Skip to content

Hypertension — statistics quick reference

Last updated: 2026-09-01

Published figures with their source, year, population and method. Conflicting estimates are shown side by side and never averaged. Every PubMed identifier was resolved by live query during the build session of 2026-09-01. Where a figure depends on a definitional choice — and in hypertension most do — the definition is stated in the row.

1. Prevalence

Figure Value Population Year Method Source
Adults 30–79 with hypertension (≥140/90 or on treatment) 331M women (95% CrI 306–359); 317M men (292–344) Global 1990 Bayesian hierarchical model over 1,201 population-representative studies, 104M participants NCD-RisC, PMID 34450083
Same 626M women (584–668); 652M men (604–698) Global 2019 Same NCD-RisC, PMID 34450083
Age-standardised prevalence trend 1990–2019 Essentially flat globally Global 1990–2019 Same NCD-RisC, PMID 34450083
Adult prevalence 31.1% (95% CI 30.0–32.2); 1.39 billion (1.34–1.44) people Global, 90 countries 2010 Systematic analysis of 135 population-based studies, 968,419 adults Mills, PMID 27502908
Prevalence, high-income vs LMIC 28.5% (27.3–29.7) vs 31.5% (30.2–32.9) Global 2010 Same Mills, PMID 27502908
Age-standardised prevalence change 2000→2010 −2.6% high-income; +7.7% LMIC Global 2000–2010 Same Mills, PMID 27502908
US crude prevalence under JNC7 (≥140/90) 31.9% (95% CI 30.1–33.7) US adults 2011–2014 NHANES, 3 standardised readings averaged, n=9,623 Muntner, PMID 29133599
US crude prevalence under 2017 ACC/AHA (≥130/80) 45.6% (43.6–47.6) US adults 2011–2014 Same Muntner, PMID 29133599
Prevalence, sub-Saharan Africa 30% (95% CI 27–34); 16%/26%/35%/44% at mean ages 30/40/50/60 33 surveys, 110,414 participants 2000–2013 Systematic review and meta-analysis Ataklte, PMID 25385758
US prevalence, ages 18–39 (≥130/80 or treated) 21.3% (20.4 million) US young adults 2021–2023 NHANES, n=51,291 across cycles Tang, PMID 40156902
US prevalence, ages 20–44 9.3% (95% CI 8.1–10.5) → 11.5% (9.6–13.4) US adults 20–44 2009–2010 → 2017–2020 NHANES, n=12,924 Aggarwal, PMID 36871237
US prevalence, ages 20–44, Black adults 16.2% (14.0–18.4) → 20.1% (16.8–23.3) Same Same Same Aggarwal, PMID 36871237
Residual lifetime risk of hypertension from age 55 or 65 ~90%; lifetime probability of antihypertensive use 60% Framingham, n=1,298 free of hypertension at baseline 1976–1998 Community cohort; ≥140/90 or medication Vasan, PMID 11866648
Neighbourhood prevalence gradient, most- vs least-deprived quintile 50.7% vs 25.5% 56,387 adults aged 35–50, one US county 2019 Geocoded EHR linked to area deprivation index across 1,157 block groups Blazel, PMID 39177999

2. The care cascade

Step 44 LMICs (Geldsetzer, PMID 31327566) Global 2019 (NCD-RisC, PMID 34450083) US 2017–2018 (Muntner, PMID 32902588)
Ever had BP measured 73.6% (95% CI 72.9–74.3)
Diagnosed / aware 39.2% (38.2–40.3) 59% women / 49% men
Treated 29.9% (28.6–31.3) 47% women / 38% men
Controlled 10.3% (9.6–11.0) 23% women / 18% men 43.7% (40.2–47.2) to <140/90

Method notes. Geldsetzer: pooled individual-level data from nationally representative surveys (mainly WHO STEPS) in 44 low- and middle-income countries, 1,100,507 participants, of whom 192,441 (17.5%) had hypertension; ≥140/90 or reported medication. NCD-RisC: modelled estimates for ages 30–79, self-reported diagnosis and treatment. Muntner: NHANES serial cross-sections, 18,262 US adults with hypertension across 10 cycles, control defined as <140/90.

US control trend Value Method
1999–2000 31.8% (95% CI 26.9–36.7) NHANES, age-adjusted, <140/90
2007–2008 48.5% (45.5–51.5) Same
2013–2014 53.8% (48.7–59.0) Same
2017–2018 43.7% (40.2–47.2) Same

(All: Muntner, PMID 32902588.)

