Letter: Blood Pressure Targets After Aneurysmal Subarachnoid Hemorrhage: Is Lower Better?

To the Editor: We read with interest the recent article by Eagles et al,1 "Blood Pressure Targets After Aneurysmal Subarachnoid Hemorrhage: Is Lower Better?," which explores the association between maximal systolic blood pressure (sBP) before aneurysm securing and 3-month functional outcomes. While the findings are intriguing, several important limitations deserve consideration before they can inform clinical practice. First, the principal rationale for lowering sBP in the immediate hours after aneurysmal rupture, before definitive surgical or endovascular treatment, is to prevent rebleeding.2 However, the study excluded patients who experienced rebleeding before aneurysm securing, thereby limiting its relevance to the population most likely to benefit from early blood pressure control. In addition, it remains unclear how brief reductions in blood pressure, often maintained for only a few hours before aneurysm treatment, could exert a meaningful influence on long-term neurological outcomes in aneurysmal subarachnoid hemorrhage, a condition characterized by delayed and multifactorial secondary brain injury. Furthermore, the reliance on a single maximal sBP value, without methodological safeguards against measurement artifact, raises concerns about data validity. This is particularly relevant in critically ill patients, where transient fluctuations and spurious readings are common, making interpretation of these values inherently difficult.3 Second, elevated sBP in the setting of aneurysmal subarachnoid hemorrhage often represents a compensatory response to raised intracranial pressure, helping to preserve cerebral perfusion.4 The study did not account for intracranial dynamics, such as the presence of intracranial hypertension or hydrocephalus, key clinical variables that can affect the safety of blood pressure reduction. Third, the exclusion of high-risk patients, including those with World Federation of Neurosurgical Societies (WFNS) grade 5 or chronic kidney disease (who are particularly vulnerable to hypoperfusion), and those with hypotension (sBP <90 mm Hg) may artificially minimize the harms of low sBP, biasing the findings toward more favorable outcomes and limiting the generalizability.4 Finally, and most critically, blood pressure management was not standardized or described. It remains unknown whether patients had lower sBP due to active pharmacologic intervention or simply as a reflection of baseline physiology. Lowering BP in a chronically hypertensive patient is vastly different from observing a spontaneously normotensive patient. Without distinguishing between these mechanisms, the clinical applicability of the 118 mm Hg cutoff is significantly weakened. While the authors mentioned the proven association of larger sBP variability with worse outcomes, they did not evaluate this important variable in their analysis. It is hardly the same to lower the sBP to 118 mm Hg from a baseline 240 mm Hg than from a baseline of 140 mm Hg.5 We appreciate the authors' effort to address a major clinical question but believe these limitations underscore the need for caution in interpretation and for prospective studies with standardized blood pressure lowering protocols that include higher-risk patient populations.