Publication

• Title: HIgh versus STAndard blood Pressure target in hypertensive high-risk patients undergoing elective major abdominal surgery: the HISTAP multicentre randomised clinical trial
• Acronym: HISTAP
• Year: 2026
• Journal published in: Intensive Care Medicine
• Citation: Cecconi M, Cortegiani A, Noto A, Sotgiu G, Antonelli M, Anderloni M, et al. HIgh versus STAndard blood Pressure target in hypertensive high-risk patients undergoing elective major abdominal surgery: the HISTAP multicentre randomised clinical trial. Intensive Care Med. 2026.

Context & Rationale

• Background

  • Major postoperative complications after abdominal surgery are common and are associated with mortality, prolonged hospital stay, escalation of care, and long-term functional impairment.
  • Intraoperative hypotension has been repeatedly associated with postoperative acute kidney injury, myocardial injury, stroke, delirium, and death.
  • Much of the pre-HISTAP evidence was observational, so it could not prove that raising arterial pressure itself improves outcomes.¹
  • Consensus statements support avoiding sustained low intraoperative MAP, particularly below approximately 60–65 mmHg, but acknowledge uncertainty around higher targets and patient-specific thresholds.²
  • Chronic hypertension is physiologically important because renal, cerebral, and coronary autoregulation may be shifted to higher pressures.
  • Observational work suggested that hypertensive patients may require less cumulative time below any given MAP threshold to incur the same increase in 30-day mortality risk as non-hypertensive patients.³
  • Previous randomised perioperative blood-pressure trials gave mixed results, differing in patient risk, target definition, monitoring intensity, fluid strategy, and outcome selection.
• Research Question/Hypothesis

  • HISTAP tested whether a fixed higher intraoperative MAP target would improve postoperative outcomes in a deliberately selected high-risk hypertensive surgical population.
  • The experimental strategy targeted MAP ≥80 mmHg.
  • The control strategy targeted MAP ≥65 mmHg.
  • The trialists hypothesised that higher intraoperative MAP, delivered with continuous haemodynamic monitoring and protocolised fluid therapy, would reduce a composite of 30-day mortality and major postoperative organ dysfunction.
  • The published protocol used a fixed MAP threshold rather than an autoregulation-derived, ambulatory-pressure-derived, or relative-to-baseline target, prioritising clinical implementability over physiological individualisation.⁴
• Why This Matters

  • Blood pressure is one of the most actively manipulated intraoperative variables.
  • A simple higher MAP target could be rapidly adopted if it prevented kidney, cardiovascular, respiratory, neurological, or infective complications.
  • A higher target may also increase vasopressor exposure, transfusion behaviour, haemodynamic complexity, and treatment burden.
  • The key clinical distinction is between preventing harmful hypotension and actively driving arterial pressure above conventional thresholds in all selected patients.
  • HISTAP therefore tested whether “more pressure” is beneficial when fluids and haemodynamic monitoring are already protocolised.

