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Hypertension — overview

TL;DR — Hypertension is the single largest risk-attributable cause of death and disability on earth, and the defining feature of the field is that the science is decades ahead of the delivery. The number of people aged 30–79 living with it doubled between 1990 and 2019 — 331 million women (95% CrI 306–359) and 317 million men (292–344) to 626 million (584–668) and 652 million (604–698) — while age-standardised prevalence stayed flat, so the growth is demographic (NCD-RisC 2021, PMID 34450083). In that same year only 59% of women and 49% of men with hypertension had ever been diagnosed, and control rates were 23% and 18% (NCD-RisC 2021, PMID 34450083). The pharmacology is not in doubt: in 344,716 participants from 48 randomised trials, each 5 mm Hg fall in systolic pressure cut major cardiovascular events by about 10%, with no reliable heterogeneity by baseline pressure or prior disease (BPLTTC 2021, PMID 33933205). What remains genuinely contested is how low to go and in whom (SPRINT 2021, PMID 34010531; ACCORD 2010, PMID 20228401), how much of what is called "essential" hypertension is really unrecognised aldosterone excess (Brown 2020, PMID 32449886), and how to move a population-level control rate that has been stuck or falling for a decade in the country that spends most on health (Muntner 2020, PMID 32902588).

What this condition covers here — and what it does not

Hypertension borders four other conditions in this knowledge base. The rule for this build is cross-link, never restate: a trial that matters to two conditions is cited on each page for its own endpoint.

Owned here Owned elsewhere
Measurement, thresholds, diagnostic phenotypes Hypertensive cardiac end-organ disease → hypertensive-heart-disease
Epidemiology and the detection–treatment–control cascade Stroke and its secondary prevention → stroke
Mechanism, genetics, secondary causes Coronary disease management → ischemic-heart-disease
Targets, drugs, lifestyle, devices, resistant disease Blood-pressure lowering as dementia prevention → vascular-dementia
Pregnancy, special populations, implementation, emergencies Diabetes management → type-2-diabetes

Definition, and why the number is contested

Hypertension has no biological discontinuity. Usual blood pressure relates continuously to vascular mortality with no threshold detectable down to at least 115/75 mm Hg: in a million adults across 61 prospective studies, each 20 mm Hg higher usual systolic pressure at ages 40–69 was associated with more than a doubling of stroke death and of ischaemic heart disease death (Lewington 2002, PMID 12493255). Any cut-point is therefore an administrative decision about where treatment begins, not a description of nature — which is why guideline bodies working from overlapping evidence set different numbers.

Document Hypertension defined as Note
2017 ACC/AHA ≥130/80 mm Hg Raised US crude prevalence from 31.9% to 45.6% (Muntner 2018, PMID 29133599)
2025 AHA/ACC ≥130/80 mm Hg retained Retires and replaces the 2017 document (Writing Committee 2025, PMID 40811516)
2023 ESH ≥140/90 mm Hg (Mancia 2023, PMID 37345492)
2024 ESC ≥140/90, with a new "elevated BP" 120–139/70–89 category (McEvoy 2024, PMID 39210715)
2020 ISH ≥140/90 mm Hg, with essential/optimal care tiers (Unger 2020, PMID 32370572)
2021 WHO ≥140/90 mm Hg Treatment-focused, resource-stratified (Al-Makki 2022, PMID 34775787)
2025 Hypertension Canada ≥130/80 mm Hg Moved to the lower definition and a <130 systolic target (Goupil 2025, PMID 40419299)

The reclassification argument is quantitative: applying the 2017 ACC/AHA definition to NHANES 2011–2014 raised US hypertension prevalence by 13.7 percentage points but increased the share of adults recommended for drug therapy by only 1.9 points (36.2% vs 34.3%), because most of the newly labelled group qualified for lifestyle intervention alone (Muntner 2018, PMID 29133599). See definition, measurement and diagnosis and guidelines.

Burden

Measure Estimate Source
Adults 30–79 with hypertension, 2019 626M women, 652M men (NCD-RisC 2021, PMID 34450083)
Ever diagnosed, 2019 59% women, 49% men (NCD-RisC 2021, PMID 34450083)
Treated, 2019 47% women, 38% men (NCD-RisC 2021, PMID 34450083)
Controlled <140/90, 2019 23% women, 18% men (NCD-RisC 2021, PMID 34450083)
Deaths attributable to high systolic BP, 2019 10.8 million (95% UI 9.51–12.1), 19.2% of all deaths (GBD 2019 Risk Factors, PMID 33069327)
Share of all global DALYs attributable to high systolic BP, 2023 8.4% (6.9–10.0), the leading risk factor (GBD 2023, PMID 41092926)
Deaths attributable to SBP >115 mm Hg, 2015 8.5 million, 88% in low- and middle-income countries (Zhou 2021, PMID 34050340)
Residual lifetime risk of hypertension from age 55 ~90% (Vasan 2002, PMID 11866648)

Prevalence has fallen in high-income regions since the 1970s and risen in East, South and Southeast Asia, Oceania and sub-Saharan Africa, so the burden is now concentrated where treatment capacity is weakest (Zhou 2021, PMID 34050340). Across 44 low- and middle-income countries and 1.1 million adults, of those with hypertension 73.6% had ever had a blood pressure measured, 39.2% had been diagnosed, 29.9% treated and 10.3% controlled (Geldsetzer 2019, PMID 31327566). Detail in epidemiology and burden.

The evidence that treatment works

  • Across the pressure range. The BPLTTC individual-participant analysis of 48 trials and 344,716 participants found hazard ratios per 5 mm Hg systolic reduction of 0.91 (95% CI 0.89–0.94) without and 0.89 (0.86–0.92) with prior cardiovascular disease, with no reliable heterogeneity across seven baseline systolic strata from <120 to ≥170 mm Hg (BPLTTC 2021, PMID 33933205).
  • In the very old. HYVET randomised 3,845 people aged ≥80 with systolic ≥160 mm Hg to indapamide ± perindopril or placebo; active treatment reduced all-cause death by 21% (95% CI 4–35) and heart failure by 64% (42–78), with fewer serious adverse events than placebo (Beckett 2008, PMID 18378519).
  • Beyond drugs. Cluster-randomising 600 Chinese villages to a 25%-potassium salt substitute reduced stroke (rate ratio 0.86, 95% CI 0.77–0.96), major cardiovascular events (0.87, 0.80–0.94) and death (0.88, 0.82–0.95) over 4.74 years, without excess hyperkalaemia events (Neal 2021, PMID 34459569).

The three live controversies

How low. SPRINT achieved 121.4 vs 136.2 mm Hg and cut the primary composite (1.77% vs 2.40% per year; HR 0.73, 95% CI 0.63–0.86) and all-cause mortality (HR 0.75, 0.61–0.92) in its final report, at the cost of more hypotension, syncope, electrolyte abnormality and acute kidney injury (SPRINT 2021, PMID 34010531). ACCORD-BP, in type 2 diabetes, found no significant benefit for the same target (HR 0.88, 95% CI 0.73–1.06) though stroke fell (HR 0.59, 0.39–0.89) (ACCORD 2010, PMID 20228401). ESPRIT then randomised 11,255 high-risk Chinese adults including 4,359 with diabetes and found benefit (HR 0.88, 95% CI 0.78–0.99) with no heterogeneity by diabetes status (Liu 2024, PMID 38945140). A pooled participant-level analysis of six trials and 80,220 participants put the number needed to treat at 58 and the number needed to harm at 55, with net benefit still positive (Guo 2025, PMID 40902616). See blood-pressure targets.

How much is not primary. Systematic oral sodium suppression testing across the blood-pressure spectrum found biochemically overt primary aldosteronism in 11.3% of normotensive people (95% CI 5.9–16.8), 15.7% of stage 1, 21.6% of stage 2 and 22.0% of resistant hypertension, with the aldosterone-renin ratio showing poor sensitivity and negative predictive value (Brown 2020, PMID 32449886). If that continuum is real, a screening policy keyed to resistant hypertension misses most of it. See secondary hypertension.

Whether devices belong. SYMPLICITY HTN-3 was the field's discipline event: 535 patients, sham-controlled, and no significant office systolic difference (−2.39 mm Hg, 95% CI −6.89 to 2.12) (Bhatt 2014, PMID 24678939). Subsequent sham-controlled trials with revised technique and selection were positive but small in effect — SPYRAL HTN-OFF MED Pivotal −3.9 mm Hg 24-hour systolic (Bayesian 95% CrI −6.2 to −1.6) (Böhm 2020, PMID 32234534), pooled ultrasound denervation −5.9 mm Hg daytime ambulatory (95% CI −8.1 to −3.8) (Kirtane 2023, PMID 36853627). See device and interventional therapy.

