Hypertension: diagnosis and staging

Overview and definitions

ESC 2024 describes a continuous and log-linear association between BP and adverse CVD outcomes, with relative risk rising from systolic levels as low as 90 mmHg.^[1] AHA/ACC 2025 describes a graded, log-linear association with an approximate doubling of the risk of fatal and nonfatal cardiovascular events for each 20 mm Hg higher SBP and 10 mm Hg higher DBP.^[2]

ESC 2024 says no categorisation of BP can be considered immutable or flawless.^[1] AHA/ACC 2025 says its category names rest on a pragmatic interpretation of BP-related CVD risk and the benefit of BP reduction in clinical trials.^[2]

Why keep 140/90 mmHg as the hypertension line? ESC 2024 gives three reasons. First, trial meta-analyses show benefit from BP-lowering therapy above it, among all adults and across settings.^[1] Second, most adults above it are at increased CVD risk, typically with 10-year estimates of fatal and non-fatal CVD events of 10% or more.^[1] Third, policymakers already use it to define a disease state, and keeping it avoids labelling most adults with what is widely considered a disease.^[1]

Classification: ESC 2024 versus AHA/ACC 2025

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Comparing the two schemes side by side: First, office BP with systolic 130–139 mmHg and diastolic below 90 mmHg, or diastolic 80–89 mmHg with systolic below 140 mmHg, is ESC elevated BP but AHA/ACC stage 1 hypertension.^[1][2] For AHA/ACC, the category rests on the average of 2 or more careful readings on 2 or more occasions.^[2] Second, the diastolic lines differ: ESC elevated BP starts at a diastolic of 70 mmHg, whereas AHA/ACC normal and elevated both require a DBP below 80 mm Hg.^[1][2] Third, for its lowest category ESC 2024 avoids terms such as normal BP and uses non-elevated BP, while AHA/ACC 2025 keeps a normal category.^[1][2]

ESC 2024 defines its categories by office BP and gives corresponding home and ambulatory thresholds in Table 5; AHA/ACC 2025 categorises average BP measured in a health care setting (office BP).^[1][2] AHA/ACC 2025 adds that its classification is most valuable for untreated adults when deciding how to prevent or treat high BP, though it also helps judge whether interventions are working.^[2]

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Epidemiology and risk factors

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Hypertension is the most prevalent modifiable CVD risk factor and the leading cause of death and disability worldwide (AHA/ACC 2025).^[2] ESC 2024 calls it the most important modifiable risk factor for all-cause and CVD morbidity and mortality globally.^[1]

Higher BP is associated with higher risk of total CVD, coronary heart disease, heart failure, aortic and peripheral vascular disease, kidney disease, ischaemic and haemorrhagic stroke, dementia and cognitive impairment (AHA/ACC 2025).^[2] Among individuals without major risk factors, relative CVD event rates start rising at SBP levels as low as 90 mm Hg.^[2] In middle-aged and older adults, higher SBP carries greater prevalence and risk than higher DBP.^[2] ESC 2024 notes that some studies suggest a stronger relative risk for CVD at a given BP in females than in males.^[1]

With ageing, population SBP tends to rise steadily to the end of life, whereas DBP rises until the fifth decade, plateaus for a decade and then declines (AHA/ACC 2025).^[2] Hypertension frequently co-occurs with other CVD risk factors (AHA/ACC 2025).^[2] From 2017 to 2020, 16.6% of US adults with hypertension were current smokers, 72.6% were overweight or obese, 12.3% had diabetes and 13.4% had diagnosed CKD.^[2] AHA/ACC 2025 states that most US adults with hypertension are not controlled to below 130/80 mm Hg, and more than 50% are unaware that they have hypertension.^[2]

AHA/ACC 2025 Table 8: environmental, behavioural and genetic causes of hypertension

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Among dietary factors, higher sodium intake, lower potassium intake and alcohol overuse predominate, while low intake of fibre, calcium, magnesium and plant protein also influence BP (AHA/ACC 2025).^[2] Weight gain, overweight or obesity and related metabolic issues (i.e. insulin resistance) contribute to the increase in BP across the lifespan, particularly in recent decades.^[2] Factors such as increasing age, obesity and insulin resistance influence how BP is affected by sodium.^[2] Emerging data also implicate environmental exposures and chemical toxins, including air pollution and heavy metals.^[2]

BP is a highly heritable trait and hundreds of genetic loci affecting BP have been described; each has small effects alone, and all loci described to date explain less than 10% of BP variance (AHA/ACC 2025).^[2]

Pathophysiology

Most patients have essential or primary hypertension, with no known exact cause. ESC 2024 estimates that 10% have secondary hypertension with an identifiable cause, while noting that some studies indicate the prevalence may be substantially higher with modern systematic screening.^[1] The mechanism involves complex interactions between environmental and behavioural factors, genes, hormonal networks and several organ systems (renal, cardiovascular and central nervous system), plus vascular and immune mechanisms.^[1] Dysregulation of these processes leads to hypertension, which, if uncontrolled, can lead to hypertension-mediated organ damage (HMOD) and adverse CVD outcomes.^[1] ESC 2024 adds that the contribution of these factors may differ between males and females.^[1]

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From pressure to organ damage

Longstanding hypertension causes organ damage and ultimately cardiovascular, cerebrovascular and clinical renal disease (ESC 2024).^[1] Organs adversely affected by elevated BP and hypertension include the heart, brain, kidneys, eyes and vessels, which undergo structural and functional changes.^[1] ESC 2024 uses the term hypertension-mediated organ damage for subclinical complications of hypertension that indicate high risk of later clinical events, while acknowledging that factors besides BP (dyslipidaemia, hyperglycaemia) can contribute to these changes.^[1]

HMOD usually indicates long-standing elevated BP or hypertension and adds prognostic information on CVD risk in all BP categories (ESC 2024).^[1] Unless treated, it can progress from asymptomatic to symptomatic and ultimately to overt CVD events.^[1] Its profile may differ by sex: left ventricular hypertrophy (LVH) and left atrial dilatation are more frequent in women.^[1]

What the cuff actually measures

Systolic BP is the maximum arterial pulsatile pressure; by auscultation it is the onset of the first Korotkoff sound (ESC 2024).^[1] Diastolic BP is the minimum pulsatile pressure, read at complete disappearance of the Korotkoff sounds (the fifth sound), or at muffling (the fourth sound) if the sounds never disappear.^[1] Oscillometric devices work differently: at maximum cuff oscillation the cuff pressure equals mean arterial pressure, and SBP and DBP are then estimated by proprietary manufacturer algorithms (AHA/ACC 2025).^[2] That is why AHA/ACC 2025 recommends only oscillometric devices validated with a rigorous standardised protocol against a reference standard.^[2]

