3rd ACE inhibitor or angiotensin-II receptor
antagonist + thia zide diuretic
Primary options
-or-
» valsartan: 40-80 mg orally once daily
initially, increase gradually according to
response, maximum 320 mg/day
--AND--
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Essential hypertension Management
Acute
» hydrochlorothiazide: 12.5 to 25 mg orally
once daily initially, increase gradually
according to response, maximum 50 mg/day
-or-
» chlortalidone: 12.5 mg orally once daily
initially, increase gradually according to
response, maximum 25 mg/day
-or-
» indapamide: 1.25 mg orally once daily
initially, increase gradually according to
response, maximum 2.5 mg/day
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Essential hypertension Management
Acute
men and <88 cm (<35 inches) for women and
weight loss to a body mass index of about 25
kg/m²; increased physical activity consisting
of at least 30 minutes of moderate-intensity,
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
concomitant heart failure (HF)
» Beta-blockers
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Essential hypertension Management
Acute
receive ACE inhibitors, angiotensin-II receptor
antagonists, or ARNi because of intolerance or
contraindications.[126] [127]
OR
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Essential hypertension Management
Acute
» irbesartan: 75 mg orally once daily initially,
increase gradually according to response,
maximum 300 mg/day
OR
OR
OR
OR
Secondary options
OR
OR
OR
MANAGEMENT
OR
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Essential hypertension Management
Acute
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Essential hypertension Management
Acute
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
concomitant chronic renal disease
without cardiovascular disease
OR
OR
OR
OR
Secondary options
OR
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Essential hypertension Management
Acute
» irbesartan: 75 mg orally once daily initially,
increase gradually according to response,
maximum 300 mg/day
OR
OR
OR
OR
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Essential hypertension Management
Acute
titrated for a therapeutic effect, while observing
for potential adverse effects.
Primary options
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Essential hypertension Management
Acute
OR
OR
OR
OR
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Essential hypertension Management
Acute
Hypertension (DASH) diet (8-10 servings of
fruit and vegetables daily, whole grains, low
sodium, low-fat proteins); maintaining waist
circumference of <102 cm (<40 inches) for
men and <88 cm (<35 inches) for women and
weight loss to a body mass index of about 25
kg/m²; increased physical activity consisting
of at least 30 minutes of moderate-intensity,
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
2nd thia zide diuretic
Primary options
OR
OR
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Essential hypertension Management
Acute
plus lifestyle modification
Treatment recommended for ALL patients in
selected patient group
» All patients should be given a thorough
explanation of the risks associated with
hypertension and the need for adequate control
and adherence to therapy.
-or-
» perindopril: 4 mg orally once daily initially,
increase gradually according to response,
maximum 16 mg/day as a single dose or in 2
divided doses
-or-
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Essential hypertension Management
Acute
» ramipril: 2.5 mg orally once daily initially,
increase gradually according to response,
maximum 20 mg/day as a single dose or in 2
divided doses
--AND--
» hydrochlorothiazide: 12.5 to 25 mg orally
once daily initially, increase gradually
according to response, maximum 50 mg/day
-or-
» chlortalidone: 12.5 mg orally once daily
initially, increase gradually according to
response, maximum 25 mg/day
-or-
» indapamide: 1.25 mg orally once daily
initially, increase gradually according to
response, maximum 2.5 mg/day
Secondary options
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Essential hypertension Management
Acute
American College of Cardiology (ACC)/American
Heart Association (AHA) defines stage 2
hypertension as BP ≥140/90 mmHg.[3]
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Essential hypertension Management
Acute
weight loss to a body mass index of about 25
kg/m²; increased physical activity consisting
of at least 30 minutes of moderate-intensity,
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
2nd ACE inhibitor or angiotensin-II receptor
antagonist + calcium-channel blocker
Primary options
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Essential hypertension Management
Acute
» diltiazem: 120-180 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 480 mg/day
-or-
» verapamil: 120-180 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 480 mg/day
Secondary options
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Essential hypertension Management
Acute
Heart Association (AHA) defines stage 2
hypertension as BP ≥140/90 mmHg.[3]
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Essential hypertension Management
Acute
dynamic aerobic exercise (walking, jogging,
cycling, or swimming) 5 days per week to total
150 minutes/week, as tolerated or recommended
by physician; limited alcohol consumption (≤2
standard drinks [<20-30 g alcohol] per day in
hypertensive men, ≤1 standard drink [<10-20 g
alcohol] in hypertensive women). Total weekly
alcohol consumption should not exceed 14
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
3rd ACE inhibitor or angiotensin-II receptor
antagonist + thia zide diuretic +
spironolactone
Primary options
--AND--
» spironolactone: 12.5 mg orally once daily
initially, increase gradually according to
response, maximum 25 mg/day
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Essential hypertension Management
Acute
Secondary options
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Essential hypertension Management
Acute
» All patients should be given a thorough
explanation of the risks associated with
hypertension and the need for adequate control
and adherence to therapy.
