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Blood-pressure targets

TL;DR — Lowering BP reduces cardiovascular events across broad baseline risks, but the “right target” depends on measurement method, population, tolerability and guideline. Per 10-mm Hg systolic reduction, a 123-trial meta-analysis found RR 0.80 (95% CI 0.77–0.83) for major CVD, 0.73 for stroke and 0.72 for HF (Ettehad 2016, PMID 26724178). SPRINT and STEP favored intensive strategies in high-risk nondiabetic adults and Chinese adults aged 60–80, while ACCORD BP did not significantly reduce its primary composite in diabetes and increased treatment-attributed serious adverse events (SPRINT 2021, PMID 34010531; Zhang 2021, PMID 34491661; ACCORD 2010, PMID 20228401). HHD does not have a trial-validated imaging-specific BP target. Office and ambulatory values are not interchangeable, and benefit must be balanced against hypotension, syncope, electrolyte disturbance, kidney-function change and treatment burden.

1. Target is inseparable from measurement

Measurement context Typical strength Target-translation problem
Routine office Accessible Technique and white-coat effect
Standardized automated office Trial-like when protocol reproduced Often lower than casual clinic BP
Home BP Repeated real-world values No sleep measurement
24-hour ABPM Day/night load and masked phenotypes Availability and reproducibility
Central BP Mechanistic interest Limited outcome-target evidence

SPRINT’s target cannot be copied without considering its standardized measurement and eligibility. ESC, AHA/ACC and WHO documents use distinct labels, resource assumptions and treatment frameworks (Jones 2025, PMID 40815242; McEvoy 2024, PMID 39210715; Al-Makki 2022, PMID 34775787).

2. Continuous treatment effect

A meta-analysis of 123 randomized studies and 613,815 participants reported per 10-mm Hg lower systolic BP:

Outcome Relative risk (95% CI)
Major cardiovascular disease 0.80 (0.77–0.83)
Coronary heart disease 0.83 (0.78–0.88)
Stroke 0.73 (0.68–0.77)
Heart failure 0.72 (0.67–0.78)
All-cause mortality 0.87 (0.84–0.91)
Renal failure 0.95 (0.84–1.07)

These estimates come from Ettehad 2016 (PMID 26724178) and are averages across heterogeneous trials, not a single HHD target.

An individual-participant analysis of 344,716 participants found each 5-mm Hg systolic reduction lowered major cardiovascular events similarly with prior CVD (HR 0.89, 95% CI 0.86–0.92) and without prior CVD (HR 0.91, 0.89–0.94) (BPLTTC 2021, PMID 33933205).

3. SPRINT

SPRINT randomized 9,361 adults with systolic BP ≥130 mm Hg and increased cardiovascular risk, excluding diabetes and prior stroke, to targets <120 or <140 mm Hg (SPRINT 2015, PMID 26551272).

Result Intensive Standard Effect
Achieved SBP at 1 year 121.4 136.2 mm Hg —
Primary outcome, initial report 1.65%/year 2.19%/year HR 0.75 (95% CI 0.64–0.89)
All-cause mortality, initial — — HR 0.73 (0.60–0.90)
Final primary outcome 1.77%/year 2.40%/year HR 0.73 (0.63–0.86)
Final all-cause mortality 1.06%/year 1.41%/year HR 0.75 (0.61–0.92)

Hypotension, syncope, electrolyte abnormalities and acute kidney injury/failure were more frequent with intensive treatment; injurious falls were not increased in the initial report (SPRINT 2015, PMID 26551272; SPRINT 2021, PMID 34010531).

4. STEP

STEP randomized 8,511 Chinese adults aged 60–80 to systolic targets 110–<130 versus 130–<150 mm Hg. Achieved one-year systolic BP was 127.5 versus 135.3 mm Hg; the primary composite occurred in 3.5% versus 4.6%, HR 0.74 (95% CI 0.60–0.92) (Zhang 2021, PMID 34491661).

Component Hazard ratio (95% CI)
Stroke 0.67 (0.47–0.97)
Acute coronary syndrome 0.67 (0.47–0.94)
Acute decompensated HF 0.27 (0.08–0.98)
Atrial fibrillation 0.96 (0.55–1.68)
Cardiovascular death 0.72 (0.39–1.32)

Hypotension was more frequent; other safety/renal outcomes did not significantly differ (Zhang 2021, PMID 34491661).

5. Diabetes: ACCORD BP

ACCORD BP randomized 4,733 adults with type 2 diabetes and high cardiovascular risk to <120 versus <140 mm Hg. At one year, systolic BP was 119.3 versus 133.5 mm Hg (ACCORD 2010, PMID 20228401).

Outcome Intensive vs standard Effect
Primary composite annual rate 1.87% vs 2.09% HR 0.88 (95% CI 0.73–1.06), P=0.20
Stroke annual rate 0.32% vs 0.53% HR 0.59 (0.39–0.89)
All-cause death 1.28% vs 1.19% HR 1.07 (0.85–1.35)
Treatment-attributed serious adverse events 3.3% vs 1.3% P<0.001

The result is not “intensive control fails in diabetes”; it is a nonsignificant primary composite, a significant stroke reduction and greater treatment-attributed harm within a factorial trial and specific risk population.