How BP changes with age

Systolic BP rises with age until the eighth decade, while diastolic BP rises until the fifth or sixth decade and then plateaus or falls, so pulse pressure widens from middle age (ESC 2024).^[1] ESC 2024 relates these changes to increased aortic stiffening with age.^[1]

Two secondary mechanisms worth knowing

Primary aldosteronism is a group of disorders in which aldosterone production is inappropriately high for sodium and volume status, relatively autonomous of angiotensin II and potassium, and not completely suppressible with sodium loading (AHA/ACC 2025).^[2] The excess aldosterone causes intravascular volume expansion, suppressed plasma renin activity, sodium retention, increased potassium excretion, hypertension, and cardiovascular and kidney damage.^[2]

Renovascular hypertension is renal artery occlusion or stenosis that lowers renal perfusion pressure enough to activate the renin–angiotensin–aldosterone system and raise BP (ESC 2024).^[1] Its major causes are atherosclerosis, the most common form especially in older adults, and fibromuscular dysplasia.^[1]

Clinical presentation and screening

Hypertension is predominantly an asymptomatic condition, typically found by systematic or opportunistic screening in a healthcare setting (ESC 2024).^[1] Systematic screening invites people solely to measure BP and CVD risk profile; opportunistic screening measures BP whenever a patient attends for any reason.^[1] The ESC patient-communication table puts it plainly: for most people hypertension has no noticeable signs or symptoms.^[1]

Unless treated, HMOD can progress from asymptomatic to symptomatic and ultimately to overt CVD events (ESC 2024).^[1] Populations in which masked hypertension is more prevalent include men, people who smoke, those with excessive alcohol intake and those with diabetes or obesity (ESC 2024).^[1]

ESC 2024 Recommendation Table 5 (all rows) and Recommendation Table 1 opportunistic-measurement row

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Differential diagnosis: office and out-of-office phenotypes, pseudo-resistance and secondary causes

AHA/ACC 2025 notes that out-of-office monitoring separates several clinically relevant categories by the concordance or discordance of office and out-of-office BP.^[2] These include white-coat and masked hypertension in people not taking antihypertensive medication, and white-coat effect and masked uncontrolled hypertension in those who are.^[2]

BP categories based on office and out-of-office measurement

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ESC 2024 defines white-coat hypertension as BP above the diagnostic threshold in the office but below it in home or ambulatory settings.^[1] For example, 140/90 mmHg or more in the office but below 135/85 mmHg at home or on daytime ambulatory BP (or 24-h BP below 130/80 mmHg).^[1] Masked hypertension is the reverse: for example, below 140/90 mmHg in clinic but 135/85 mmHg or more at home or on daytime ambulatory BP (or 24-h BP of 130/80 mmHg or more).^[1]

ESC 2024 makes excluding pseudo-resistance a prerequisite in diagnosing resistant hypertension.^[1] ESC 2024 lists its causes as poor adherence to and persistence with treatment, the white-coat phenomenon, poor BP measurement method, marked brachial artery calcification (Osler phenomenon), clinician inertia (inadequate doses, inappropriate combinations) and Munchausen syndrome (rare).^[1]

The triggers for secondary-hypertension screening are set out under Investigations below. ESC 2024 reports a secondary hypertension prevalence of 10%–35% in all hypertensive patients, depending on the definition and cohort.^[1] It reports up to 50% in resistant hypertension, an estimate that included people with eGFR below 40 mL/min/1.73 m².^[1] AHA/ACC 2025 gives approximately 5% to 25% of adults with hypertension.^[2]

Clinical and bedside assessment: measuring office BP properly

All BP measurements can be influenced by the circumstances of measurement, including position, ambient temperature, measurement technique, equipment accuracy and the patient’s physical condition (ESC 2024).^[1] Both guidelines recommend a standardised method. AHA/ACC 2025 recommends standardised methods for accurate measurement and documentation of in-office BP when diagnosing and managing high BP (COR 1, LOE C-LD).^[2][1] ESC 2024 recommends a validated, calibrated device, the correct technique and a consistent approach for each patient (Class I, Level B).^[1]

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ESC 2024 Recommendation Table 1 (all rows)

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On device type, AHA/ACC 2025 states it is reasonable to use the oscillometric method with an automated device over the auscultatory method when measuring in-office BP in adults (COR 2a, LOE C-EO).^[2] It notes that potential limitations of the auscultatory method include improper stethoscope placement, too-fast cuff deflation, digit preference and observer hearing deficits.^[2] A single reading is inadequate for decisions; AHA/ACC 2025 says an average of 2 or more measurements on 2 or more separate occasions may minimise error.^[2]

Automated office BP (AOBP) can be attended or unattended. ESC 2024 finds no clear evidence that unattended AOBP is superior to attended AOBP for managing BP to reduce rates of CVD.^[1] Because readings may differ between the two, it advises a consistent approach, depending on local resource and preference.^[1] It notes that AOBP correlates more closely with mean ABPM than with the manual auscultatory technique and may reduce measurement error and white-coat effects.^[1] AHA/ACC 2025 adds that mean unattended AOBP is lower than mean office BP taken with a clinician present using a standardised protocol.^[2] It also notes that within-person differences between unattended AOBP and out-of-office BP can be large.^[2]

In AF, the ESC 2024 text notes that oscillometric monitors are not always accurate because of the greater beat-to-beat variability of BP, so multiple auscultatory measurements are recommended.^[1] The formal recommendation is that BP measurement should be considered using a manual auscultatory method in AF where possible (Class IIa, Level C).^[1] AHA/ACC 2025 notes that oscillometric validation has typically been done in sinus rhythm and evidence in AF is limited.^[2] Some oscillometric monitors include an AF-detection algorithm, but an ECG is still required to confirm the diagnosis (ESC 2024).^[1]

ESC 2024 does not currently recommend any cuffless modality for routine clinical use, citing insufficient consensus on accuracy standards and validation.^[1] AHA/ACC 2025 states that cuffless BP devices are not recommended for diagnosing or managing high BP in adults (COR 3: No Benefit, LOE C-LD).^[2]

Beyond the cuff, the clinical evaluation aims to diagnose hypertension, find contributing factors and other CVD risk factors, define comorbidities, screen for secondary causes where indicated, and establish whether there is HMOD or existing cardiac, cerebrovascular or renal disease (ESC 2024).^[1] Checking the inter-arm difference may itself identify a subclavian stenosis as vascular HMOD.^[1]