1st beta-blocker
Primary options
OR
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Essential hypertension Management
Acute
should be tapered over 1-2 weeks and patients
should be monitored for symptoms of angina.
OR
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Essential hypertension Management
Acute
» verapamil: 120-180 mg orally (extended-
release) once daily initially, increase gradually
according to response, maximum 480 mg/day
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Essential hypertension Management
Ongoing
refractory/resistant to optimised
triple therapy at any stage: without
congestive heart failure
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Essential hypertension Management
Ongoing
generally avoided because of its adverse-effect
profile.
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Essential hypertension Management
Ongoing
standard drinks (140 g) for men and 8 standard
drinks (80 g) for women.
MANAGEMENT
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Essential hypertension Management
Emerging
Chronotherapy
Studies have investigated whether hypertension therapy taken at bedtime results in improved cardiovascular
disease (CVD) risk reduction compared with medication taken upon awakening. The Hygia Chronotherapy
Trial, conducted in primary care, found that hypertensive patients taking ≥1 prescribed blood pressure (BP)-
lowering medications at bedtime had improved ambulatory BP control compared with those who took their
medications upon awakening, and they also had a reduced occurrence of major CVD events.[175] However,
excessive lowering of nocturnal BP with night-time dosing may increase the potential risk of retinal, cerebral,
and myocardial ischaemia, and may lower medication adherence. The Treatment in Morning versus Evening
(TIME) study compared evening and morning dosing of usual antihypertensive medication in participants
followed up for a median of 5.2 years and found no difference between the groups for the primary composite
outcome of vascular death or hospitalisation for non-fatal myocardial infarction.[176] The 2023 European
guidelines note that patients have a choice as to when to take hypertension therapy, but that adherence
is generally better in the morning.[5] Bedtime dosing may be considered in patients with documented high
night-time BP.
L-arginine supplementation
Oral supplementation with L-arginine, an amino acid and a substrate of nitric oxide synthase, has been
shown to significantly lower both systolic and diastolic BP.[198]
Vitamin C supplementation
Vitamin C supplementation has been shown to reduce systolic and diastolic BP in short-term trials. Long-
term trials examining the effects of vitamin C supplementation on BP and clinical events are needed.[199]
[200]
Vitamin D supplementation
MANAGEMENT
Data from cross-sectional studies report that low levels of 25-hydroxy vitamin D are associated with higher
systolic BP and higher incidence of hypertension.[201] Large observational studies show a weaker, yet
similar, association. This effect is thought to be partly mediated through regulation of the renin-angiotensin-
aldosterone axis.[202] Randomised controlled trials conflict with observational data, probably due to
differences in populations studied, doses of vitamin D used, and unmeasured confounders. One systematic
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Essential hypertension Management
review found that in studies to date, vitamin D supplementation was ineffective for BP lowering.[203] Large
randomised trials focusing on patients with severe vitamin D deficiency and hypertension are needed before
vitamin D can be recommended for the prevention or treatment of hypertension.