Design & Methods

• Research Question: In high-risk hypertensive patients aged ≥60 years undergoing elective major abdominal surgery, does targeting intraoperative MAP ≥80 mmHg, compared with MAP ≥65 mmHg, reduce postoperative major organ dysfunction and 30-day mortality?
• Study Type: Multicentre, randomised, stratified, assessor-blinded, investigator-initiated clinical trial conducted in 18 Italian centres between March 2023 and April 2025; the intervention was delivered in the operating theatre from induction of anaesthesia to awakening in theatre.
• Population:
  • Adults aged ≥60 years.
  • Required chronic hypertension treated with stable home therapy at the preoperative visit.
  • Scheduled for elective major abdominal surgery by laparoscopic, robotic, or open approach.
  • Expected surgical duration had to be at least 3 hours.
  • Invasive arterial and haemodynamic monitoring had to be required as judged by the attending anaesthesiologist.
  • At least one additional high-risk criterion was required.
  • High-risk criteria included ASA III–IV status, coronary artery disease, peripheral vascular disease, treated heart failure, ejection fraction <30%, moderate-to-severe diastolic dysfunction or chronic hypertensive cardiomyopathy, moderate-to-severe valvular disease, COPD, diabetes, morbid obesity, hypoalbuminaemia, low anaerobic threshold, or exercise tolerance ≤6 METs.
  • Key exclusions included refusal of consent, pregnancy, severe chronic kidney disease with GFR <30 mL/min/1.73 m² or renal replacement therapy, acute or decompensated heart failure or acute coronary syndrome within 30 days, urgent or time-critical surgery, neurosurgery, aortic or renal vascular surgery, planned liver surgery, palliative surgery, and ASA V status.
  • Of 1,040 screened patients, 636 were randomised and 630 underwent surgery and were included in the final intention-to-treat analysis.
• Intervention:
  • Intraoperative MAP target ≥80 mmHg.
  • The intervention period ran from anaesthesia induction to awakening in theatre.
  • Hypotension was defined as MAP below the assigned target for more than 1 minute.
  • All patients received continuous haemodynamic monitoring based on invasive arterial waveform analysis.
  • Pressure management used ephedrine 2.5 mg boluses, etilefrine 1 mg boluses, or continuous noradrenaline infusion at clinician discretion.
  • Maintenance crystalloid fluid was 5 mL/kg/h for laparotomy and 3 mL/kg/h for laparoscopy, adjustable if judged inadequate.
  • Fluid challenges were guided by pulse pressure variation or stroke volume variation during laparotomy.
  • Mini-fluid challenge testing was used during laparoscopy, atrial fibrillation, or other conditions where dynamic indices were unreliable.
• Comparison:
  • Intraoperative MAP target ≥65 mmHg.
  • The same continuous haemodynamic monitoring, maintenance fluid strategy, functional haemodynamic testing, and rescue drug options were used.
  • Interventions were triggered at the lower MAP threshold.
  • Other anaesthetic, surgical, postoperative, and chronic antihypertensive management followed local practice and contemporary guideline recommendations.
• Blinding: Intraoperative blinding was not feasible because anaesthesiologists had to know the assigned MAP target. Postoperative outcome assessors and statisticians were blinded to allocation, and postoperative data entry was separated from the randomisation and intraoperative allocation processes.
• Statistics: A total of 636 patients was required to detect a 12.5% absolute reduction in the primary composite outcome, assuming a 41% event rate in the control group, with 90% power at a two-sided 5% significance level and 5% anticipated dropout.⁴ The primary analysis used the intention-to-treat population of randomised patients who underwent surgery. The primary outcome was analysed with an unadjusted chi-squared test, reporting absolute risk difference and relative risk with 95% confidence intervals; time-to-event analyses used Cox models. Missing primary and secondary outcome data were not imputed.
• Follow-Up Period: Major organ dysfunction was assessed from postoperative day 1 to day 7; mortality and follow-up were assessed to day 30. Troponin, creatinine, and urine output were mandatory for the first 3 postoperative days and were collected to day 7 thereafter when clinically indicated.

Key Results

This trial was not stopped early. It completed planned randomisation of 636 patients; 6 patients allocated to MAP ≥80 mmHg were excluded because surgery was cancelled after randomisation for technical reasons unrelated to the study protocol, leaving 315 patients in each group for the final intention-to-treat analysis.