Control by access, US 2017–2018 Value Source
Healthcare visit in past year vs not 49.1% vs 8.0% (adjusted PR 5.23, 95% CI 2.88–9.49) Muntner, PMID 32902588
Usual healthcare facility vs not 48.4% vs 26.5% (adjusted PR 1.48, 1.13–1.94) Muntner, PMID 32902588
Non-Hispanic Black vs non-Hispanic White 41.5% vs 48.2% (adjusted PR 0.88, 0.81–0.96) Muntner, PMID 32902588
Young adults 18–39: aware / controlled to <130/80 28.3% / 5.6% Tang, PMID 40156902
Adults with hypertension + diabetes + hyperlipidaemia, all three controlled 26.3% (95% CI 20.8–32.6) Lee, PMID 41295934

3. Attributable burden

Figure Value Year Method Source
Deaths attributable to high systolic BP 10.8 million (95% UI 9.51–12.1); 19.2% (16.9–21.3) of all deaths — leading Level 2 risk 2019 GBD comparative risk assessment, 87 risk factors, 204 countries GBD 2019 Risk Factors, PMID 33069327
Share of all global DALYs attributable to high systolic BP 8.4% (6.9–10.0) — leading Level 3 risk 2023 GBD 2023, 88 risk factors GBD 2023, PMID 41092926
Deaths attributable to systolic BP >115 mm Hg 8.5 million, 88% in LMICs 2015 Review of global burden estimates Zhou, PMID 34050340
Leading risk for DALYs at ages 50–74 and ≥75 High systolic blood pressure 2019 GBD GBD 2019 Risk Factors, PMID 33069327

4. Dose–response and risk

Relationship Estimate Population Method Source
Stroke death per 20 mm Hg higher usual systolic, ages 40–69 >2-fold 1 million adults, 61 prospective studies, 12.7M person-years Individual-data meta-analysis with time-dependent regression-dilution correction Lewington, PMID 12493255
IHD death per 20 mm Hg, ages 40–69 >2-fold Same Same Lewington, PMID 12493255
Proportional effect at ages 80–89 vs 40–49 About half as extreme; absolute differences larger Same Same Lewington, PMID 12493255
Threshold below which association disappears None detectable to 115/75 mm Hg Same Same Lewington, PMID 12493255
Peripheral arterial disease per 20 mm Hg usual systolic HR 1.63 (95% CI 1.59–1.66) 4,222,459 UK adults aged 30–90 Linked primary-care EHR, 1990–2013 Emdin, PMID 26419648
Atrial fibrillation per 20 mm Hg usual systolic HR 1.21 (1.19–1.22) overall; 1.91 (1.75–2.09) at 30–40y; 1.01 (0.97–1.04) at 80–90y 4.3 million UK adults Same Emdin, PMID 27143136
Heart failure risk from systolic ≥130 mm Hg at ages 18–39 +37%, independent of exposure after age 40 36,030 people, 6 pooled US cohorts, median 17y follow-up Imputed risk-factor trajectories from age 18 Zhang, PMID 31319915
Stroke per top-decile visit-to-visit systolic SD (7 visits) HR 6.22 (95% CI 4.16–9.29) UK-TIA trial cohort Independent of mean systolic Rothwell, PMID 20226988
Stroke per top-decile maximum systolic (7 visits) HR 15.01 (6.56–34.38) Same Adjusted for mean systolic Rothwell, PMID 20226988
Residual on-treatment variability, stroke HR 3.25 (2.32–4.54) top decile ASCOT-BPLA Independent of clinic and ambulatory mean Rothwell, PMID 20226988
Diastolic <60 vs 80–89 mm Hg: odds of hs-troponin-T ≥14 ng/L 2.2 11,565 ARIC participants, 21 years Community cohort McEvoy, PMID 27590090