Calcium supplementation
Data indicate that increased calcium intake slightly reduces systolic and diastolic BP in people with normal
BP, particularly young people. This could have implications for prevention and public health, but more and
larger studies are needed.[204]
Amiloride
In the PATHWAY-2 study of resistant hypertension, the potassium-sparing diuretic amiloride was shown to
be as effective at reducing BP as spironolactone, suggesting it may be an alternative option for resistant
hypertension.[205]
Baxdrostat
In one phase 2 trial, baxdrostat, an aldosterone synthase inhibitor, was shown to reduce BP in patients with
resistant hypertension over 12 weeks compared with placebo. Reductions were dose-related.[206]
Aprocitentan
In one phase 3, multi-centre trial (PRECISION), aprocitentan, a novel dual endothelin antagonist, reduced
BP compared with placebo at 4 weeks of treatment.[207]
Zilebesiran
Zilebesiran is an investigational RNA interference therapeutic agent that inhibits synthesis of hepatic
angiotensinogen (the precursor of all angiotensin peptides). It has been investigated in a phase 1 study,
which found that patients receiving zilebesiran had decreases in serum angiotensinogen and BP that were
sustained for up to 24 weeks.[208]
Primary prevention
The lifetime risk for development of hypertension is high. Efforts should be made to minimise risk factors.
The 2017 American College of Cardiology (ACC)/American Heart Association (AHA) guideline recommends
lifestyle modifications for patients with elevated blood pressure (BP), which is defined as 120 to 129/<80
mmHg.[3] Recommended lifestyle modifications include dietary changes, smoking cessation, increased
physical activity, and reduced alcohol intake.[49] [50]
Population-based approaches to prevent hypertension have been proposed: the American Public Health
Association (APHA) has advocated for reduced sodium in the food supply, particularly in processed
foods.[51] Although sodium reduction has a modest effect on BP lowering, the population effect on the
huge number of at-risk people would potentially have significant consequences for cardiovascular morbidity
and mortality.[52] Use of salt substitutes has demonstrated BP-mediated protective effects for major
cardiovascular events and mortality.[53] [54]
The US Preventive Services Task Force (USPSTF) recommends that adults at increased risk of
cardiovascular disease are offered behavioural counselling interventions to promote a healthy diet and
physical activity; those not at high risk may also be considered for behavioural counselling interventions.[55]
[56]
MANAGEMENT
Secondary prevention
Aggressive lifestyle modifications (dietary changes, smoking cessation, increased physical activity, reduced
alcohol intake) should be initiated in patients with pre-hypertension (blood pressure [BP] 120-139/80-89
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Essential hypertension Management
mmHg) to delay or prevent the onset of overt hypertension. The 2017 American College of Cardiology
(ACC)/American Heart Association (AHA) guideline defines elevated BP as 120 to 129/<80 mmHg and
recommends lifestyle modification for these patients, which should be reassessed 3-6 months after
initiation.[3] Other cardiovascular risk parameters should be aggressively managed. For example, statins
should be used in accordance with guidelines in people with diabetes. Accordingly, patients with pre-
hypertension or elevated BP should be evaluated for occult cardiovascular risk by screening for diabetes
or dyslipidaemia with fasting blood sugar and lipid levels. Global cardiovascular risk should be assessed.
[American College of Cardiology: ASCVD risk estimator plus] (https://tools.acc.org/ASCVD-Risk-Estimator-
Plus/#!/calculate/estimate)
Patient discussions
As with most chronic conditions, hypertension requires a lifelong commitment from both patient and
physician to pursue aggressive management with healthy lifestyle choices and medical therapy.[10]
Patients should be counselled about diet (Dietary Approaches to Stop Hypertension [DASH] diet, sodium
≤1.5 g/day, in consultation with a nutritionist) and physical activity.[55]
• Smoking raises blood pressure (BP) acutely and transiently, but long-term studies have not
found an association between smoking and the risk of developing chronic hypertension.[231]
Nevertheless, smoking cessation should be encouraged to reduce cardiovascular risk.
