Early Blood Pressure Variability and Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage

Technical Summary: Early Blood Pressure Variability and Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage

Problem Statement
Aneurysmal subarachnoid hemorrhage (aSAH) presents a complex clinical challenge where optimal blood pressure management remains controversial. While maintaining adequate cerebral perfusion is critical, excessive fluctuations may be detrimental. Cerebral vasospasm, occurring in up to 70% of aSAH patients, is a major cause of delayed cerebral ischemia (DCI) and poor prognosis. Although risk factors such as smoking, hypertension, and hemorrhage severity are established, the specific relationship between early acute blood pressure variability (BPV) and the subsequent development of cerebral vasospasm within the first 24 hours of admission remains uncertain. This study investigates whether acute-phase BPV can serve as a predictive marker for cerebral vasospasm.

Methodology
This retrospective, single-center study analyzed data from 85 patients with aSAH admitted to the First People's Hospital of Lianyungang between May 2024 and May 2025. The cohort was divided into a vasospasm group (n=26) and a non-vasospasm group (n=59). Inclusion criteria required confirmed aSAH via CT, single anterior circulation aneurysm rupture, admission within 8 hours of symptom onset, and age between 18 and 75. Patients were excluded if they had secondary SAH, severe comorbidities (e.g., heart failure, renal failure), or incomplete data.

Blood pressure was recorded every 2 hours during the first 24 hours of admission using automated monitors. The study calculated multiple BPV metrics for both systolic (SBP) and diastolic (DBP) pressure, including:

• Mean, maximum, and minimum values.
• Range (ΔBP: max − min).
• Standard Deviation (SD).
• Coefficient of Variation (CV).
• Successive Variation (SV).

Cerebral vasospasm was diagnosed based on new-onset hypodensity on non-contrast head CT indicative of cerebral infarction in a vascular territory distinct from the aneurysm. Statistical analysis involved univariate and multivariate logistic regression to identify independent predictors, alongside Receiver Operating Characteristic (ROC) curve analysis to evaluate the predictive accuracy (AUC) of various BPV indices.

Key Results
The study found that all calculated BPV metrics were significantly associated with the development of cerebral vasospasm (P < 0.05).

• Comparative Analysis: Patients who developed vasospasm exhibited significantly higher maximum SBP and DBP, lower minimum SBP and DBP, and greater variability (higher SD, CV, and SV) compared to the non-vasospasm group. Conversely, the mean SBP was significantly lower in the vasospasm group.
• Regression Analysis: In multivariate logistic regression adjusted for confounders (smoking, hypertension, Modified Fisher Scale, creatinine, and albumin), most BPV indices remained significant predictors. Notably, SBPmax, SBPmin, SBP range, SBP SD, SBP CV, and SBP SV were independent risk factors. For DBP, mean, minimum, range, SD, CV, and SV were significant, though DBPmax lost significance after adjustment.
• Predictive Performance: ROC analysis demonstrated that variability indices generally outperformed mean blood pressure levels in predictive ability. The Coefficient of Variation (CV) and Successive Variation (SV) for both SBP and DBP showed the strongest performance. Specifically, SBP SV achieved the highest Area Under the Curve (AUC = 0.854), followed by SBP SD and SBP CV (both AUC = 0.835). DBP SD and SV also performed well (AUC = 0.847).
• Time-Dependent Trends: Time-dependent analysis revealed that patients developing vasospasm had significantly lower average SBP between 2 and 24 hours post-ictus compared to those without vasospasm.

Significance and Claims
The authors conclude that acute-phase blood pressure variability is significantly associated with cerebral vasospasm following aSAH. The study posits that BPV indices, particularly CV and SV, hold potential utility as hemodynamic markers for identifying patients at increased risk of vasospasm.

The paper suggests that these findings could inform clinical management by highlighting the importance of stabilizing blood pressure fluctuations during the critical first 24 hours, a period associated with early brain injury. However, the authors maintain a modest tone regarding clinical application. They explicitly state that these values should serve as general references rather than fixed targets, as individual patient management must be tailored to their overall clinical presentation.

Limitations and Future Directions
The study acknowledges several limitations inherent to its design:

• Retrospective Nature: The single-center, retrospective design limits the ability to fully account for confounders such as the intensity of antihypertensive treatment, sedation strategies, and the precise timing of aneurysm repair.
• Sample Size: The relatively small sample size (n=85) raises the possibility of model overfitting.
• Validation: The findings require validation in larger, prospective studies to establish clinical utility definitively.
• Scope: The analysis was restricted to the first 24 hours; longer-term monitoring was not assessed.

Ultimately, the paper frames BPV as a promising but unproven tool that warrants further investigation before it can be integrated into standard clinical protocols for preventing or predicting cerebral vasospasm.