5. Prognostic value of measurement method

Comparison Estimate Population Source
24-h systolic vs clinic systolic, all-cause death per 1 SD HR 1.41 (95% CI 1.36–1.47) vs 1.18 (1.13–1.23) 59,124 Spanish primary-care patients, median 9.7y Staplin, PMID 37156250
Clinic systolic after adjustment for 24-h HR 1.04 (1.00–1.09) Same Staplin, PMID 37156250
Night-time systolic informativeness vs clinic (=100%) 591% for all-cause death; 604% for CV death Same Staplin, PMID 37156250
Night-time systolic per 20/10 mm Hg, total mortality HR 1.23 (1.17–1.28) 11,135 adults, 13 populations, median 13.8y Yang, PMID 31386134
24-h systolic per 20/10 mm Hg, CV events HR 1.45 (1.37–1.54) Same Yang, PMID 31386134
Incremental AUC from adding 24-h or night-time systolic 0.0013–0.0027 (mortality); 0.0031–0.0075 (CV) Same Yang, PMID 31386134
Home vs 24-h ambulatory, per 10 mm Hg systolic HR 1.36 (1.23–1.50) vs 1.38 (1.22–1.57), NS difference 4,439 people, 5 studies Kollias, PMID 38164947
Time in target range (24-h), standardised HR 0.57 (0.46–0.71) mortality; 0.30 (0.23–0.39) CV endpoints 14,230 people, 14 cohorts, median 10.9y Zhang, PMID 40249369

6. Phenotype prevalence and risk

Phenotype Prevalence Risk vs normotension Source
Untreated white-coat hypertension CV events HR 1.36 (95% CI 1.03–2.00); all-cause death 1.33 (1.07–1.67); CV death 2.09 (1.23–4.48) Cohen, PMID 31181575 (27 studies, 25,786 vs 38,487)
Treated white-coat effect CV events HR 1.12 (0.91–1.39), NS Cohen, PMID 31181575
White-coat hypertension, Spanish registry No excess all-cause or CV mortality Staplin, PMID 37156250
Masked hypertension All-cause death HR 1.24 (1.12–1.37); CV death 1.37 (1.15–1.63) Staplin, PMID 37156250
Sustained hypertension All-cause death HR 1.24 (1.15–1.32); CV death 1.38 (1.22–1.55) Staplin, PMID 37156250
Masked asleep hypertension (2017 ACC/AHA criteria) 22.7% (95% CI 20.6–24.8) — 53.7 million US adults Li, PMID 33112362
Isolated masked asleep hypertension (2017 criteria) 13.3% — 31.5 million US adults Li, PMID 33112362
Masked asleep hypertension (JNC7 criteria) 18.8% (16.7–20.8) — 44.4 million Li, PMID 33112362
Apparent treatment-resistant hypertension 14.7% (13.1–16.3) of treated patients Noubiap, PMID 30087099 (91 studies, 3,207,911 patients)
Pseudo-resistant hypertension 10.3% (6.0–15.5) Noubiap, PMID 30087099
True resistant hypertension 10.3% (7.6–13.2) Noubiap, PMID 30087099
True resistant hypertension in CKD 22.9% (19.1–27.0) Noubiap, PMID 30087099
True resistant hypertension in renal transplant 56.0% (52.7–59.3) Noubiap, PMID 30087099
Non-adherence in apparent resistant hypertension 31.2% (20.2–44.7) pooled; range 3.3–86.1% by method Durand, PMID 28777133 (24 studies)
Complete non-adherence by chemical testing 15.0% pooled (I²=94.6%); any non-adherence 33.0% (I²=95.6%) Highton, PMID 40371625 (70 papers)

7. Secondary causes

Cause Prevalence Population Method Source
Biochemically overt primary aldosteronism 11.3% (95% CI 5.9–16.8) Normotension (n=289) Oral sodium suppression test in all, urinary aldosterone >12 μg/24h Brown, PMID 32449886
Same 15.7% (8.6–22.9) Stage 1 hypertension (n=115) Same Brown, PMID 32449886
Same 21.6% (16.1–27.0) Stage 2 hypertension (n=203) Same Brown, PMID 32449886
Same 22.0% (17.2–26.8) Resistant hypertension (n=408) Same Brown, PMID 32449886
Primary aldosteronism, Endocrine Society criteria 5.9% overall; 3.9% stage 1 → 11.8% stage 3 1,672 unselected primary-care hypertensives, Italy ARR screening then confirmatory testing and AVS Monticone, PMID 28385310
Primary aldosteronism in resistant hypertension 5–25% depending on criteria Review Azizi, PMID 41870448
Stroke odds, primary aldosteronism vs essential hypertension OR 2.58 (95% CI 1.93–3.45) 3,838 vs 9,284 patients, 31 studies, median 8.8y Meta-analysis of observational studies Monticone, PMID 29129575
Atrial fibrillation odds, same OR 3.52 (2.06–5.99) Same Same Monticone, PMID 29129575
CV events on MRA therapy vs essential hypertension 56.3 (48.8–64.7) vs 26.6 (26.1–27.2) per 1,000 py; adjusted HR 1.91 (1.63–2.25) 602 vs 41,853 patients Registry cohort, matched by age decade Hundemer, PMID 29129576
Excess confined to persistently suppressed renin (<1 μg/L/h) Adjusted HR 2.83 (2.11–3.80); no excess if renin unsuppressed Same Same Hundemer, PMID 29129576
Complete clinical success after adrenalectomy 37% (range across centres 17–62); clinical benefit 84%; complete biochemical success 94% (83–100) 705 patients, 12 centres, 9 countries PASO consensus criteria Williams, PMID 28576687