• Acute consumption of coffee and black tea has a mild pressor effect; however, long-term studies
have found slightly lower BP in patients who consume caffeine daily.[90] [232] Therefore, moderate
caffeine consumption is acceptable.
• Patients should be advised to begin and maintain aerobic exercise, with a goal of at least 30
minutes of moderate-intensity, dynamic aerobic exercise (walking, jogging, cycling, or swimming) 5
days per week to total 150 minutes as tolerated or recommended by a physician.
• Medication adherence is important and it should be discussed with patients in whom drug therapy
for hypertension is often a lifelong commitment.[233]
• Regular use of paracetamol has been associated with increased systolic BP in those with
hypertension; continued regular use in these patients should be reviewed.[71]
MANAGEMENT
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Essential hypertension Follow up
Monitoring
Monitoring
FOLLOW UP
While adjusting medication dosage, blood pressure (BP) should be monitored every 2-4 weeks. Once
stabilised, BP should be checked and medications reviewed every 6-12 months. Serum potassium and
creatinine should be checked annually. Patients taking thiazide and thiazide-type diuretics should also
have serum sodium checked annually.
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Essential hypertension Follow up
Complications
FOLLOW UP
coronary artery disease long term high
For every 20/10 mmHg increase in blood pressure (BP), there is a lifetime doubling of mortality related
to ischaemic heart disease or cerebrovascular accident.[219] As with all other associated complications
and comorbid diseases, aggressive BP control, along with therapy specific for the individual condition,
may retard the progression of disease. A longer duration of hypertension has also been associated with
increased risks of cardiovascular disease and overall death in a linear fashion.[220]
The risk of developing cerebrovascular accident (CVA) varies linearly with blood pressure (BP), and BP
control reduces the risk of recurrent CVA.[220] [221]
Left ventricular hypertrophy (LVH) on echocardiography is seen in more than 30% of hypertensive
patients.[225]
Linked to cardiovascular morbidity and mortality.[226] LVH patterns vary based on haemodynamic loading
conditions.[227]
Patients with hypertension are 3 times more likely to develop congestive heart failure (systolic or diastolic
dysfunction) than are normotensive patients.[222]
ACE inhibitors, angiotensin-II receptor antagonists, beta-blockers, aldosterone antagonists, and sodium-
glucose co-transporter 2 inhibitors confer a mortality benefit. Diuretics do not, but loop diuretics are
frequently used to relieve symptoms of fluid overload.
Hypertension is also a major risk factor for development of other retinal vascular diseases, such as retinal
vein or artery occlusion, or ischaemic optic neuropathy.
Treatment of hypertension in patients with peripheral artery disease reduces the risk of myocardial
infarction, stroke, or congestive heart failure.
Hypertension is closely associated with the development of renal disease and end-stage renal disease
(ESRD). However, while many hypertensive patients will develop a mild degree of nephrosclerosis, few
progress to ESRD.[228]
A more malignant course of hypertensive kidney disease is seen in black than in white people.[229]
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Essential hypertension Follow up
More than 70% of patients with aortic dissection have a history of hypertension.
Despite improved methods of diagnosis and increased awareness, aortic dissection remains associated
with high mortality rates, particularly proximal (type A) dissections.[223] [224]
Undiagnosed or inadequately treated essential hypertension is the most common cause of hypertensive
emergency.[230]
Prognosis
Several trials have shown that uncontrolled hypertension is a major risk factor for the development of cardiac,
vascular, renal, and cerebrovascular disease, morbidity, and mortality. However, even modest reductions
in blood pressure (BP) decrease morbidity and mortality.[3] Systolic BP may have a greater effect on
cardiovascular outcomes, but both systolic and diastolic hypertension have been shown to independently
influence the risk of adverse cardiovascular events.[209] The association between BP and mortality from
cardiovascular disease (CVD) may be sex-specific, with increased CVD mortality seen at lower systolic BP in
women compared with men.[210]
There is currently no randomised controlled trial evidence for the benefit of treating white-coat hypertension.
