Blood pressure variability (BPV) has emerged as a prognostic hemodynamic marker in acute ischemic stroke (AIS), with observational studies consistently associating early systolic fluctuations with infarct progression, neurological deterioration, hemorrhagic transformation, and worse functional outcomes. Whether BPV directly mediates injury or primarily reflects underlying stroke severity and physiological instability remains uncertain. Biologically plausible mechanisms exist in the context of impaired cerebral autoregulation, where systemic pressure fluctuations may translate into cerebral perfusion instability, particularly in the ischemic penumbra and during reperfusion. Despite consistent associations, clinical interpretation of BPV is limited by substantial heterogeneity in measurement methods, monitoring frequency, and analytic approaches. Most studies derive BPV from intermittently sampled oscillometric measurements, which may miss rapid fluctuations and are susceptible to artifacts. BPV is also strongly influenced by stroke severity, treatment intensity, and hemodynamic interventions, raising the possibility that observed variability reflects disease burden rather than an independent injury mechanism. This review summarizes evidence linking BPV to outcomes in AIS, examines methodological variability in its measurement, and highlights limitations restricting its translation into standardized monitoring or therapeutic strategies. BPV should be interpreted as a prognostic marker of disease severity rather than a confirmed causal mediator of injury, and its role as a modifiable treatment target remains unestablished. The HOPE randomized trial provided the first evidence that a reperfusion-guided, individualized systolic BP strategy may improve functional outcomes after endovascular thrombectomy (EVT), though findings require confirmation in larger trials.
Shah et al. (Tue,) studied this question.