Investigations

Home and ambulatory monitoring

Home BP measurement (HBPM) is done by the patient with a validated monitor, usually an upper-arm oscillometric cuff device (ESC 2024).^[1] Ambulatory BP measurement (ABPM) uses a fully automated oscillometric device, usually for 24 h, at set intervals.^[1]

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An average HBPM of 135/85 mmHg or more, equivalent to office BP of 140/90 mmHg or more, should be used to diagnose hypertension, and an average systolic BP of 120–134 mmHg or diastolic BP of 70–84 mmHg to diagnose elevated BP (ESC 2024).^[1] ABPM readings are usually taken every 15–30 min by day (typically 7 a.m. to 11 p.m.) and every 30–60 min at night (typically 11 p.m. to 7 a.m.) (ESC 2024).^[1] A valid session needs at least 70% usable readings, typically 27 or more over 24 h, and preferably seven night readings.^[1] Emerging data indicate that 8 or more waking and 4 or more sleeping readings may be adequate if more cannot be obtained, and raw readings should be reviewed for outliers before the means are used.^[1]

ESC 2024 Table 5: office, home and ambulatory thresholds (mmHg); the office thresholds assume standardised measurement

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AHA/ACC 2025 Table 7: home and ambulatory values corresponding to office levels (mm Hg)

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AHA/ACC 2025 provides these as a guide to be interpreted with caution, because the data are primarily from European, Australian and Asian populations, with few data for establishing appropriate thresholds for US populations.^[2] Further, the data are derived primarily from observational studies.^[2]

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ESC 2024 notes overlap between home and ambulatory monitoring in differentiating hypertensive phenotypes.^[1] However, around 15% of people will have diagnostic disagreement between them, of whom approximately 50% will have clinically significant differences of more than 5 mmHg.^[1] AHA/ACC 2025 notes that ABPM has been the de facto reference standard for out-of-office BP monitoring because more data link ABPM than HBPM to CVD events, while there are scarce data on whether ABPM or HBPM is superior for CVD risk prediction.^[2] It adds that HBPM is often a more practical approach in clinical practice than ABPM and may be more reproducible and accessible, supporting its use for longitudinal management and titration of BP-lowering medication.^[2]

For management, AHA/ACC 2025 recommends HBPM to monitor titration of BP-lowering medication in adults taking antihypertensive medication, along with cointerventions such as patient education, telehealth counselling and clinical interventions (COR 1, LOE A).^[2] ESC 2024 notes that in clinical practice some patients may not provide reliable information on their home BP, and both their device and measurement technique need to be checked.^[1]

Confirming the diagnosis: the pathway

ESC 2024 proposes a confirmation protocol with out-of-office measurement as the preferred method for confirming elevated BP or hypertension.^[1] Office BP has lower specificity than ABPM for detecting hypertension, so diagnosis based on office BP alone is less desirable unless resources do not allow out-of-office measurements.^[1] A single screening office BP does not typically have sufficient diagnostic performance, especially for values close to diagnostic thresholds, so it needs some form of repeat assessment.^[1] The BP threshold for acting on a screening office BP by arranging repeat assessment should also be lower than the office BP threshold used for diagnosing hypertension, particularly in the presence of increased CVD risk or markers of HMOD.^[1]

ESC 2024 Recommendation Table 6 (all rows; the last two lines are the two bullets of the 160/100 mmHg or more row). Each row is scoped to its own screening office BP band.

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The ESC text (not a table row) adds that, at screening BP above 180/110 mmHg without a hypertensive emergency, prompt confirmation (preferably within a week) can be considered before treatment.^[1] It also says that, for an initial screening systolic BP above 160 mmHg and/or diastolic above 100 mmHg, prompt re-evaluation is advisable, within days to weeks but not more than 1 month, preferably with ABPM or HBPM.^[1] A screening office BP above 160/100 mmHg is almost always consistent with hypertension, though a small proportion of patients have extreme white-coat effects that motivate prompt repeat assessment.^[1]

AHA/ACC 2025 recommends out-of-office BP measurement by ABPM or HBPM to confirm the diagnosis in adults with suspected hypertension (COR 1, LOE A), and adds a scoped row on white-coat hypertension.^[2] Its row covers adults with untreated office SBP of 130 mm Hg or more or DBP of 80 mm Hg or more, and without office SBP of 160 mm Hg or more or DBP of 100 mm Hg or more.^[2] In them, it is reasonable to exclude white-coat hypertension with out-of-office monitoring before a diagnosis of hypertension is made (COR 2a, LOE B-NR).^[2] The supporting text adds a caveat: adults with office SBP/DBP of 160/100 mm Hg or more should be treated promptly with dose titration as needed, and the prevalence of white-coat hypertension is low in this range.^[2] For people not on treatment, AHA/ACC 2025 prefers ABPM for excluding white-coat and masked hypertension; for people on treatment it prefers HBPM for excluding white-coat effect and masked uncontrolled hypertension, because ABPM is harder to repeat.^[2]

Baseline tests

ESC 2024 Table 8: routine tests in the initial work-up of elevated BP or hypertension (all rows)

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AHA/ACC 2025 recommends that adults diagnosed with hypertension have laboratory tests (complete blood count, serum electrolytes, serum creatinine, lipid profile, glucose or HbA1c, TSH, urinalysis and urine albumin-to-creatinine ratio) and a 12-lead ECG to optimise management (COR 1, LOE C-EO).^[2] Its Table 6 adds detail: serum sodium, potassium and calcium; serum creatinine with eGFR by the 2021 CKD-EPI creatinine equation; fasting blood glucose or HbA1c; and urine albumin-to-creatinine ratio and urine protein-to-creatinine ratio.^[2] Basic tests should be repeated at least annually, or sooner if glucose intolerance, electrolyte imbalance or uric acid changes appear.^[2]

Hypertension-mediated organ damage

ESC 2024 Recommendation Tables 8, 9 and 10 (all rows)

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ESC 2024 defines CKD as abnormalities of kidney structure or function, present for at least 3 months with implications for health.^[1] Its definition of moderate-to-severe CKD requires an eGFR below 60 mL/min/1.73 m² or albuminuria of 30 mg/g or more (3 mg/mmol or more).^[1] Renal function is evaluated initially with serum creatinine and an eGFR equation, preferably race-free CKD-EPI, and typically for proteinuria.^[1]

The ECG is part of the initial routine work-up for everyone with hypertension and should be repeated whenever an irregular pulse or cardiac symptoms appear; it is analysed for LVH and AF (ESC 2024).^[1] Echocardiography is recommended in patients with hypertension when the ECG is abnormal, murmurs are detected or there are cardiac symptoms.^[1] It can be considered for all patients with newly diagnosed hypertension if local resources and reimbursement policies allow.^[1] Sex-specific thresholds are used for cardiac HMOD to avoid under-diagnosis in women.^[1]