One meta-analysis found that untreated white-coat hypertension is associated with an increased risk for
cardiovascular events and all-cause mortality; there was no significant association between treated white
coat effect and cardiovascular events or mortality.[211] Similarly, there are no data on the risks and benefits
of treating masked hypertension; however, the American College of Cardiology (ACC)/American Heart
Association (AHA) guideline notes that masked hypertension and masked uncontrolled hypertension are
associated with an increased prevalence of target organ damage and risk of cardiovascular disease, stroke,
and mortality compared with normotensive individuals and those with white coat hypertension.[3] [212] Out-
of-clinic BP monitoring is critical in the management of hypertension and improving outcomes.
Further studies are needed to confirm optimal BP targets in diabetes. In one randomised clinical trial
(ACCORD), a more stringent BP goal for patients with type 2 diabetes did not significantly reduce the primary
cardiovascular outcome or most secondary outcomes compared with standard BP goals. In this study, the
number of total and non-fatal strokes was lower in the intensive therapy group, although the clinical benefit
was limited (number needed to treat = 89 for 5 years to prevent one stroke).[85] Data from the ACCORD
study and the Veterans Affairs Diabetes Trials were also used in an analysis to show an association between
BP variability and risk of heart failure in patients with type 2 diabetes, possibly related to diastole.[213]
In patients with diabetes, the decrease in asleep BP - a novel therapeutic target requiring evaluation by
ambulatory monitoring - has been shown to be the most significant independent predictor of event-free
survival in some studies.[214] [215] [216] [217] [218]
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Essential hypertension Guidelines
Diagnostic guidelines
United Kingdom
Europe
2023 ESH Guidelines for the management of arterial hypertension (ht tps://
GUIDELINES
www.eshonline.org/guidelines/2023-guidelines)
Published by: European Society of Hypertension Last published: 2023
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Essential hypertension Guidelines
North America
The seventh report of the Joint National Commit tee on the Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (ht tps://
www.nhlbi.nih.gov/health-topics/seventh-report-of-joint-national-commit tee-
on-prevention-detection-evaluation-and-treatment-high-blood-pressure)
Published by: National Heart, Lung, and Blood Institute Last published: 2004
Treatment guidelines
United Kingdom
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Essential hypertension Guidelines
Europe
2023 ESH Guidelines for the management of arterial hypertension (ht tps://
www.eshonline.org/guidelines/2023-guidelines)
Published by: European Society of Hypertension Last published: 2023
GUIDELINES
Published by: European Society of Cardiology; European Society of Last published: 2018
Hypertension
International
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Essential hypertension Guidelines
North America
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Essential hypertension Guidelines
North America
The seventh report of the Joint National Commit tee on the Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (ht tps://
www.nhlbi.nih.gov/health-topics/seventh-report-of-joint-national-commit tee-
on-prevention-detection-evaluation-and-treatment-high-blood-pressure)
Published by: National Heart, Lung, and Blood Institute Last published: 2004
Asia
GUIDELINES
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Essential hypertension Online resources
Online resources
1. American College of Cardiology: ASCVD risk estimator plus (https://tools.acc.org/ASCVD-Risk-
Estimator-Plus/#!/calculate/estimate) (external link)
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Essential hypertension Evidence tables
Evidence tables
How does pharmacotherapy affect outcomes in people aged 60 years or older
EVIDENCE TABLES
with hypertension?
This table is a summary of the analysis reported in a Cochrane Clinical Answer that focuses on the
above important clinical question.
