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Purpose <p>Delayed cerebral ischemia (DCI) remains a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (aSAH). Despite identification of numerous predictors, risk remains variable even among patients with similar hemorrhage severity suggesting presence of unrecognized modifiers. One factor receiving little attention is intracranial arterial disease (ICAD): stenosis and calcification. We aim to examine their additive impacts to known modifiers.</p> Methods <p>We analyzed 526 patients with aSAH treated at a single, tertiary care center between 2015 and 2025. DCI was defined as new neurologic deficits and/or new cerebral infarction ≥ 48&#xa0;h from hemorrhage not explained by other etiologies. Stenosis (≥ 25% of luminal diameter) and calcification (CTA hyperdensity ≥ 100 HU) were assessed in all arteries including and distal to the petrous ICA on admission CTA. Multivariable logistic regressions were used to determine independent associations with DCI. For easy clinical applicability, ICAD was dichotomized as presence vs. absence.</p> Results <p>Among 526 patients with aSAH, 440 survived ≥ 48&#xa0;h and were included (median age = 56 IQR [45–64], 63.7% female). 132/440 (30.1%) developed DCI. DCI was associated with significantly worse outcomes (median mRS DCI: 4, No DCI 2, <i>p</i> &lt; 0.001). Stenosis, not calcification, was an independent predictor of DCI (aOR:3.556, 95%CI: 1.90–6.65, <i>p</i> &lt; 0.001). Vasospasm significantly correlated with DCI (OR:5.89, 95%CI: 3.62–9.57, <i>p</i> &lt; 0.001), and more common in patients with stenosis (aOR:2.391 95%CI: 1.240–4.608, <i>p</i> &lt; 0.001).</p> Conclusion <p>Pre-existing ICAD confers substantial, independent DCI risk after aSAH, enhancing rather than competing with traditional predictors. This suggests that baseline cerebrovascular integrity meaningfully predicts ischemic vulnerability following hemorrhage.</p>

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Pre-existing intracranial arterial stenosis independently predicts delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

  • 期刊论文

  • 发表日期：

    2026年7月2日

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  • Ross Moseley,
  • Ahmed Helal,
  • Mohamed Salem,
  • Yan Zhou,
  • Hayley Granberg,
  • Daron Assatoury,
  • Zach Folzenlogen,
  • Christopher Roark,
  • Joshua Seinfeld,
  • David Case

摘要

Purpose

Delayed cerebral ischemia (DCI) remains a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (aSAH). Despite identification of numerous predictors, risk remains variable even among patients with similar hemorrhage severity suggesting presence of unrecognized modifiers. One factor receiving little attention is intracranial arterial disease (ICAD): stenosis and calcification. We aim to examine their additive impacts to known modifiers.

Methods

We analyzed 526 patients with aSAH treated at a single, tertiary care center between 2015 and 2025. DCI was defined as new neurologic deficits and/or new cerebral infarction ≥ 48 h from hemorrhage not explained by other etiologies. Stenosis (≥ 25% of luminal diameter) and calcification (CTA hyperdensity ≥ 100 HU) were assessed in all arteries including and distal to the petrous ICA on admission CTA. Multivariable logistic regressions were used to determine independent associations with DCI. For easy clinical applicability, ICAD was dichotomized as presence vs. absence.

Results

Among 526 patients with aSAH, 440 survived ≥ 48 h and were included (median age = 56 IQR [45–64], 63.7% female). 132/440 (30.1%) developed DCI. DCI was associated with significantly worse outcomes (median mRS DCI: 4, No DCI 2, p < 0.001). Stenosis, not calcification, was an independent predictor of DCI (aOR:3.556, 95%CI: 1.90–6.65, p < 0.001). Vasospasm significantly correlated with DCI (OR:5.89, 95%CI: 3.62–9.57, p < 0.001), and more common in patients with stenosis (aOR:2.391 95%CI: 1.240–4.608, p < 0.001).

Conclusion

Pre-existing ICAD confers substantial, independent DCI risk after aSAH, enhancing rather than competing with traditional predictors. This suggests that baseline cerebrovascular integrity meaningfully predicts ischemic vulnerability following hemorrhage.