Outcome	MAP ≥80 mmHg	MAP ≥65 mmHg	Effect	p value / 95% CI	Notes
Achieved mean intraoperative MAP	88 ± 9 mmHg	77 ± 7 mmHg	Mean difference 11 mmHg	P<0.001	Clear separation, although the control group averaged well above 65 mmHg.
Primary composite outcome 30-day mortality or ≥1 major organ dysfunction by day 7	120/315 (38.1%)	154/315 (48.9%)	RR 0.78 Absolute difference -10.8%	95% CI 0.65 to 0.93; P=0.006 Absolute difference 95% CI -18.5 to -3.1	Primary endpoint met.
Time-to-primary composite event	Lower cumulative probability	Higher cumulative probability	HR 0.72	95% CI 0.57 to 0.92; log-rank P=0.004	Consistent with the primary binary result.
Acute kidney injury AKIN stage ≥1	74/315 (23.5%)	106/315 (33.7%)	RR 0.70 Absolute difference -10.1%	95% CI 0.54 to 0.90; P=0.005 Absolute difference 95% CI -17.2 to -3.2	Main driver of the primary composite result.
AKIN stage 1	67/315 (21.3%)	94/315 (29.8%)	RR 0.71 Absolute difference -8.57%	95% CI 0.54 to 0.94; P=0.01 Absolute difference 95% CI -15.35 to -1.79	Mild AKI reduction.
AKIN stage 2	17/315 (5.4%)	35/315 (11.1%)	RR 0.49 Absolute difference -5.71%	95% CI 0.28 to 0.85; P=0.009 Absolute difference 95% CI -9.99 to -1.44	Moderate AKI reduction.
AKIN stage 3	4/315 (1.3%)	4/315 (1.3%)	RR 1.00 Absolute difference 0.00%	95% CI 0.25 to 3.96; P=1.00	No difference in severe AKI.
Cardiovascular major events	18/315 (5.7%)	17/315 (5.4%)	RR 1.06	95% CI 0.56 to 2.02; P=0.86	No cardiovascular-event reduction.
Myocardial injury after non-cardiac surgery	14/315 (4.4%)	10/315 (3.2%)	RR 1.40	95% CI 0.63 to 3.10; P=0.41	No signal of myocardial protection.
Respiratory major events	23/315 (7.3%)	34/315 (10.8%)	RR 0.68	95% CI 0.41 to 1.12; P=0.13	Direction favoured MAP ≥80 mmHg, but did not meet conventional statistical significance.
Acute respiratory distress or hypoxaemia	15/315 (4.8%)	28/315 (8.9%)	RR 0.54	95% CI 0.29 to 0.98; P=0.04	Component-level signal; not adjusted for multiplicity.
Sepsis or septic shock	21/315 (6.7%)	20/315 (6.3%)	RR 1.05	95% CI 0.58 to 1.90; P=0.87	No infective-event difference.
Neurological major events	3/315 (1.0%)	10/315 (3.2%)	RR 0.30	95% CI 0.08 to 1.08; P=0.09	Few events; imprecise estimate.
30-day mortality	8/315 (2.5%)	6/315 (1.9%)	RR 1.33	95% CI 0.47 to 3.80; P=0.59	No mortality benefit; event rate was low.
Hospital stay	6 days [4–11]	7 days [5–11]	Median difference not reported	P=0.01	Statistically shorter stay; clinical magnitude modest.
ICU stay	1 day [1–3]	1 day [1–4]	Median difference not reported	P=0.86	No ICU length-of-stay difference.
ICU readmission	1/315 (0.3%)	5/315 (1.6%)	RR 0.20	95% CI 0.02 to 1.70; P=0.11	Rare event; imprecise estimate.
Need for reoperation	13/315 (4.2%)	19/315 (6.1%)	RR 0.68	95% CI 0.34 to 1.35; P=0.26	No significant difference.
Noradrenaline infusion	127/315 (40.3%)	71/315 (22.5%)	Not reported	P<0.001	Substantially greater vasopressor exposure with MAP ≥80 mmHg.
Time spent on noradrenaline among recipients	64% [33–81]	48% [23–69]	Median difference not reported	P=0.005	Higher treatment intensity in the high-MAP group.
Highest noradrenaline dose among recipients	0.16 [0.10–0.25] micrograms/kg/min	0.12 [0.10–0.25] micrograms/kg/min	Median difference not reported	P=0.046	Reported as tartrate-equivalent dosing.
Patients receiving ≥1 unit packed red cells	37/315 (11.8%)	21/315 (6.7%)	Not reported	P=0.03	Potential treatment-burden signal; median blood loss was 200 mL [100–400] vs 200 mL [100–300].
Major intraoperative bleeding ≥4 units red cells	1/315 (0.32%)	1/315 (0.32%)	No difference	P=0.99	Only prespecified adverse event.