8. Treatment effect sizes — drugs

Intervention Effect Population Source
Per 5 mm Hg systolic reduction, no prior CVD HR 0.91 (95% CI 0.89–0.94) for major CV events 186,988 participants BPLTTC, PMID 33933205
Per 5 mm Hg systolic reduction, prior CVD HR 0.89 (0.86–0.92) 157,728 participants BPLTTC, PMID 33933205
Per 5 mm Hg, ages <55 / 55–64 / 65–74 / 75–84 / ≥85 0.82 (0.76–0.88) / 0.91 (0.88–0.95) / 0.91 (0.88–0.95) / 0.91 (0.87–0.96) / 0.99 (0.87–1.12) 358,707 participants, 51 trials BPLTTC, PMID 34461040
Low-dose thiazide vs control Mortality RR 0.89 (0.82–0.97); stroke 0.68 (0.60–0.77); CHD 0.72 (0.61–0.84); total CV 0.70 (0.64–0.76) 24 trials, 58,040 patients Wright, PMID 29667175
β-blocker vs control Mortality RR 0.96 (0.86–1.07) NS; stroke 0.83 (0.72–0.97); total CV 0.89 (0.81–0.98) Same Wright, PMID 29667175
ACE inhibitor vs control Mortality RR 0.83 (0.72–0.95); stroke 0.65 (0.52–0.82); CHD 0.81 (0.70–0.94) Same Wright, PMID 29667175
Calcium channel blocker vs control Stroke RR 0.58 (0.41–0.84); total CV 0.71 (0.57–0.87); mortality 0.86 (0.68–1.09) NS Same Wright, PMID 29667175
ACEi+amlodipine vs ACEi+HCTZ (ACCOMPLISH) HR 0.80 (0.72–0.90) for composite; 9.6% vs 11.8% 11,506 high-risk patients, 36 months Jamerson, PMID 19052124
Chlorthalidone vs hydrochlorothiazide (DCP) HR 1.04 (0.94–1.16); 10.4% vs 10.0%; hypokalaemia 6.0% vs 4.4% 13,523 veterans ≥65, median 2.4y Ishani, PMID 36516076
Losartan vs atenolol (LIFE) Composite RR 0.87 (0.77–0.98); stroke 0.75 (0.63–0.89) 9,193 patients with ECG LVH Dahlöf, PMID 11937178
Quadpill vs monotherapy (QUARTET), 12 weeks Systolic −6.9 mm Hg (95% CI 4.9–8.9); control 76% vs 58% (RR 1.30, 1.15–1.47) 591 Australian adults Chow, PMID 34469767
Triple pill vs usual care (TRIUMPH), 6 months Target attainment 70% vs 55% (risk difference 12.7%, 3.2–22.0) 700 adults, Sri Lanka Webster, PMID 30120478
Spironolactone vs placebo (PATHWAY-2) Home systolic −8.70 mm Hg (95% CI 7.69–9.72) 335 resistant-hypertension patients, crossover Williams, PMID 26414968
Spironolactone vs placebo (network meta-analysis) Office systolic −13.3 mm Hg (−17.89 to −8.72); 24-h −8.46 (−12.54 to −4.38) 24 RCTs, 3,485 resistant-hypertension patients Azizi, PMID 41870448
Aprocitentan 12.5/25 mg vs placebo, 4 weeks Office systolic −3.8 (97.5% CI −6.8 to −0.8) / −3.7 (−6.7 to −0.8) mm Hg; 24-h −4.2 / −5.9 730 randomised Schlaich, PMID 36356632