Carotid ultrasound detects plaque (wall thickness of 1.5 mm or more) and stenosis, and carotid or femoral plaque improves CVD risk prediction in asymptomatic patients on top of conventional risk factors (ESC 2024).^[1] Systematic use of intima-media thickness does not appear to consistently improve prediction.^[1] ESC 2024 notes that PWV is currently used mostly for research or in specialist referral centres.^[1] In hypertensive individuals, mild or moderate hypertensive retinopathy is associated with increased risk of CVD events.^[1]

ESC 2024 Table 9: optional tests that may be used as clinically indicated in the initial work-up of elevated BP or hypertension to assess HMOD or established CVD (all rows)

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Optional tests should be considered in the initial assessment if they are likely to change management, mainly to improve CVD risk stratification (ESC 2024).^[1] For adults with elevated BP and a 10-year risk of 5% to below 10%, optional tests including HMOD tests may be considered if an abnormal result could up-classify risk and prompt BP-lowering therapy.^[1] HMOD assessment is also an important way to identify young adults under 40 years with increased CVD risk, because SCORE2 cannot be calculated in this age group.^[1]

ESC 2024 states genetic testing should be considered in specialist centres for patients suspected to have rare monogenic causes of secondary hypertension or with phaeochromocytoma/paraganglioma (Class IIa, Level B), and routine genetic testing for hypertension is not recommended (Class III, Level C).^[1]

CVD risk assessment when BP is elevated

Why does ESC 2024 recommend risk scoring in the elevated range?^[1] Because the heterogeneity in CVD risk among adults with elevated BP is larger than in those with hypertension: they tend to be younger, and their absolute CVD risk depends more on the prevalence of other CVD risk factors.^[1] So formally estimating CVD risk is recommended to guide BP-lowering treatment decisions in elevated BP.^[1] Using hypertension thresholds alone would under-treat many high-risk patients, and the efficacy of BP lowering in preventing CVD events extends down to a systolic BP of 120 mmHg and a diastolic BP of 70 mmHg.^[1]

ESC 2024 Recommendation Table 3 (all rows); established CVD in this table means coronary artery disease, cerebrovascular disease, peripheral arterial disease or heart failure

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For BP-lowering treatment decisions, ESC 2024 uses one risk threshold, a SCORE2 or SCORE2-OP 10-year risk of 10% or more, rather than age-specific thresholds.^[1] It calls such patients sufficiently high risk or increased risk, rather than high or very high risk, to avoid confusion with the 2021 ESC prevention guideline.^[1] SCORE2 and SCORE2-OP are preferred because they predict fatal and non-fatal events, are validated and recalibrated for European populations, and SCORE2-OP adjusts for competing non-cardiovascular mortality.^[1]

ESC 2024 gives an example: in elevated BP with borderline 10-year risk by SCORE2 or SCORE2-OP (5% to below 10%), non-traditional risk modifiers may help up-classify risk and thereby prompt BP-lowering treatment.^[1]

ESC 2024 Recommendation Table 4 (all rows)

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ESC 2024 thresholds for these tests: a CAC score above 100 Agatston units or at or above the 75th percentile for age, sex and ethnicity favours up-classification.^[1] Common arterial stiffness thresholds for increased risk include carotid–femoral PWV above 10 m/s and brachial–ankle PWV above 14 m/s.^[1] Risk stratification is not required to allocate BP-lowering treatment when BP is non-elevated, though risk assessment may still be needed for other prevention therapies such as lipid lowering.^[1] And once hypertension is confirmed, BP-lowering treatment is recommended with no further risk stratification needed.^[1]

AHA/ACC 2025 uses PREVENT instead.^[2] Increased short-term or 10-year risk is a 10-year predicted risk of CVD events of 7.5% or more on PREVENT, and adults with hypertension are also at increased risk if they have diabetes or CKD.^[2] The PREVENT equations are validated for US adults aged 30 to 79 years, and the 7.5% PREVENT threshold is equivalent to the Framingham score threshold of 15% used for SPRINT entry.^[2]

When to screen for secondary hypertension

This topic covers the triggers for screening; the confirmatory work-up is outside its scope. ESC 2024 recommends that patients with hypertension who present with suggestive signs, symptoms or medical history of secondary hypertension are appropriately screened (Class I, Level B).^[1] It also states that screening for primary aldosteronism by renin and aldosterone measurement should be considered in all adults with confirmed hypertension (BP of 140/90 mmHg or more) (Class IIa, Level B).^[1] For adults diagnosed before 40 years, comprehensive screening for the main causes is recommended, except in obese young adults, in whom it is recommended to start with an obstructive sleep apnoea evaluation (Class I, Level B).^[1]

AHA/ACC 2025 Sections 3.2.3 and 3.2.3.1 (all rows)

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AHA/ACC 2025 says secondary hypertension is more common with stage 2 hypertension, treatment-resistant hypertension, sudden onset, and increased BP in hypertension previously controlled on drug therapy.^[2] It is also more common with early-onset hypertension (age under 30 years), diastolic hypertension in older adults, and target organ damage disproportionate to the duration or severity of hypertension.^[2] Common forms include primary aldosteronism and obstructive sleep apnoea.^[2]

The AHA/ACC 2025 synopsis puts primary aldosteronism at 5% to 10% of patients with hypertension and 20% of patients with resistant hypertension, with exceptionally low screening rates (1% to 2%) in appropriate patients.^[2] Spontaneous hypokalaemia is present in only 20% to 50% of patients with primary aldosteronism, so the decision to screen should not rely on hypokalaemia alone.^[2] ESC 2024 notes that a history of hypokalaemia is absent in most patients diagnosed with the condition and that the aldosterone-to-renin ratio can be influenced by drugs taken at the time of testing.^[1]

AHA/ACC 2025 Table 10, selected rows and columns (the drug- or alcohol-induced, hypothyroidism, hyperthyroidism, primary hyperparathyroidism, congenital adrenal hyperplasia, other mineralocorticoid excess and acromegaly rows are not shown)

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ESC 2024 Table 13: optional tests that should be used to screen for secondary hypertension in the presence of suggestive signs, symptoms or medical history (all rows)

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The ESC text also addresses adrenal incidentalomas: patients with an incidental adrenal nodule warrant screening for elevated BP and hypertension.^[1] Those with an adrenal incidentaloma and hypertension warrant a basic work-up for secondary hypertension including screening for primary aldosteronism, Cushing’s syndrome and phaeochromocytoma.^[1] Obstructive sleep apnoea should be suspected in patients with hypertension and suggestive symptoms, in all patients with resistant hypertension, and with a non-dipping or reverse-dipping 24-h pattern, especially if obese; lack of suggestive symptoms does not rule it out.^[1]