• The primary composite was significantly reduced with MAP ≥80 mmHg, but the clinical signal was driven mainly by fewer AKIN stage 1–2 acute kidney injuries.
• The intervention achieved meaningful pressure separation: mean intraoperative MAP 88 ± 9 mmHg versus 77 ± 7 mmHg.
• The higher target increased treatment intensity: noradrenaline infusion 40.3% versus 22.5%, and red-cell transfusion 11.8% versus 6.7%.

Internal Validity

• Randomisation and Allocation: Randomisation was centralised through REDCap, used 1:1 allocation, block size 6, and stratification by age ≥75 years and preoperative systolic arterial pressure ≥140 mmHg. This provides strong allocation concealment.
• Dropout and Post-Randomisation Exclusions: Six patients, all initially assigned to MAP ≥80 mmHg, were excluded because surgery was cancelled after randomisation. This is a small post-randomisation exclusion, but the reason was unrelated to the study intervention and the final analysed groups were balanced at 315 patients each.
• Missing Data: Primary and secondary outcome data were obtained for all patients who underwent surgery. No imputation was performed.
• Performance Bias: Intraoperative blinding was impossible. Anaesthesiologists knew the assigned target and may have modified vasopressor, transfusion, anaesthetic depth, or rescue decisions in ways beyond MAP alone.
• Detection Bias: Postoperative outcome assessors were blinded. The dominant outcome component, AKI, was defined by AKIN creatinine and urine-output criteria, reducing subjective ascertainment bias.
• Protocol Adherence: No true major protocol violations were reported. One patient in the Treatment group was initially flagged because the target blood pressure was not maintained throughout the procedure, but this was reviewed and not considered a protocol violation.
• Baseline Characteristics: Groups were broadly comparable: median age 73 versus 74 years; age ≥75 years 45.1% versus 47.6%; ASA III 69.2% versus 72.1%; RCRI >2 7.6% versus 7.6%; chronic kidney disease 7.0% versus 7.0%; serum creatinine 0.91 [0.77–1.13] versus 0.90 [0.76–1.11] mg/dL.
• Severity of Illness: The trial successfully enriched for risk, with a control primary composite event rate of 48.9%. However, 30-day mortality was only 1.9–2.5%, meaning the trial is informative for postoperative organ dysfunction rather than survival.
• Heterogeneity: The trial included colorectal, pancreatic, urological, gynaecological, oesophagogastric, and other abdominal surgery, using laparoscopic, robotic, and open approaches. This improves pragmatic relevance but introduces variation in surgical stress, bleeding risk, postoperative pathways, and anaesthetic practice.
• Timing: The intervention was delivered during the biologically relevant intraoperative exposure window from induction to awakening. Postoperative blood pressure was not protocolised, so renal outcomes may still have been influenced by postoperative hypotension or ward-level haemodynamics.
• Dose: MAP ≥80 mmHg is simple and reproducible, but not personalised. It does not account for baseline ambulatory pressure, renal autoregulation, pulse pressure, cardiac output, venous pressure, arterial stiffness, or organ-specific perfusion thresholds.
• Separation of the Variable of Interest: Mean intraoperative MAP was 88 ± 9 mmHg versus 77 ± 7 mmHg, a between-group difference of 11 mmHg. Median MAP remained separated at recorded intraoperative time points, although the control group’s achieved MAP was substantially above its nominal ≥65 mmHg target.
• Fluid Balance Separation: Fluids were well balanced: fluid balance 1681 mL [998–2502] versus 1630 mL [945–2561]; crystalloid 2500 mL [1800–3500] versus 2500 mL [1700–3600]; blood loss 200 mL [100–400] versus 200 mL [100–300]; diuresis 500 mL [300–790] versus 500 mL [300–750]. This supports pressure and vasoactive exposure as the main treatment separation rather than fluid volume.
• Key Delivery Aspects: Continuous arterial waveform-derived haemodynamic monitoring and protocolised fluid therapy were central to the intervention. The result should be interpreted as a combined pressure-plus-haemodynamic-management strategy, not simply as a vasopressor-only strategy.
• Crossover: No meaningful crossovers were reported; the per-protocol population coincided with the intention-to-treat population.
• Adjunctive Therapy Use: The high-MAP group received more noradrenaline infusion (40.3% vs 22.5%), spent more intraoperative time on noradrenaline among recipients (64% [33–81] vs 48% [23–69]), received higher peak noradrenaline doses (0.16 [0.10–0.25] vs 0.12 [0.10–0.25] micrograms/kg/min), received more ephedrine (5 [0–20] vs 0 [0–12.5] mg), and received more red-cell transfusion (11.8% vs 6.7%). These are part of the intervention strategy but complicate attribution to MAP alone.
• Outcome Assessment: The primary endpoint was a broad composite of 30-day mortality and renal, respiratory, cardiovascular, neurological, and infective dysfunction by day 7. It captured global postoperative morbidity but was driven mainly by AKI, especially AKIN stage 1 and 2.
• Renal Outcome Robustness: The trial oversight committee requested renal classification using KDIGO as well as AKIN; the classifications were concordant. In a post hoc AKI model, Treatment group assignment remained associated with lower AKI risk: HR 0.58; 95% CI 0.40 to 0.83.
• Statistical Rigor: The protocol and SAP were published before trial completion and no revisions were reported.⁴ The primary analysis matched the SAP. Component and secondary outcomes were not adjusted for multiplicity and should be interpreted supportively.