9. Treatment effect sizes — targets

Trial n Achieved systolic Primary result Source
SPRINT (final) 9,361 121.4 vs 136.2 (1y) 1.77 vs 2.40 %/yr, HR 0.73 (0.63–0.86); all-cause death HR 0.75 (0.61–0.92) PMID 34010531
ACCORD-BP 4,733 119.3 vs 133.5 1.87 vs 2.09 %/yr, HR 0.88 (0.73–1.06) NS; stroke HR 0.59 (0.39–0.89) PMID 20228401
STEP 8,511 127.5 vs 135.3 3.5% vs 4.6%, HR 0.74 (0.60–0.92) PMID 34491661
STEP 6-year 8,511 127.9 vs 129.5 1.12 vs 1.33 %/yr, HR 0.82 (0.71–0.96) PMID 41105077
ESPRIT 11,255 119.1 vs 134.8 9.7% vs 11.1%, HR 0.88 (0.78–0.99); syncope HR 3.00 (1.35–6.68) PMID 38945140
BPROAD 12,821 121.6 vs 133.2 1.65 vs 2.09 per 100 py, HR 0.79 (0.69–0.90) PMID 39555827
SPS3 3,020 127 vs 138 All stroke HR 0.81 (0.64–1.03) NS; ICH HR 0.37 (0.15–0.95) PMID 23726159
HYVET 3,845 15.0/6.1 mm Hg lower on treatment Stroke −30% (−1 to 51); all-cause death −21% (4–35); heart failure −64% (42–78) PMID 18378519
Pooled participant-level (6 trials) 80,220 CV composite 5.3% vs 7.1%, HR 0.76 (95% CrI 0.72–0.81); ARR 1.73% (NNT 58); AE ARI 1.82% (NNH 55) PMID 40902616

10. Treatment effect sizes — lifestyle

Intervention Effect Population Source
Sodium reduction, per 50 mmol/day Systolic −1.10 mm Hg (95% CI 0.66–1.54); diastolic −0.33 (0.04–0.63) 133 trials, 12,197 participants, 24h urine verified Huang, PMID 32094151
Sodium reduction, mean 130 mmol/day contrast Systolic −4.26 mm Hg (3.62–4.89); diastolic −2.07 (1.67–2.48) Same Huang, PMID 32094151
Trials <15 days vs longer, per 50 mmol/day −1.05 (0.40–1.70) vs −2.13 (0.85–3.40) mm Hg Same Huang, PMID 32094151
DASH vs control, hypertensive participants Systolic −11.4, diastolic −5.5 mm Hg 133 of 459 participants Appel, PMID 9099655
DASH + low sodium vs control + high sodium Systolic −11.5 mm Hg (hypertensive); −7.1 (non-hypertensive) 412 participants, feeding study Sacks, PMID 11136953
DASH4D + low sodium vs comparison + high sodium Systolic −4.6 mm Hg (95% CI 2.0–7.2); diastolic −2.3 (0.9–3.7) 102 adults with type 2 diabetes, crossover feeding Pilla, PMID 40489102
Salt substitute (75/25), stroke Rate ratio 0.86 (95% CI 0.77–0.96); 29.14 vs 33.65 per 1,000 py 20,995 people, 600 villages, 4.74y Neal, PMID 34459569
Salt substitute, major CV events 0.87 (0.80–0.94); 49.09 vs 56.29 per 1,000 py Same Neal, PMID 34459569
Salt substitute, all-cause death 0.88 (0.82–0.95); 39.28 vs 44.61 per 1,000 py Same Neal, PMID 34459569
Salt substitute, hyperkalaemia SAEs 1.04 (0.80–1.37); 3.35 vs 3.30 per 1,000 py Same Neal, PMID 34459569
Salt substitute, blood pressure Systolic −4.61 mm Hg (−6.07 to −3.14); diastolic −1.61 (−2.42 to −0.79) 21 trials, 31,949 participants Yin, PMID 35945000
Salt substitute, per 10% lower NaCl content Additional systolic −1.53 mm Hg (−3.02 to −0.03) Same Yin, PMID 35945000
Alcohol reduction (≥6 drinks/day, halved) Systolic −5.50 mm Hg (−6.70 to −4.30); diastolic −3.97 (−4.70 to −3.25) 36 trials, 2,865 participants Roerecke, PMID 29253389
Alcohol reduction (≤2 drinks/day) No significant reduction Same Roerecke, PMID 29253389
DASH in network meta-analysis of 22 interventions Systolic −6.97 mm Hg (95% CrI 4.50–9.47); diastolic −3.54 (1.80–5.28); ranked first 120 trials, 14,923 participants Fu, PMID 32975166
Exercise vs drugs, all populations Drugs better by 3.96 mm Hg (95% CrI 2.91–5.02) 391 RCTs (197 exercise, 194 drug) Naci, PMID 30563873
Exercise vs drugs, hypertensive populations No detectable difference 56 exercise trials, 3,508 hypertensive participants Naci, PMID 30563873