AHA/ACC 2025 says a careful history should be taken, with close attention to prescription medications, over-the-counter substances, illicit drugs and herbal products.^[2] When feasible, drugs associated with increased BP should be reduced or discontinued and alternative agents used.^[2]

Management: BP of 180/110 mmHg or more and hypertensive emergency

ESC 2024 recommends assessment for hypertensive emergency at BP of 180/110 mmHg or more, immediate BP-lowering treatment if an emergency is present; otherwise, prompt confirmation (preferably within a week) can be considered before starting treatment.^[1] Fundoscopy is recommended if BP is above 180/110 mmHg in the work-up of hypertensive emergency and malignant hypertension, as well as in hypertensive patients with diabetes (Class I, Level C).^[1]

In its section on non-pregnant adults without acute stroke, AHA/ACC 2025 defines hypertensive emergency as BP above 180 and/or 120 mm Hg with evidence of acute target organ damage.^[2] For these patients it recommends ICU admission for continuous monitoring of BP and target organ damage and for consideration of parenteral therapy (COR 1, LOE B-NR).^[2] Emergencies with acute ICH or acute ischaemic stroke, and in pregnant adults, are covered in other sections of that guideline.^[2] Its What Is New table lists new terminology: severe hypertension, in place of the 2017 term hypertensive urgency.^[2] Acute treatment is covered in the hypertensive emergency topic.

Management: thresholds and targets

ESC 2024 defines the threshold as the BP at which treatment starts and the target as the BP goal on treatment.^[1] In ESC 2024 the target is always 120–129/70–79 mmHg, but only if treatment is tolerated and with certain exceptions where more lenient targets are advised; the threshold may differ with CVD risk inside the elevated range.^[1]

ESC 2024 Table 14: initiation of BP-lowering treatment by confirmed BP category and CVD risk (risk and treatment rows)

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The target row of the same table reads: maintain BP below 120/70 mmHg (non-elevated BP), and aim for 120–129/70–79 mmHg, with a footnote urging caution in adults with orthostatic hypotension, moderate-to-severe frailty or limited life expectancy, and in older patients aged 85 years or more.^[1]

ESC 2024 Recommendation Table 17 (all rows)

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ESC 2024 Recommendation Table 18 (all rows)

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For confirmed hypertension (sustained BP of 140/90 mmHg or more), ESC 2024 recommends starting BP-lowering treatment irrespective of CVD risk, as a simultaneous combination of lifestyle interventions and pharmacological therapy.^[1] After treatment initiation, the patient should be seen frequently (e.g. every 1–3 months with a GP or specialist) until BP is controlled; BP should be controlled preferably within 3 months.^[1] The ESC text then turns to elevated BP (office 120–139/70–89 mmHg).^[1] At sufficiently high CVD risk (e.g. 10-year risk of 10% or more), or with high-risk conditions, or with borderline 10-year risk (5% to below 10%) plus risk modifiers or abnormal risk tool tests, BP-lowering lifestyle measures should be initiated for 3 months.^[1] Following this, pharmacological therapy is recommended for confirmed BP of 130/80 mmHg or more when these lifestyle changes have not worked or are not being implemented.^[1] At 120–129/70–79 mmHg, ongoing and intensified lifestyle intervention is preferred.^[1] For elevated BP without increased risk (10-year risk below 10%, and no other high-risk conditions or risk modifiers), BP-lowering lifestyle measures are recommended.^[1] ESC 2024 makes no formal drug recommendation here; if lifestyle measures are not successful after 6–12 months, drug treatment might be discussed individually when BP is between 130/80 and below 140/90 mmHg.^[1] ESC 2024 also recommends that, in elevated BP, BP-lowering treatment should always be started on the basis of individual clinical judgement and shared decision-making.^[1]

ESC 2024 endorses a trust but verify approach to office BP measurement.^[1] Where possible, confirming BP with accurate out-of-office measurements (ABPM, HBPM) is recommended before starting treatment and to monitor the treatment effect.^[1] It states that it is well established that an on-treatment systolic BP of 135 mmHg is not optimal relative to more intensive control.^[1]

AHA/ACC 2025 Section 5.2.2: initiation of BP-lowering medication (all rows)

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AHA/ACC 2025 Section 5.2.7 (all rows)

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AHA/ACC 2025 judges achievement of target from an average of 2 or more readings at 2 or more visits rather than from an individual measurement.^[2] Hypotension, syncope, injurious falls, electrolyte abnormalities and a fall in eGFR are the most commonly recognised adverse events of intensive therapy, but they are infrequent and usually mild.^[2]

Specific phenotypes and scenarios

White-coat hypertension

AHA/ACC 2025 notes that systematic reviews and meta-analyses of observational studies show that, compared with sustained normotension, white-coat hypertension is associated with no risk to a moderately increased risk of CVD.^[2] That risk may only be increased among older adults with high baseline CVD risk.^[2] CVD risk is still higher in sustained hypertension than in white-coat hypertension among adults with high office BP.^[2]

AHA/ACC 2025 notes that studies have shown that, compared with individuals with sustained normotension, a higher proportion of individuals with white-coat or masked hypertension have sustained hypertension during follow-up.^[2] Its formal row: in adults with white-coat hypertension or masked hypertension, out-of-office BP monitoring is reasonable to exclude transition to a diagnosis of sustained hypertension (COR 2a, LOE B-NR).^[2] The frequency of follow-up monitoring is unclear, because only a single follow-up visit was conducted in these studies, approximately 7 to 11 years after the baseline visit.^[2]

Masked hypertension

AHA/ACC 2025 notes that systematic reviews and meta-analyses of observational studies show that, compared with sustained normotension, masked hypertension is associated with an increased risk of CVD events, in a range similar to sustained hypertension.^[2] AHA/ACC 2025 states that, in adults with untreated office SBP below 130 mm Hg and DBP below 80 mm Hg, it may be reasonable to exclude masked hypertension with out-of-office monitoring (COR 2b, LOE B-NR).^[2] Studies have examined whether using office BP ranges approaching the high office BP threshold, or prediction models, to target out-of-office monitoring would be a better approach than screening all individuals who do not have high office BP.^[2] Clinicians may consider these targeted screening approaches, particularly in patients with unexplained BP-related target organ damage, but which diagnostic approach is best remains unclear.^[2] ESC 2024 notes that out-of-office measurement may also help diagnose masked hypertension at office BP of 130–139/85–89 mmHg.^[1]