Conclusion on Internal Validity: Internal validity is strong for the pragmatic question of whether a fixed high intraoperative MAP target, delivered with continuous haemodynamic monitoring and protocolised fluids, reduces the prespecified composite outcome in this selected population. Internal validity is more moderate for the mechanistic claim that MAP itself, rather than vasopressor exposure, transfusion behaviour, postoperative events, or unmeasured flow variables, caused the observed renal benefit.

External Validity

• Population Representativeness: HISTAP enrolled a highly selected group: older patients, treated hypertension, elective major abdominal surgery, planned invasive haemodynamic monitoring, and at least one additional postoperative-risk criterion.
• Screening and Selection: Of 1,040 screened patients, 404 were excluded: 83 did not meet eligibility criteria, 234 had no adjunctive severity criterion, and 87 had at least one exclusion criterion.
• Surgical Mix: The trial included laparoscopic, robotic, and open surgery, with colorectal surgery comprising approximately 41–42%, urological surgery 22.5–25.1%, and pancreatic surgery 15.3–17.9% of cases.
• Centre and System Context: The trial was conducted exclusively in Italian centres where pulse-contour haemodynamic monitoring for this high-risk population is recommended by national guidance and was already embedded in routine practice.
• Monitoring Dependency: The findings should not be transferred directly to settings without arterial waveform analysis, protocolised fluid algorithms, reliable arterial waveform quality control, and teams familiar with dynamic preload assessment.
• Patient Groups Not Answered: The trial does not directly apply to normotensive patients, younger patients, emergency surgery, vascular surgery, neurosurgery, liver surgery, severe chronic kidney disease, ASA V patients, palliative surgery, or patients not selected for invasive monitoring.
• Outcome Generalisability: The most defensible generalisation is prevention of mild-to-moderate postoperative AKI. The trial does not establish improved survival, dialysis-free survival, cardiovascular protection, neurological protection, long-term renal recovery, or functional recovery.
• Resource-Limited Settings: Generalisability is limited where continuous haemodynamic monitoring, blinded postoperative assessment, standardised postoperative laboratory surveillance, or protocolised fluid therapy cannot be reproduced.

Conclusion on External Validity: External validity is good for selected older hypertensive high-risk patients undergoing elective major abdominal surgery in well-resourced perioperative systems using continuous haemodynamic monitoring. It is limited for broader surgical populations and for hospitals where the monitoring and fluid-management infrastructure cannot be replicated.