11. Devices

Intervention Effect Population Source
Renal denervation vs sham, office systolic (SYMPLICITY HTN-3) −2.39 mm Hg (95% CI −6.89 to 2.12), NS 535 patients Bhatt, PMID 24678939
Sham-arm office systolic fall in the same trial −11.74±25.94 mm Hg Same Bhatt, PMID 24678939
Renal denervation vs sham, 24-h systolic (SPYRAL OFF MED Pivotal) −3.9 mm Hg (Bayesian 95% CrI −6.2 to −1.6) 331 patients off drugs Böhm, PMID 32234534
Ultrasound denervation vs sham, daytime ambulatory systolic (pooled) −5.9 mm Hg (95% CI −8.1 to −3.8) 506 patients, 3 trials Kirtane, PMID 36853627
Ultrasound denervation vs sham at 6 months after blinded medication escalation −3.0 mm Hg (−5.7 to −0.2), with fewer added drugs (p=0.004) Same Azizi, PMID 37883784
Renal denervation vs sham, meta-analysis 24-h systolic −4.4 mm Hg (−6.1 to −2.7); office −6.6 (−9.7 to −3.6) 10 sham-controlled RCTs, 2,478 participants Azizi, PMID 41870448
Baroreflex activation therapy, SBP ≤140 mm Hg at 6 months 42% vs 24% (p=0.005) 265 implanted, randomised 2:1 Bisognano, PMID 21816315
Central iliac AV anastomosis, office systolic at 12 months −25.1±23.3 mm Hg; ipsilateral venous stenosis in 33% 39 patients (intention-to-treat) Lobo, PMID 29061728

12. Implementation

Programme Effect Population Source
Village-doctor-led intervention (CRHCP), control <130/80 at 18 months 57.0% vs 19.9%; difference 37.0 percentage points (95% CI 34.9–39.1) 33,995 people, 326 villages Sun, PMID 35500594
CRHCP cardiovascular composite, 36 months 1.62% vs 2.40% per year; HR 0.67 (95% CI 0.61–0.73); all-cause death HR 0.85 (0.76–0.95); hypotension 1.75% vs 0.89% Same cluster-randomised population He, PMID 36871573
CRHCP cardiovascular composite, 7 years 2.4% vs 3.0% per year; HR 0.76 (95% CI 0.72–0.81); post-trial years 4–7 HR 0.79 (0.73–0.85); hypotension RR 1.58 (1.39–1.79) 31,334 entered post-trial follow-up Sun, PMID 42666029
Same, systolic change −26.3 vs −11.8 mm Hg; difference −14.5 (−15.7 to −13.3) Same Sun, PMID 35500594
Barbershop pharmacist intervention, systolic at 6 months −27.0 vs −9.3 mm Hg; difference 21.6 (14.7–28.4); <130/80 in 63.6% vs 11.7% 319 Black men, 52 barbershops Victor, PMID 29527973
HOPE 4 community NPHW model Systolic −11.45 mm Hg greater (−14.94 to −7.97); control <140 in 69% vs 30% 1,371 people, 30 communities, Colombia and Malaysia Schwalm, PMID 31488369
Kaiser Permanente NC programme, control 43.6% (39.4–48.6) → 80.4% (75.6–84.4), 2001–2009 Registry to 652,763 patients Jaffe, PMID 23989679
US national mean over the same period 55.4% → 64.1% NCQA HEDIS commercial Jaffe, PMID 23989679
Team-based care Control +12 percentage points (median); systolic −5.4 mm Hg (median) 80 studies Proia, PMID 24933494
Self-monitoring alone, 12-month clinic systolic −1.0 mm Hg (95% CI −3.3 to 1.2), NS 25 trials, 7,138 participants Tucker, PMID 28926573
Self-monitoring with intensive support −6.1 mm Hg (−9.0 to −3.2) Same Tucker, PMID 28926573
Fixed-dose combination (polypill) primary prevention CV composite 3.0% vs 4.9%, HR 0.62 (0.53–0.73) 18,162 participants, 3 trials, median 5y Joseph, PMID 34469765