Treated patients: white-coat effect and masked uncontrolled hypertension

AHA/ACC 2025 notes that studies have consistently shown that, compared with controlled hypertension, white-coat effect is not associated with an increased risk of CVD events and mortality.^[2] In apparent treatment-resistant hypertension on office BP, AHA/ACC 2025 states it is reasonable to exclude white-coat effect, a form of pseudo-resistance, with out-of-office monitoring (COR 2a, LOE C-LD).^[2] A second row covers adults taking antihypertensive medication with elevated office BP (SBP 130 mm Hg or more or DBP 80 mm Hg or more).^[2] It excludes those with resistant hypertension or office SBP of 160 mm Hg or more or DBP of 100 mm Hg or more.^[2] In them, it is also reasonable to exclude white-coat effect with out-of-office monitoring (COR 2a, LOE B-NR).^[2]

AHA/ACC 2025 notes that systematic reviews and meta-analyses show that, compared with controlled hypertension, masked uncontrolled hypertension is associated with an increased risk of CVD events and mortality.^[2] In adults taking antihypertensive medication with office SBP below 130 mm Hg and DBP below 80 mm Hg, it may be reasonable to exclude it with out-of-office monitoring (COR 2b, LOE B-NR).^[2] ESC 2024 reports that it occurs in 30% of patients treated for hypertension and is more often due to poorly controlled nocturnal than daytime BP on ABPM.^[1]

Isolated systolic and isolated diastolic hypertension

Isolated systolic hypertension is typically defined as systolic BP of 140 mmHg or more with diastolic BP below 90 mmHg (ESC 2024).^[1] It is uncommon in younger patients but the most common type in older patients: more than 80% of untreated patients with hypertension aged over 60 years have it.^[1] In the young, out-of-office measurement is recommended to exclude white-coat hypertension, which often accompanies isolated systolic hypertension.^[1]

Isolated diastolic hypertension is systolic BP below 140 mmHg with diastolic BP of 90 mmHg or more (ESC 2024).^[1] It is seen more commonly in younger adults, particularly those with obesity or other metabolic derangements; in older adults with this phenotype, consider whether diastolic BP was accurately measured.^[1] These patients should be followed up because they are at increased risk of systolic hypertension.^[1]

Nocturnal hypertension and dipping

Nocturnal hypertension is night-time BP above 120 mmHg systolic and/or above 70 mmHg diastolic on 24-h ABPM; it can be day–night sustained or isolated nocturnal hypertension (daytime BP below 135/85 mmHg), and BP is normally expected to fall by 10%–20% during sleep (ESC 2024).^[1] It has been observed in up to half of patients with hypertension and is more common in secondary hypertension.^[1]

• Inverse dipping (riser): nocturnal increase in BP (night-to-day ratio above 1.0) (ESC 2024)^[1]
• Non-dipper: night-time dip below 10% (night-to-day ratio above 0.9 and up to 1.0)^[1]
• Normal dipping: night-time fall above 10% and below 20% (ratio 0.8 to 0.9)^[1]
• Extreme dipping: night-time fall above 20% (ratio below 0.8)^[1]

Long-term reproducibility of dipping patterns appears to be low (ESC 2024).^[1]

Resistant hypertension: definition and pseudo-resistance

ESC 2024 defines resistance by the failure of a treatment strategy that includes appropriate lifestyle measures and maximum or maximally tolerated doses of a diuretic (thiazide or thiazide-like), a RAS blocker and a calcium channel blocker.^[1] Hypertension is resistant when this strategy fails to lower office systolic and diastolic BP to below 140 mmHg and/or below 90 mmHg, respectively, and these uncontrolled values must be confirmed by out-of-office measurement (HBPM or ABPM).^[1] It has been reported in 10%–20% of patients with hypertension.^[1]

• Resistant hypertension is not a disease but an indicator of high CVD risk, in which secondary hypertension is also frequent (ESC 2024 key considerations).^[1]
• Pseudo-resistant hypertension, including non-adherence, must be excluded.^[1]
• With eGFR below 30 mL/min/1.73 m², an adequately up-titrated loop diuretic is necessary to define resistant hypertension.^[1]
• The key considerations add that patients with suspected resistant hypertension should be referred to specialised centres; the formal recommendation row is that patients with resistant hypertension should be considered for referral to clinical centres with expertise in hypertension management for further testing (Class IIa, Level B).^[1]
• ESC 2024 does not use the terms controlled resistant hypertension (BP at target but needing 4 or more medications) or refractory hypertension (BP not at target despite 5 or more medications).^[1]

Excluding pseudo-resistance is a prerequisite: verify adherence by careful questioning in the first instance, exclude white-coat hypertension, and also consider objective adherence testing (directly observed treatment or detecting prescribed drugs in blood or urine) if resources allow (ESC 2024).^[1] ESC 2024 lists causes of true resistance as behavioural factors (overweight or obesity, physical inactivity, excess daily dietary sodium and excess habitual alcohol consumption), drugs or substances that may increase BP, and undetected secondary hypertension.^[1] Patients with resistant hypertension should be considered for referral to clinical centres with expertise in hypertension management for further testing (Class IIa, Level B).^[1]

Orthostatic hypotension

Orthostatic hypotension is a fall of 20 mmHg or more systolic and/or 10 mmHg or more diastolic at 1 and/or 3 min after standing, following 5 min sitting or lying (ESC 2024).^[1] It is present in approximately 10% of hypertensive adults and up to 50% of older institutionalised adults.^[1] ESC 2024: diagnosis is made in the office, and routine ABPM is not currently suitable for formally assessing it, though it may help in some cases, particularly when accompanied by a patient symptom diary.^[1]

Complications and pitfalls

• Labelling on one reading. A single office screening BP does not typically have enough diagnostic performance, especially near thresholds, and needs repeat assessment, preferably out of office (ESC 2024).^[1]
• Wrong cuff. An under-sized cuff artificially elevates BP and an over-sized cuff reduces it (ESC 2024).^[1]
• Rolled-up sleeve. Clothing at the cuff site should be removed, and rolling up shirt sleeves should be avoided because it can cause a tourniquet effect (ESC 2024).^[1]
• Unsupported arm. The arm should be supported to avoid isometric exercise-induced rises in BP (ESC 2024).^[1]
• One arm only. A between-arm systolic difference of more than 10 mmHg is associated with increased CVD risk and may indicate arterial stenosis, so ESC 2024 recommends measuring both arms at least at the first visit (Class I, Level B).^[1]
• Oscillometry in AF. Most automated oscillometric monitors have not been validated for BP measurement in AF (ESC 2024).^[1]
• Untrained staff. AHA/ACC 2025 asks for initial and ongoing training with competency checks ideally every 6 to 12 months.^[2]
• Calling resistance too early. Pseudo-resistant hypertension, including that caused by non-adherence, must be excluded; its causes include the white-coat phenomenon and poor measurement method (ESC 2024).^[1]
• Waiting for hypokalaemia. Hypokalaemia is absent in most patients with primary aldosteronism (ESC 2024; AHA/ACC 2025).^[1][2]
• Mistaking a bystander lesion. Bystander renal artery stenosis may be present in essential hypertension without causing secondary hypertension due to renovascular hypertension (ESC 2024).^[1]