Strengths & Limitations

• Strengths:
  • Large multicentre randomised trial in a clinically important perioperative population.
  • Focused on high-risk hypertensive patients, a biologically plausible subgroup for higher pressure targets.
  • Clear intraoperative MAP separation: 88 ± 9 versus 77 ± 7 mmHg.
  • Both groups received continuous haemodynamic monitoring and structured fluid algorithms.
  • Blinded postoperative outcome assessment and blinded statistical analysis.
  • Central electronic randomisation with allocation concealment.
  • Published protocol and SAP, with no reported revisions.
  • Near-complete follow-up among patients who underwent surgery.
  • Useful implementation data on vasopressors, fluid balance, transfusion, operative duration, discharge destination, and adverse events.
• Limitations:
  • Open-label intraoperative care, creating unavoidable performance-bias risk.
  • Broad composite primary endpoint, driven mainly by AKIN stage 1–2 AKI.
  • No significant reduction in mortality, cardiovascular events, severe AKI, ICU stay, reoperation, or major intraoperative bleeding.
  • Control-group achieved mean MAP was 77 ± 7 mmHg, so the trial compared approximately 88 versus 77 mmHg rather than sustained 80 versus 65 mmHg physiology.
  • Higher MAP required more noradrenaline, more ephedrine, and more red-cell transfusion.
  • Postoperative blood pressure management was not protocolised.
  • Postoperative nephrotoxic exposures and AKI-management pathways were not collected or standardised.
  • Vasopressor choice was flexible, so the effect cannot be attributed exclusively to MAP.
  • Haemodynamic data were systematically recorded at 10-minute intervals, limiting detailed analysis of MAP variability and hypotension burden.
  • Conducted exclusively in Italy, limiting international and resource-context generalisability.

Interpretation & Why It Matters

• Clinical meaning

  • HISTAP supports considering MAP ≥80 mmHg in selected high-risk hypertensive patients undergoing elective major abdominal surgery when continuous haemodynamic monitoring and protocolised fluid management are already in place.
  • It should not be simplified to “MAP 80 for everyone”.
• What improved

  • The main improvement was renal: AKI fell from 33.7% to 23.5%.
  • The reduction was concentrated in AKIN stage 1 and stage 2 events.
  • Severe AKI was unchanged at 1.3% in both groups.
• What did not improve

  • There was no demonstrated reduction in 30-day mortality.
  • There was no demonstrated reduction in cardiovascular major events.
  • There was no demonstrated reduction in ICU stay or need for reoperation.
• Practice implication

  • The result is most applicable to a monitored, protocolised perioperative haemodynamic strategy.
  • Implementation requires attention to vasopressor exposure, transfusion practice, fluid responsiveness, postoperative hypotension, and renal-protective postoperative care.
• Scientific implication

  • HISTAP strengthens the argument that high-risk hypertensive patients may be a subgroup in whom avoiding lower intraoperative MAPs protects the kidney.
  • It does not prove that pressure alone is the sufficient therapeutic target.

Controversies & Other Evidence

• The primary endpoint was positive, but the clinically strongest signal is narrower than the composite suggests. The primary composite fell from 48.9% to 38.1%, but severe AKI, cardiovascular events, ICU stay, reoperation, and mortality were not reduced. The most defensible clinical claim is fewer mild-to-moderate AKI events.
• The control group was not “low pressure” care. The control group target was MAP ≥65 mmHg, but achieved mean MAP was 77 ± 7 mmHg. HISTAP therefore tested a higher target against already well-maintained MAP, not against prolonged hypotension.
• The treatment burden is part of the result. The high-MAP group received noradrenaline more often (40.3% vs 22.5%), spent more time on noradrenaline among recipients (64% vs 48%), received more ephedrine, and received more red-cell transfusion (11.8% vs 6.7%). These exposures may be acceptable if renal protection is valued, but they should not be treated as clinically neutral.
• MAP is not organ perfusion. Raising arterial pressure with vasopressors may improve renal perfusion pressure in some patients, but can also affect cardiac output, venous pressure, renal microcirculation, and regional blood flow. HISTAP did not fully capture these mechanisms.
• INPRESS remains the closest positive predecessor. INPRESS reported fewer postoperative organ dysfunction events with individualised systolic blood-pressure management in high-risk surgical patients: 38% versus 51%; relative risk reduction 27%; P=0.03.⁵ HISTAP differs by using a fixed MAP threshold, enrolling a hypertensive-only population, and embedding continuous haemodynamic monitoring and protocolised fluids in both groups.
• Large contemporary trials have not consistently supported higher or individualised pressure targets. POISE-3 reported similar 30-day major vascular complications with a hypotension-avoidance strategy versus a hypertension-avoidance strategy: 520/3742 (13.9%) versus 524/3748 (14.0%); HR 0.99; 95% CI 0.88 to 1.12; P=0.92.⁶ BP-CARES found that MAP ≥80 mmHg did not reduce 30-day cardiovascular events compared with conventional management: 107/739 (14.5%) versus 100/738 (13.6%); RR 1.07; 95% CI 0.83 to 1.38; P=0.61.⁷
• Individualised or proactive strategies have also disappointed in broader major-surgery populations. IMPROVE-multi found no reduction in its 7-day composite outcome with individualised perioperative blood pressure management: 190/567 (33.5%) versus 173/567 (30.5%); RR 1.10; 95% CI 0.93 to 1.30; P=0.31.⁸ PRETREAT found no improvement in 6-month WHODAS disability scores with proactive risk-stratified MAP targets: 17.7 ± 20.1 versus 18.2 ± 20.5; mean difference -0.5; 95% credible interval -1.9 to 0.9.⁹
• Fluid strategy is a major co-intervention. HISTAP achieved similar fluid balance between groups, approximately +1.6 litres. This matters because RELIEF showed that excessively restrictive fluid therapy in major abdominal surgery can increase AKI despite reducing fluid administration.¹⁰
• Guideline context remains cautious. The 2025 ESAIC statement recommends basing intraoperative arterial-pressure management on MAP and keeping intraoperative MAP above 60 mmHg; it does not mandate a universal high-MAP target for all adults having non-cardiac surgery.¹¹
• The broader literature argues against blood-pressure-centred thinking alone. Contemporary synthesis emphasises that higher pressure targets can reduce hypotension exposure yet fail to improve patient-centred outcomes, because hypotension may be a marker of vulnerability, postoperative hypotension is often unrecognised, vasopressors may have microcirculatory trade-offs, and fixed targets do not reflect organ-specific autoregulation.¹²¹³
• Systematic review evidence remains heterogeneous. A 2025 systematic review of randomised blood-pressure optimisation strategies found that many interventions reduce hypotension exposure, but there are few consistent data showing prevention of postoperative complications across intervention classes.¹⁴

Summary

• HISTAP randomised 636 high-risk hypertensive patients undergoing elective major abdominal surgery to MAP ≥80 mmHg or MAP ≥65 mmHg; 630 underwent surgery and were analysed.
• The high-MAP strategy reduced the primary composite outcome: 38.1% versus 48.9%; RR 0.78; 95% CI 0.65 to 0.93; P=0.006.
• The benefit was mainly renal: AKI fell from 33.7% to 23.5%, driven by reductions in AKIN stage 1 and stage 2 events.
• Severe AKI, 30-day mortality, cardiovascular events, ICU stay, and need for reoperation were not significantly reduced.
• The high-MAP strategy required more noradrenaline, more ephedrine, and more red-cell transfusion.

Overall Takeaway

HISTAP is an important perioperative haemodynamics trial because it shows that a fixed higher intraoperative MAP target can reduce a composite postoperative organ dysfunction endpoint in carefully selected high-risk hypertensive abdominal surgery patients, largely through fewer mild-to-moderate AKI events. It should shape practice as a targeted, monitored haemodynamic strategy for selected patients, not as a universal mandate to target MAP ≥80 mmHg in all non-cardiac surgery.

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