13. Harms

Harm Estimate Method Source
Falls RR 1.05 (95% CI 0.89–1.24) — no association 7 trials within a 58-trial, 280,638-participant meta-analysis Albasri, PMID 33568342
Acute kidney injury RR 1.18 (1.01–1.39) 15 trials Albasri, PMID 33568342
Hyperkalaemia RR 1.89 (1.56–2.30) 26 trials Albasri, PMID 33568342
Hypotension RR 1.97 (1.67–2.32) 35 trials Albasri, PMID 33568342
Syncope RR 1.28 (1.03–1.59) 16 trials Albasri, PMID 33568342
Orthostatic hypotension with intensive treatment OR 0.93 (0.86–0.99) — reduced 18,466 participants, 127,882 visits, 5 target trials Juraschek, PMID 32909814
Orthostatic hypertension with intensive treatment OR 0.93 (0.90–0.96) — reduced; prevalence 17% 31,124 participants, 315,497 standing measurements, 9 trials Juraschek, PMID 40132860
Intensive inpatient BP treatment, composite adverse outcome Weighted OR 1.28 (1.18–1.39); 1.90 (1.65–2.19) with IV agents 66,140 veterans ≥65, propensity overlap weighting Anderson, PMID 37252732
Inpatient treatment, acute kidney injury / myocardial injury 10.3% vs 7.9% / 1.2% vs 0.6% 22,834 admissions, propensity matched Rastogi, PMID 33369614
As-needed BP medication, acute kidney injury Adjusted HR 1.23 (1.18–1.29); composite MI/stroke/death HR 1.69 (1.49–1.92) 133,760 hospitalised veterans, target trial emulation Canales, PMID 39585709
Cuff size error: regular cuff on extra-large arm +19.5 mm Hg systolic (16.1–22.9) 195 adults, randomised crossover Ishigami, PMID 37548984
Cuff size error: regular cuff on small arm −3.6 mm Hg (−5.6 to −1.7) Same Ishigami, PMID 37548984
Unvalidated home devices online 92.4% of 972 devices; 0% of 532 wrist-band wearables validated Marketplace survey, one country Picone, PMID 32275193
Terminal-digit preference (systolic ending in zero) 41.7% → 37.7% (2015→2019) vs 10–20% expected Nationally representative physician survey, ~60M visits/yr Foti, PMID 33246327

14. Genetics

Figure Value Source
Independent genome-wide significant BP signals 2,103 (113 novel), explaining >60% of SNP-based BP heritability Keaton, PMID 38689001 (n=1,028,980)
Top vs bottom PRS decile, systolic difference 16.9 mm Hg (95% CI 15.5–18.2) Keaton, PMID 38689001
Top vs bottom PRS decile, hypertension odds OR 7.33 (5.54–9.70) Keaton, PMID 38689001
AUROC gain from adding PRS 0.791 (0.781–0.801) → 0.826 (0.817–0.836); ΔAUROC 0.035 Keaton, PMID 38689001
Rare-variant associations 106 new regions, 87 rare-variant signals; average effects ~8× common-variant Surendran, PMID 33230300 (n≈1.3 million)
Heritability, twin/family ~40% Salfati, PMID 26162070
Heritability, genomic relatedness, European ancestry ~20% systolic / ~50% diastolic Salfati, PMID 26162070 (ARIC, n=8,901)
Heritability, genomic relatedness, African ancestry ~27% systolic / ~39% diastolic Salfati, PMID 26162070 (n=2,860)
BP tracking childhood→adulthood, correlation 0.38 systolic / 0.28 diastolic (average) Chen, PMID 18559702 (50 cohorts, 617 data points)
Maintaining elevated BP/hypertension over 38 years OR 2.16 (95% CI 1.95–2.39) Meng, PMID 39495520 (n=2,918)