Prognosis and follow-up

HMOD adds prognostic information in every BP category, and some individuals may be at heightened risk when cardiac and vascular HMOD, such as LVH and increased PWV, does not regress over time despite appropriate treatment and BP control (ESC 2024).^[1] AHA/ACC 2025 reports that people with diagnosed hypertension whose treated BP is below 120/80 mm Hg have twice the CVD risk of adults without hypertension with untreated BP below 120/80 mm Hg, highlighting the importance of primordial prevention of BP elevation.^[2]

For white-coat and masked hypertension, AHA/ACC 2025 cites systematic reviews and meta-analyses of observational studies.^[2] Compared with sustained normotension, masked hypertension is associated with an increased CVD risk in a range similar to sustained hypertension (AHA/ACC 2025).^[2] Compared with sustained normotension, white-coat hypertension is associated with no risk to a moderately increased risk of CVD, which may only be increased among older adults with high baseline CVD risk.^[2] In resistant hypertension, the risk of myocardial infarction, stroke, end-stage renal disease and death may be two- to six-fold higher than in treated patients who achieve BP control (ESC 2024).^[1] Nocturnal hypertension is a risk factor for adverse CVD events, cerebrovascular disease (including stroke) and cardiovascular mortality (ESC 2024).^[1] AHA/ACC 2025 cites meta-analyses of studies that matched patients with primary aldosteronism to those with primary hypertension: primary aldosteronism carried a 2.0-fold risk of heart failure, 2.8-fold risk of stroke, 1.7-fold risk of coronary artery disease and 4.0-fold risk of AF, and increased kidney damage.^[2]

In ESC 2024 Table 14, elevated BP managed with lifestyle measures alone has BP and CVD risk monitored yearly.^[1] That column covers all adults with systolic 120–129 mmHg, and those with systolic 130–139 mmHg, 10-year risk below 10% and no high-risk conditions, risk modifiers or abnormal risk tool tests.^[1] Patients on drug treatment have BP monitored yearly once treatment control is established.^[1] In elevated BP not yet meeting risk thresholds for treatment, a repeat BP measurement and risk assessment within 1 year should be considered (ESC 2024, Class IIa, Level C).^[1] Isolated diastolic hypertension needs follow-up because of the risk of later systolic hypertension (ESC 2024).^[1]

Special populations

Young adults (18–40 years)

ESC 2024 defines young adulthood as 18–40 years.^[1] Secondary hypertension is more frequent in younger than in later-onset hypertension, with a prevalence of 15%–30% in hypertensive young adults reported from some referral centres; major causes include drug-induced hypertension (e.g. oestrogen-progesterone oral contraceptives, cold medication) and primary aldosteronism.^[1] Fibromuscular dysplasia should be considered in young women, and in obese young adults primary hypertension is more common, though OSA should also be considered.^[1] Out-of-office measurement is recommended to confirm the diagnosis, because the white-coat phenomenon occurs in the young.^[1]

SCORE2 is not validated under 40 years, so ESC 2024 states screening for HMOD may be considered in young people with elevated BP without other increased-risk conditions to identify more individuals for possible treatment (Class IIb, Level B).^[1] Without established CVD, diabetes, familial hypercholesterolaemia or moderate or severe CKD, an office treatment threshold of 140/90 mmHg is appropriate in most young adults (ESC 2024).^[1] AHA/ACC 2025 notes that for adults under 30 years, in whom risk models are limited, drug therapy could be considered at average SBP of 130 mm Hg or more after a lifestyle trial, but data are limited.^[2]

Older and frail adults

ESC 2024 recommends maintaining BP-lowering drugs lifelong, even beyond 85 years, if well tolerated (Class I, Level A).^[1] With pre-treatment symptomatic orthostatic hypotension, age 85 years or older, clinically significant moderate-to-severe frailty and/or limited predicted lifespan (under 3 years), ESC 2024 says BP-lowering treatment should only be considered from 140/90 mmHg or more (Class IIa, Level B).^[1] The row gives its reasons: the benefit in reducing CVD outcomes is uncertain in these settings, and close monitoring of treatment tolerance is advised.^[1] The ESC text gives eGFR below 30 mL/min/1.73 m² as an example of the high competing risk behind a limited predicted lifespan.^[1] It notes that patients with elevated BP in these settings are less likely to obtain sufficient net benefit from BP-lowering drug therapy or to tolerate intensive drug therapy.^[1]

AHA/ACC 2025 recommends initiation at 130/80 mm Hg or more in adults aged 80 years or older, for whom risk models are limited, when clinical judgement suggests benefit outweighs harm and it aligns with the patient’s goals of care.^[2] In older adults who may be frail or have limited life expectancy, it asks for a clinician-patient assessment of the potential benefits and harms of BP lowering.^[2]

Pregnancy

Only a small number of automated oscillometric monitors have been adequately validated in pregnancy, so auscultatory sphygmomanometry is the clinical standard (ESC 2024).^[1] Oscillometric devices tend to under-estimate true BP and are unreliable in severe pre-eclampsia; only devices validated for pregnancy and pre-eclampsia should be used.^[1] BP tends to reach a nadir at 20–30 weeks before rising towards term.^[1]

ESC 2024 states that hypertension in pregnancy includes:^[1]

• Chronic hypertension: precedes pregnancy, develops before 20 weeks of gestation, persists for more than 6 weeks post-partum, and may be associated with proteinuria.^[1]
• Gestational hypertension: develops after 20 weeks of gestation and usually resolves within 6 weeks post-partum.^[1]
• Antenatally unclassifiable hypertension: BP is first recorded after 20 weeks and hypertension is diagnosed, but it is unclear whether it is chronic; reassessment is necessary 6 weeks post-partum.^[1]
• Pre-eclampsia: gestational hypertension accompanied by new-onset (i) proteinuria (above 0.3 g/day or ACR of 30 mg/mmol or more), (ii) other maternal organ dysfunction, including acute kidney injury (serum creatinine 1 mg/dL or more), liver dysfunction (transaminases above 40 IU/L with or without right upper quadrant or epigastric pain), neurological complications (convulsions, altered mental status, blindness, stroke, severe headaches, persistent visual scotomata) or haematological complications (platelets below 150 000/µL, disseminated intravascular coagulation, haemolysis), or (iii) uteroplacental dysfunction (such as foetal growth restriction, abnormal umbilical artery Doppler waveform or stillbirth).^[1]