6. Very old adults and frailty

HYVET randomized 3,845 adults aged ≥80 with systolic BP ≥160 mm Hg to indapamide-based treatment or placebo, targeting 150/80 mm Hg. Active treatment lowered sitting BP by 15.0/6.1 mm Hg and reduced all-cause death by 21% (95% CI 4–35) and HF by 64% (42–78); stroke reduction was 30% with CI crossing zero (Beckett 2008, PMID 18378519).

Post hoc HYVET analysis found no evidence that baseline frailty modified treatment benefit, but trial participants and frailty measurement limit extrapolation to severely dependent or institutionalized populations (Warwick 2015, PMID 25880068).

A meta-analysis of 18,806 participants aged >60 from SPRINT, STEP and ACCORD BP found MACE HR 0.83 (95% CI 0.74–0.94) and stroke HR 0.70 (0.56–0.88), with hypotension HR 1.46 and syncope HR 1.43 under intensive treatment (Li 2023, PMID 37099984).

7. Prior stroke

SPS3 randomized 3,020 people with recent lacunar stroke to systolic targets <130 or 130–149 mm Hg. Achieved BP was 127 versus 138 mm Hg; all-stroke HR was 0.81 (95% CI 0.64–1.03), P=0.08, while intracerebral-hemorrhage HR was 0.37 (0.15–0.95) (SPS3 2013, PMID 23726159).

The lower target accelerated early eGFR decline: rapid decline occurred in 24% versus 19%, OR 1.4 (95% CI 1.1–1.6), with no later slope difference (Peralta 2016, PMID 26762524).

8. HHD remodeling endpoints

STEP secondary analysis among 7,141 participants found intensive treatment reduced new ECG-LVH, HR 0.76 (95% CI 0.66–0.89), but did not increase regression of baseline LVH. Adjusting for time-varying LVH barely changed the cardiovascular HR (0.75 to 0.76), arguing against ECG-LVH change explaining most benefit (Deng 2023, PMID 37259845).

LIFE demonstrated that regimen and remodeling can differ despite similar achieved BP, but does not define an HHD-specific pressure target (Dahlöf 2002, PMID 11937178; Devereux 2004, PMID 15326072).

9. Out-of-office targets

ABPM is more closely associated with events than office BP and identifies nighttime and masked load (Huang 2021, PMID 33390042; Hinderliter 2018, PMID 29404785). In an 11,135-person cohort, both 24-hour and nighttime BP predicted mortality and cardiovascular events (Yang 2019, PMID 31386134). In 14,230 participants, greater 24-hour percentage time in the 2024 ESC target range was associated with lower mortality and cardiovascular endpoints; office BP misclassified most participants relative to this metric (Zhang 2025, PMID 40249369).

Home monitoring improves control chiefly when paired with support: individual-patient meta-analysis found a 3.2-mm Hg systolic difference overall, while a smartphone-coaching trial found a nonsignificant −2.0-mm Hg adjusted difference (Tucker 2017, PMID 28926573; Persell 2020, PMID 32119093).

A STEP secondary analysis anchored the achieved target in home rather than office readings. Among 7,681 participants with morning and evening home measurements taken 3–12 months after enrollment and 261 primary events over a median 3.43 years, adjusted HRs versus achieved home systolic BP ≥135 mm Hg were 0.62 (95% CI 0.42–0.90) for <125 mm Hg and 0.66 (0.47–0.94) for 125–130 mm Hg, with absolute risk reductions of 1.70% and 1.36% and a stroke HR of 0.36 (0.19–0.66); the primary safety outcome did not increase significantly in the lower categories (Ji 2026, PMID 42660976).

The same caution applies to both results: achieved BP within a randomized trial is a post-randomization variable, so neither “percentage time in range” nor an achieved home systolic band is a randomized treatment target. What they establish is that the home and ambulatory numbers corresponding to a validated office strategy are lower than the office numbers, which matters when an HHD target is transcribed between settings.

10. Benefit–harm framework

Benefit axis Harm/burden axis
Absolute cardiovascular risk Symptomatic hypotension
Stroke/HF susceptibility Syncope/falls context
HHD target-organ damage Electrolyte abnormality
Tolerated multi-drug regimen AKI/eGFR change
Long life expectancy Polypharmacy/adherence burden
Reliable measurement White-coat overtreatment

Orthostatic hypotension is itself associated with cardiovascular risk, but it can represent autonomic disease, frailty, medication effect or reverse causation (Fedorowski 2019, PMID 31713533).

Recent pooled participant-level benefit–harm work across six intensive-target trials emphasizes heterogeneity by target and patient characteristics rather than one universal threshold (Guo 2025, PMID 40902616).

Open questions

  • Does imaging-defined HHD identify a subgroup with greater absolute benefit from intensive control? (Deng 2023, PMID 37259845)
  • Which measurement protocol should anchor an HHD trial target: standardized office, home, 24-hour mean, nighttime BP or time in range? (Huang 2021, PMID 33390042; Zhang 2025, PMID 40249369; Ji 2026, PMID 42660976)
  • Can early kidney-function decline under intensive treatment be separated into hemodynamic adaptation versus injury with clinical consequences? (Peralta 2016, PMID 26762524)
  • How should severe frailty, multimorbidity and limited life expectancy change net-benefit estimates? (Warwick 2015, PMID 25880068; Li 2023, PMID 37099984)

References

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