Evidence A * Confidence in the evidence is high or moderate to high where GRADE has been
performed and the intervention is more effective/beneficial than the comparison for
key outcomes.
Population: Adults aged ≥60 years (mean age 64-84 years where reported) with moderate-to-severe
systolic and/or diastolic hypertension (average 182/95 mmHg)
Intervention: Antihypertensive drug therapy
Comparison: Placebo or no treatment/observation
† ‡
Outcome Effectiveness (BMJ rating) Confidence in evidence (GRADE)
Note
The Cochrane review which underpins this Cochrane Clinical Answer (CCA) notes that the reduction in
mortality in the antihypertensive group occurred mostly in the 60- to 79-year-old patient group. It also notes
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Essential hypertension Evidence tables
that while a statistically significant reduction in cardiovascular mortality and morbidity occurred in both those
aged 60 to 79 years and in those aged 80 years and older, the size of the absolute risk reduction was greater
in the former (3.8% vs 2.9%).
EVIDENCE TABLES
The Cochrane review also highlights that the reduction in mortality occurred in studies with the least blood
pressure reduction and lowest intensity of therapy, suggesting that less aggressive treatment be used for
those over the age of 80. Please see the Cochrane review for more details.
* Evidence levels
The Evidence level is an internal rating applied by BMJ Best Practice. See the EBM Toolkit (https://
bestpractice.bmj.com/info/evidence-tables/) for details.
Confidence in evidence
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Essential hypertension References
Key articles
• National Heart, Lung, and Blood Institute. The seventh report of the Joint National Committee on
REFERENCES
the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Aug 2004 [internet
publication]. Full text (https://www.nhlbi.nih.gov/files/docs/guidelines/jnc7full.pdf)
• Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH guidelines for the management of arterial
hypertension. Eur Heart J. 2018 Sep 1;39(33):3021-104. Full text (https://academic.oup.com/
eurheartj/article/39/33/3021/5079119) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/30165516?
tool=bestpractice.bmj.com)
• Rabi DM, McBrien KA, Sapir-Pichhadze R, et al. Hypertension Canada's 2020 comprehensive
guidelines for the prevention, diagnosis, risk assessment, and treatment of hypertension in adults
and children. Can J Cardiol. 2020 May;36(5):596-624. Full text (https://www.onlinecjc.ca/article/
S0828-282X(20)30191-4/fulltext) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/32389335?
tool=bestpractice.bmj.com)
• Wright JT Jr, Williamson JD, Whelton PK, et al; SPRINT Research Group. A randomized trial of
intensive versus standard blood-pressure control. N Engl J Med. 2015 Nov 26;373(22):2103-16. Full
text (https://www.nejm.org/doi/full/10.1056/NEJMoa1511939) Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/26551272?tool=bestpractice.bmj.com)
• Williams B, MacDonald TM, Morant S, et al; British Hypertension Society's PATHWAY Studies Group.
Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for
drug-resistant hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet.
2015 Nov 21;386(10008):2059-68. Full text (https://www.thelancet.com/journals/lancet/article/
PIIS0140-6736(15)00257-3/fulltext) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/26414968?
tool=bestpractice.bmj.com)
References
1. National Heart, Lung, and Blood Institute. The seventh report of the Joint National Committee on
the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Aug 2004 [internet
publication]. Full text (https://www.nhlbi.nih.gov/files/docs/guidelines/jnc7full.pdf)
2. Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH guidelines for the management of arterial
hypertension. Eur Heart J. 2018 Sep 1;39(33):3021-104. Full text (https://academic.oup.com/
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Oct 17, 2023.