After pregnancy the history still matters: women with hypertensive disorders of pregnancy, including gestational hypertension and pre-eclampsia, have a two-fold higher long-term CVD risk than women without these pregnancy conditions (ESC 2024).^[1] ESC 2024 states that a history of pregnancy complications (gestational diabetes, gestational hypertension, pre-term delivery, pre-eclampsia, one or more stillbirths and recurrent miscarriage) should be considered to up-classify people with elevated BP and borderline 10-year risk (5% to below 10%) (Class IIa, Level B).^[1] AHA/ACC 2025 notes that a history of hypertensive disorders of pregnancy may also identify people who have higher long-term predicted risk and may benefit from earlier initiation of antihypertensive therapy.^[2]

Other groups

• Atrial fibrillation: most automated oscillometric monitors have not been validated for BP measurement in AF, and a manual auscultatory method should be considered in these circumstances where possible (ESC 2024, Class IIa, Level C).^[1]
• Children and adolescents: opportunistic screening with office BP measurements to monitor the development of BP during late childhood and adolescence, especially if one or both parents have hypertension, should be considered to better predict adult hypertension and CVD risk (ESC 2024, Class IIa, Level B).^[1]
• Type 2 diabetes with elevated BP: the ESC 2024 text notes that some adults under 60 years with type 2 diabetes and elevated BP have a 10-year CVD risk below 10%, so SCORE2-Diabetes should be considered to confirm that risk is sufficiently high (10% or more). The formal row: SCORE2-Diabetes should be considered to estimate CVD risk among type 2 diabetes patients with elevated BP, particularly if they are under 60 years of age (Class IIa, Level B).^[1]
• Significant obesity: where a correctly fitting upper-arm cuff is not available, measurement at the lower arm or wrist can be considered (ESC 2024).^[1]
• Ethnicity: ESC 2024 lists high-risk ethnicity (e.g. South Asian) among the modifiers that should be considered to up-classify elevated BP with borderline risk (Class IIa, Level B), and AHA/ACC 2025 names Black populations as having a high prevalence of masked hypertension.^[1][2]

Evidence, guidelines and regional differences

ESC 2024 updates the 2018 ESC/ESH hypertension guideline, and the 2025 AHA/ACC guideline retires and replaces the 2017 ACC/AHA guideline.^[1][2] ESC 2024 changed its title to elevated blood pressure and hypertension, based on evidence that CVD risk attributable to BP is on a continuous exposure scale, not a binary scale of normotension versus hypertension.^[1]

Selected changes that ESC 2024 itself highlights:

• ESC 2024 keeps the 140/90 mmHg definition of hypertension and introduces the elevated BP category (office systolic 120–139 or diastolic 70–89 mmHg).^[1]
• ESC 2024 recommends a target systolic BP of 120–129 mmHg in adults receiving BP-lowering drugs, with several important caveats, including that treatment to this target is well tolerated, that more lenient targets can be considered in symptomatic orthostatic hypotension, age 85 years or older, moderate-to-severe frailty or limited life expectancy, and a strong emphasis on out-of-office measurement to confirm the target is reached.^[1]
• ESC 2024 requires evidence of benefit on CVD outcomes, not only BP lowering, for a Class I drug or procedural recommendation (lifestyle and low-risk implementation interventions excepted).^[1]

ESC 2024 and AHA/ACC 2025 side by side (each cell from that body’s own text)

^{[1] [2]}

In Australia and New Zealand

Exam pearls

• ESC 2024 elevated BP is office systolic 120–139 or diastolic 70–89 mmHg; AHA/ACC 2025 elevated BP is SBP 120–129 and DBP below 80 mm Hg. Know both.^[1][2]
• ESC 2024 avoids terms such as normal BP in defining its lowest category, which it calls non-elevated BP (below 120/70 mmHg).^[1]
• ESC 2024 out-of-office hypertension thresholds: 135/85 mmHg home and daytime ABPM, 130/80 mmHg 24-h ABPM, 120/70 mmHg night-time ABPM.^[1]
• Manual auscultation: three readings 1–2 min apart; record the average of the last two (ESC 2024).^[1]
• Inter-arm systolic difference above 10 mmHg: ESC 2024 recommends that all subsequent readings use the arm with the higher reading (Class I, Level B).^[1]
• ESC 2024 risk tools in elevated BP without increased-risk conditions: SCORE2 at 40–69 years, SCORE2-OP at 70 years or older; irrespective of age, a SCORE2 or SCORE2-OP risk of 10% or more is considered increased risk for risk-based management of elevated BP. AHA/ACC 2025 uses PREVENT, with increased risk at 7.5% or more.^[1][2]
• AHA/ACC 2025 recommends screening for primary aldosteronism in adults with resistant hypertension regardless of whether hypokalaemia is present, to increase rates of detection, diagnosis and specific targeted therapy (COR 1, LOE B-NR); ESC 2024 states that screening by renin and aldosterone measurements should be considered in all adults with confirmed hypertension (BP of 140/90 mmHg or more) (Class IIa, Level B).^[2][1]
• Cuffless devices: not recommended for diagnosis or management (AHA/ACC 2025, COR 3: No Benefit) and not currently recommended for routine clinical use (ESC 2024).^[2][1]

References7ShowHide

1. [1]McEvoy JW, et al. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J, 2024.PMID 39210715
2. [2]Jones DW, et al. 2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM 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 Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2025.PMID 40815242
3. [3]Gabb GM, et al. Guideline for the diagnosis and management of hypertension in adults - 2016. Med J Aust, 2016.PMID 27456450
4. [4]Sharman JE, et al. Automated office blood pressure measurement: a Hypertension Australia and National Hypertension Taskforce of Australia position statement. J Hypertens, 2025.PMID 40534535
5. [5]Sharman JE, et al. Home blood pressure monitoring: Australian Expert Consensus Statement. J Hypertens, 2015.PMID 26136205
6. [6]Nelson MR, et al. 2023 Australian guideline for assessing and managing cardiovascular disease risk. Med J Aust, 2024.PMID 38623719
7. [7]Ohlrogge AH, et al. Update from the National Hypertension Taskforce of Australia: prevalence, treatment and control rates of hypertension between 2022 and 2024 - implications and future directions. J Hypertens, 2026.PMID 42223442