15. Economics

Figure Value Method Source
Scaling hypertension care from SBP ≥140 mm Hg, 24 LMICs over 30 years 2.6M averted CV events; 1.2M averted deaths (7% of expected CV deaths) Societal perspective, 4% discount, 2020 USD Hutchinson, PMID 38626959
Share of that benefit from treating SBP ≥160 mm Hg 68% Same Hutchinson, PMID 38626959
Countries with positive net benefit at some cut-point 10 of the 12 highest-income; 3 of the 12 lowest-income in the set Same Hutchinson, PMID 38626959
Cut-point maximising net economic benefit in lowest-income countries SBP ≥160 mm Hg Same Hutchinson, PMID 38626959
CVD cases averted per 1,000 people with hypertension, bottom vs top wealth quintile (lower-middle-income countries, treatment scenario) 29.1 vs 17.2 Microsimulation on 44-country survey data Stein, PMID 38278990
Adrenal vein sampling vs CT-based management +€2,285 per patient (95% CI 1,323–3,248); <0.2 probability of cost-effectiveness at €30,000/QALY Randomised diagnostic trial, n=184 completing Dekkers, PMID 27325147

Known conflicts and caveats

  1. Prevalence depends on the threshold, and the two definitions differ by 13.7 percentage points in the same US survey population (31.9% vs 45.6%) (Muntner, PMID 29133599). Any prevalence figure quoted without its threshold is uninterpretable. This file states the definition in every prevalence row.
  2. White-coat hypertension risk is genuinely contested. Cohort meta-analysis finds excess risk in untreated white-coat hypertension (Cohen, PMID 31181575); the largest single registry finds none (Staplin, PMID 37156250). Both are shown; they are not averaged.
  3. The sodium J-curve is unresolved. Randomised trials show a monotonic dose–response for pressure down to low intake (Huang, PMID 32094151); PURE observational data show higher event risk below 3 g/day sodium excretion (O'Donnell, PMID 25119607). The methodological dispute is about spot-urine estimating equations and reverse causation, and it has not been settled by a trial with hard endpoints at low intake.
  4. The ACCORD-BP null in diabetes has been superseded, not reconciled. ACCORD-BP found HR 0.88 (0.73–1.06) (PMID 20228401); ESPRIT and BPROAD found benefit (PMIDs 38945140, 39555827). Any figure quoted from ACCORD-BP should carry that context.
  5. NNT and NNH for intensive targets are nearly equal (58 vs 55) (Guo, PMID 40902616). The favourable net benefit rests on the events differing in severity, not in frequency.
  6. Renal denervation figures are not comparable across trial generations. SYMPLICITY HTN-3's −2.39 mm Hg and RADIANCE's pooled −5.9 mm Hg come from different catheters, endpoints, medication protocols and populations.
  7. The 36-month SYMPLICITY HTN-3 result (−22.1 mm Hg adjusted office difference) is not a randomised comparison — patients were unblinded at 6 months and sham patients could cross over, with imputation used for crossovers (Bhatt, PMID 36130612). It is not listed alongside the 6-month randomised figure for that reason.
  8. Cascade figures are not directly comparable between sources: NCD-RisC models ages 30–79 with self-reported diagnosis; Geldsetzer pools measured survey data across 44 countries; NHANES uses three standardised readings in a single country. Differences between them are partly definitional.
  9. Non-adherence prevalence varies by more than an order of magnitude with the measurement method (3.3–86.1% across studies) (Durand, PMID 28777133). Only chemically verified figures should be compared with each other.
  10. Two records in this literature carry publication flags. A widely cited NEJM analysis of the Spanish ambulatory registry (PMID 29669232) is marked as a retracted publication in PubMed and is deliberately not used anywhere in this condition; the Hygia Chronotherapy Trial (PMID 31641769) carries a journal Expression of Concern (PMID 32318736) and is presented only as a contested claim against the neutral TIME trial (PMID 36240838).
  11. GBD estimates are model outputs, not measurements, and are revised between rounds; the 2019 and 2023 figures quoted here are from different estimation rounds and are not a time series.
  12. Effect sizes for lifestyle interventions come predominantly from feeding studies and supervised programmes. They should not be read as population effects; the salt-substitution and population-reformulation literatures are the exceptions because they change the environment rather than the behaviour.