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Essential hypertension References
eurheartj/article/39/33/3021/5079119) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/30165516?
tool=bestpractice.bmj.com)
REFERENCES
4. Hansson L, Zanchetti A, Carruthers SG, 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 Jun 13;351(9118):1755-62. Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/9635947?tool=bestpractice.bmj.com)
5. Mancia G, Kreutz R, Brunström M, et al. 2023 ESH guidelines for the management of arterial
hypertension The Task Force for the management of arterial hypertension of the European Society of
Hypertension endorsed by the International Society of Hypertension (ISH) and the European Renal
Association (ERA). J Hypertens. 2023 Jun 21. Full text (https://journals.lww.com/jhypertension/
fulltext/9900/2023_esh_guidelines_for_the_management_of_arterial.271.aspx) Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/37345492?tool=bestpractice.bmj.com)
6. World Health Organization. Guideline for the pharmacological treatment of hypertension in adults. Aug
2021 [internet publication]. Full text (https://www.who.int/publications/i/item/9789240033986)
7. NCD Risk Factor Collaboration (NCD-RisC). Worldwide trends in hypertension prevalence and
progress in treatment and control from 1990 to 2019: a pooled analysis of 1201 population-
representative studies with 104 million participants. Lancet. 2021 Sep 11;398(10304):957-80. Full text
(https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01330-1/fulltext) Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/34450083?tool=bestpractice.bmj.com)
8. Tsao CW, Aday AW, Almarzooq ZI, et al; American Heart Association Council on Epidemiology and
Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke
statistics - 2023 update: a report from the American Heart Association. Circulation. 2023 Feb
21;147(8):e93-621. Full text (https://www.ahajournals.org/doi/10.1161/CIR.0000000000001123)
Abstract (http://www.ncbi.nlm.nih.gov/pubmed/36695182?tool=bestpractice.bmj.com)
9. Vasan RS, Beiser A, Seshadri S, et al. Residual lifetime risk for developing hypertension in middle-
aged women and men: the Framingham Heart Study. JAMA. 2002 Feb 27;287(8):1003-10. Full text
(https://jamanetwork.com/journals/jama/fullarticle/194679) Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/11866648?tool=bestpractice.bmj.com)
10. Abdalla M, Bolen SD, Brettler J, et al. Implementation strategies to improve blood pressure control
in the United States: a scientific statement from the American Heart Association and American
Medical Association. Hypertension. 2023 Oct;80(10):e143-57. Full text (https://www.ahajournals.org/
doi/10.1161/HYP.0000000000000232) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/37650292?
tool=bestpractice.bmj.com)
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Essential hypertension References
11. Public Health England. Health matters: combating high blood pressure. Jan 2017 [internet publication].
Full text (https://www.gov.uk/government/publications/health-matters-combating-high-blood-pressure/
health-matters-combating-high-blood-pressure)
REFERENCES
12. Coggon DI, Martyn CN. Time and chance: the stochastic nature of disease causation. Lancet.
2005 Apr 16-22;365(9468):1434-7. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/15836893?
tool=bestpractice.bmj.com)
13. Saad MF, Rewers M, Selby J, et al. Insulin resistance and hypertension: the Insulin Resistance
Atherosclerosis Study. Hypertension. 2004 Jun;43(6):1324-31. Full text (https://www.ahajournals.org/
doi/10.1161/01.HYP.0000128019.19363.f9) Abstract (http://www.ncbi.nlm.nih.gov/
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Figure 1: US and European guidelines - classification and management.
Created by BMJ Knowledge Centre with data from Whelton PK, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/
AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of
high blood pressure in adults: a report of the American College of Cardiology/American Heart Association
Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018 May 15;71(19):e127-248 and Williams
B, et al. 2018 ESC/ESH guidelines for the management of arterial hypertension. Eur Heart J. 2018 Sep
1;39(33):3021-104.
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Contributors:
// Authors:
// Acknowledgements:
Dr Jeffrey Brettler would like to gratefully acknowledge Dr Joel Handler, Dr Jonathan N. Bella, Dr
Moustapha Atoui, Dr Liran Blum, and Dr Michael A. Spinelli, previous contributors to this topic.
DISCLOSURES: JH, JNB, MA, LB, and MAS declare that they have no competing interests.
// Peer Reviewers: