Blood Pressure Targets After Stroke: How Low Is Too Low?

Acute hypertensive response (AHR) management during the acute phase of stroke is a complex decision-making process that directly influences patient outcomes.¹ Ischemic and hemorrhagic strokes have distinct and overlapping treatment requirements (Figure 1), with the goal to balance the risks of hemorrhagic transformation, hematoma expansion, and cerebral hypoperfusion, sometimes at the same time. Although numerous trials have investigated optimal blood pressure (BP) targets during the acute stroke phase, especially after hemorrhagic stroke, definitive consensus remains elusive, and clinical practice often reflects a variety of practice modalities, institutional protocols, and individualized patient care. This article synthesizes the current evidence base for managing BP during the acute stroke phase, including key findings from landmark trials and emerging concepts, such as BP variability and sustainability, collateral flow dynamics, and the evolving role of neuroimaging in guiding therapy.

Figure 1. Blood pressure management after stroke.
Abbreviation: SBP, systolic blood pressure.

AHR in Intracerebral Hemorrhage
In people with intracerebral hemorrhage (ICH), the relationship between AHR and poor functional outcomes is well-established and largely mediated by the risk of hematoma expansion, which occurs most frequently in the first few hours after symptom onset. Early studies laid the foundation for the hypothesis that aggressive BP reduction could mitigate hematoma expansion and improve functional outcomes. The pivotal Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage (INTERACT2, NCT00716079) trial included >2800 individuals who were randomized within 6 hours of ICH onset to a systolic BP target of <140 mm Hg or a more permissive target of <180 mm Hg.² Although the primary end point (death or major disability at 90 days) did not reach statistical significance, the trial results revealed a trend toward improved functional outcomes for individuals with systolic BP of <140 mm Hg. Secondary analyses suggested that individuals with intensive BP lowering had better health-related quality of life scores.²

The Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-II, NCT01176565) trial was designed to further refine these findings. ATACH-II used an even more aggressive BP target, randomizing >1000 individuals within 4.5 hours of ICH onset to systolic BP targets of 110 to 139 mm Hg or 140 to 179 mm Hg.³ The trial demonstrated no significant difference in 90-day morbidity or mortality between groups, and the intensive treatment arm experienced a higher rate of renal adverse events. These results highlighted the probable risks of excessive BP reduction, suggesting a “low target” below which further reduction may not yield additional benefit and could in fact cause harm, perhaps by compromising perihematomal perfusion in regions where cerebral autoregulation is impaired.

More recent analyses have also emphasized the importance of BP variability rather than static thresholds alone. Post hoc analysis of the INTERACT2 trial and data from more recent observational cohorts have consistently demonstrated that fluctuations in BP, particularly within the first 24 hours, are independently associated with worse outcomes, including increased rates of hematoma expansion, neurologic deterioration, and 90-day mortality.^4,5 This growing evidence has shifted the treatment focus for people with ICH from a fixed systolic BP target toward prioritizing stability and avoiding fluctuation, as evident in most recent pooled analysis of both major trials.⁶ To this end, continuous arterial BP monitoring and the use of short-acting intravenous (IV) agents (eg, clevidipine) have become essential components of optimal BP management in indviduals with ICH.^7,8 The Clevidipine for the Antihypertensive Treatment of Acute Intracerebral Hemorrhage (CLUTCH, NCT06402968) trial is designed to compare the proportion of participants with hypertensive ICH who can achieve and maintain target SBP within 60 minutes of treatment when treated with IV clevidipine vs alternative IV antihypertensive agents. This trial is expected to complete enrollment within the first half of 2026. 

AHR in Ischemic Stroke
The management of AHR in individuals with ischemic stroke, specifically in the context of reperfusion demand, adds an additional layer of complexity. Autoregulatory capacity (ie, the ability of an organ to maintain stable blood flow despite changes in perfusion pressure) is often impaired in the ischemic penumbra, making the tissue vulnerable to both hypoperfusion and hyperperfusion injuries. 

For individuals receiving IV thrombolysis (IVT), the current guidelines suggest that BP should be maintained at or below 180/105 mm Hg for at least the first 24 hours.⁹ This target helps balance the risk of hemorrhagic transformation with the need to ensure adequate cerebral perfusion. Continuous monitoring is essential, with BP checks every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours, and hourly until 24 hours posttreatment.

The Enhanced Control of Hypertension and Thrombolysis Stroke trial (ENCHANTED, NCT01422616) included >2000 predominantly Asian participants randomized to an intensive BP target of 130 to 140 mm Hg or the standard guideline-recommended target of <180 mm Hg after administration of IVT.¹⁰ Study results demonstrated a reduction in the incidence of any ICH in the intensive BP target group, but there was no significant difference in the primary outcome of disability or death at 90 days. This underscores that although intensive BP reduction may mitigate the increased risk of ICH after IVT, it does not necessarily translate into improved functional recovery, and the benefits of aggressive BP control should be considered against the risk of hypoperfusion in ischemic tissue.

For individuals undergoing endovascular thrombectomy (EVT) for large vessel occlusion, the evidence for agressive BP control is even more limited. In the Blood Pressure Target in Acute Stroke to Reduce Hemorrhage After Endovascular Therapy (BP-TARGET, NCT03160677) study, the first randomized trial to specifically address BP management after thrombectomy, a systolic BP target of 100 to 129 mm Hg was compared with a more permissive target of 130 to 185 mm Hg after successful reperfusion (defined as Thrombolysis in Cerebral Infarction [TICI] grade 2b or 3).¹¹ No significant reduction in radiographic intraparenchymal hemorrhage rate at 24 to 26 hours or improved functional outcomes were noted in the intensive BP-lowering group. A nonsignificant trend toward increased mortality within the first week after EVT was noted among the intensive BP-lowering group. 

Additional observational studies, such as Blood Pressure in Acute Stroke Evaluation (BEST)¹² and pooled analyses, have similarly failed to identify a clear benefit of intensive BP lowering after thrombectomy. Some data suggest that overly aggressive BP reduction in the setting of incomplete recanalization (TICI grade <3) may compromise collateral flow and exacerbate infarct progression.^13,14

Collateral Circulation
The cerebral collateral circulation concept is a crucial but often underappreciated factor in BP management after stroke. In individuals with robust collateral networks, a more aggressive BP reduction strategy may be tolerated without compromising perfusion, whereas in those with poor collaterals or large infarct cores, permissive hypertension may be essential to sustain blood flow and penumbral viability.¹⁵ Advanced imaging modalities, including CT perfusion and multiphase CT angiography, are increasingly being used to assess collateral status and guide individualized BP targets. For instance, an individual with a large ischemic core on CT perfusion and poor collaterals may benefit from a more conservative BP strategy (eg, maintaining systolic BP 140–160 mm Hg) to optimize collateral circulation, whereas an individual with successful TICI grade 3 reperfusion and minimal core expansion may safely tolerate systolic BP <140 mm Hg.¹⁶

BP Management in Ischemic Stroke
Many studies have assessed the broader landscape of BP management in people with ischemic stroke, including the Scandinavian Candesartan Acute Stroke Trial (SCAST, NCT00120003), the China Antihypertensive Trial in Acute Ischemic Stroke (CATIS, NCT01840072), and Blood Pressure Optimization for Stroke Secondary Prevention (BOSS). 

In SCAST, >2000 individuals with ischemic stroke and BP of ≥140 mm Hg were randomized to candesartan (an angiotensin-receptor blocker) or placebo within 30 hours of stroke onset. No benefit was found from cautious BP lowering; in fact, the evidence suggested potential harm with early BP lowering.¹⁷

Similarly, results of the CATIS study demonstratedno significant difference in death or major disability at 14 or 90 days between intensive BP lowering and standard care in participants with acute ischemic stroke who did not receive reperfusion therapy.¹⁸ CATIS-2 (NCT03479554 ) compared early (24–48 hours) vs delayed (starting on day 8) antihypertensive therapy to achieve a BP target <140/90 mm Hg in participants with ischemic stroke who did not receive IVT of EVT.¹⁹ The study results showed no benefit from early lowering of BP, and showed evidence of harm in individuals without a previous known history of hypertension. 

The BOSS study, conducted in China, evaluated ambulatory and home-measured systolic BP parameters for 7 days after ischemic stroke or transient ischemic attack and their relationship with clinical outcomes, such as modified Rankin Scale score, stroke recurrence, and vascular events. Study results demonstrated that a decrease in the acute‐phase BP was associated with favorable clinical outcomes in people with stroke with high admission BP, especially when evaluating a whole BP trajectory rather than a singular reading in the acute phase. This observation emphasizes the importance of using BP trajectory data over the acute phase (ie, 7 days) in the prediction of clinical outcomes in people with stroke.²⁰

These studies collectively suggest that routine aggressive BP lowering in unselected individuals with ischemic stroke, particularly those not undergoing reperfusion therapy, may not improve outcomes and could pose risks, reinforcing the principle of individualized management and the need for judicious timing and patient selection.

Permissive Hypertension
The concept of permissive hypertension (Figure 2) in stroke care has gained traction, particularly for individuals not eligible for thrombolysis or thrombectomy. Current guidelines often recommend tolerating systolic BP up to 220 mm Hg and diastolic BP up to 120 mm Hg in the first 24 to 48 hours after stroke, provided there are no other compelling indications for BP reduction, such as use of IVT, successful reperfusion, myocardial infarction, aortic dissection, or hypertensive encephalopathy.⁹ However, if BP exceeds these thresholds, a cautious reduction of 15% over the first 24 hours is generally recommended to avoid abrupt changes that could precipitate hypoperfusion injury, especially in individuals who did not receive reperfusion therapies.²¹

Figure 2. Permissive hypertension vs intensive blood pressure (BP) control.
Abbreviation: TICI, Thrombolysis in Cerebral Infarction.

Conclusion
AHR management after stroke is a dynamic process that requires careful integration of clinical trial evidence, pathophysiologic principles, imaging findings, and patient-specific factors. For individuals with ICH and systolic BP <220 mm Hg on admission, a systolic BP target of <140 mm Hg appears safe and reasonable, although benefits beyond this threshold remain unproven, and excessive lowering below 110 mm Hg should be avoided. In people with ischemic stroke, a systolic BP target of <180 mm Hg is standard in the context of reperfusion therapies, with no robust evidence supporting aggressive lowering below 130 mm Hg in most cases, at least in the acute early phase. For individuals not undergoing reperfusion, permissive hypertension up to 220/120 mm Hg is acceptable in the first 24 hours, with a gradual and strategic approach to reduction when necessary. Avoiding BP fluctuation, performing continuous monitoring, and using IV agents with rapid onset and short half-lives are essential to ensure stable cerebral perfusion during the critical early hours and days poststroke. Future research should focus on refining individualized BP targets on the basis of imaging biomarkers, cerebral autoregulation profiles, and dynamic hemodynamic assessments, moving beyond rigid thresholds to a more tailored, patient-centered approach that optimizes outcomes while minimizing harm.