Mechanism in one paragraph

Long-term arterial pressure is set where the kidney's pressure-natriuresis relationship intersects sodium intake; shifting that relationship rightwards is, in the Guytonian account, necessary for sustained hypertension (Guyton 1980, PMID 6994602; Hall 1986, PMID 3536587), an account that remains actively contested on logical and empirical grounds (Kurtz 2016, PMID 28637271; Evans 2016, PMID 26582636). Layered on it are sympathetic overactivity (Esler 2015, PMID 25680900), renin-angiotensin-aldosterone signalling, large-artery stiffening that converts a flow disorder into a pressure disorder with age (Vasan 2022, PMID 35168368), and adaptive immune activation (Caillon 2019, PMID 29952002). Every Mendelian form of hypertension identified acts on renal salt handling — Liddle syndrome through gain-of-function in the epithelial sodium channel's PY motif (Schild 1996, PMID 8665845), Gordon syndrome through the WNK–KLHL3–CUL3 degradation pathway for WNK kinases (Shibata 2013, PMID 23576762) — which is the strongest single argument that the kidney is where common hypertension is decided (Lifton 2001, PMID 11239411). See pathophysiology and genetics and monogenic forms.

Therapeutic landscape

Layer Representative evidence
Sodium reduction Each 50 mmol/day fall in urinary sodium lowered systolic pressure 1.10 mm Hg (95% CI 0.66–1.54) across 133 trials; effect larger in older, non-white and higher-pressure people (Huang 2020, PMID 32094151)
Dietary pattern DASH lowered systolic pressure 11.4 mm Hg more than control in hypertensive participants (Appel 1997, PMID 9099655); DASH plus low sodium 11.5 mm Hg below control-plus-high-sodium (Sacks 2001, PMID 11136953)
Salt substitution Hard-endpoint benefit in SSaSS (Neal 2021, PMID 34459569)
Alcohol Reduction lowers pressure only above ~2 drinks/day; −5.50 mm Hg systolic (95% CI −6.70 to −4.30) in the heaviest drinkers (Roerecke 2017, PMID 29253389)
Exercise Comparable to single-drug therapy in hypertensive populations, though exercise trials in hypertension are few (Naci 2019, PMID 30563873)
First-line drugs Thiazide-type diuretics, ACE inhibitors/ARBs and calcium channel blockers; β-blockers inferior for stroke as first-line (Wiysonge 2017, PMID 28107561)
Combination-first strategy Low-dose triple pill beat usual care on control (70% vs 55%) (Webster 2018, PMID 30120478); quarter-dose quadpill beat monotherapy by 6.9 mm Hg (Chow 2021, PMID 34469767)
Resistant hypertension Spironolactone superior to bisoprolol and doxazosin as fourth drug (−8.70 mm Hg vs placebo) (Williams 2015, PMID 26414968)
New mechanisms Aldosterone synthase inhibition (Freeman 2023, PMID 36342143; Flack 2025, PMID 40888730), endothelin antagonism (Schlaich 2022, PMID 36356632), siRNA angiotensinogen knockdown (Desai 2023, PMID 37467498)

The delivery problem

Efficacy has never been the binding constraint. US control rose from 31.8% (1999–2000) to 53.8% (2013–2014) and then fell to 43.7% (2017–2018) (Muntner 2020, PMID 32902588). What has moved population control is system redesign, not new drugs: a Kaiser Permanente Northern California registry programme raised control from 43.6% to 80.4% between 2001 and 2009 while the national rate rose from 55.4% to 64.1% (Jaffe 2013, PMID 23989679); a village-doctor-led intervention in rural China, a barbershop-based pharmacist programme, and a community health-worker model in Colombia and Malaysia all produced large control differences (Sun 2022, PMID 35500594; Victor 2018, PMID 29527973; Schwalm 2019, PMID 31488369). See adherence and implementation.

Open questions

  • Does treating masked asleep hypertension — present in an estimated 13.3% of US adults as an isolated finding under 2017 ACC/AHA thresholds — reduce events, or only numbers? (Li 2021, PMID 33112362)
  • Should screening for primary aldosteronism be uncoupled from resistant hypertension, given a prevalence continuum that begins in normotension and a screening ratio with poor negative predictive value? (Brown 2020, PMID 32449886)
  • What explains the ACCORD-BP/ESPRIT divergence in diabetes — chance, event rates, or the factorial glycaemia arm? (ACCORD 2010, PMID 20228401; Liu 2024, PMID 38945140)
  • Which of the implementation models that moved control in one health system transfer to another, and what is the active ingredient? (Jaffe 2013, PMID 23989679; Sun 2022, PMID 35500594)
  • Can any cuffless device meet a validation standard adequate for diagnosis rather than trend-tracking? (Stergiou 2023, PMID 37303198; Hu 2023, PMID 37688763)

References

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