# Calcification of the Internal Carotid Artery and Its Influence on the Severity of Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

## TL;DR

This study finds that calcification in the carotid artery may protect against cerebral vasospasm but is linked to worse outcomes in brain aneurysm patients.

## Contribution

The study identifies carotid siphon calcification as a novel protective factor against cerebral vasospasm and a risk factor for poor functional recovery.

## Key findings

- CSC is an independent predictor of reduced angiographic cerebral vasospasm severity and delayed ischemic neurological deficit.
- Higher levels of CSC correlate with worse 6-month functional outcomes in aneurysmal subarachnoid hemorrhage patients.
- CSC does not significantly affect transcranial Doppler-measured cerebral vasospasm presence or severity.

## Abstract

Background/Objectives: Cerebral vasospasm (CV) is a serious complication of aneurysmal subarachnoid hemorrhage (aSAH). Carotid siphon calcification (CSC) has been associated with a reduced risk of CV. This study investigates the influence of CSC on the clinical and radiographic severity of CV and functional outcome of aSAH. Methods: A total of 475 patients with aSAH treated at the University Hospital Essen (2008–2016) were analyzed retrospectively. CSC was assessed using the Woodcock score. Study endpoints were the CV severity in digital subtraction angiography, presence of CV in transcranial Doppler (TCD) ultra-sonography, occurrence of delayed ischemic neurological deficit (DIND) and the functional outcome at 6 months measured with the modified Rankin scale. Results: CSC was confirmed as an independent predictor for the occurrence (aOR 0.76; 95% CI 0.60–0.97; p = 0.025) and severity (RC −0.14; 95% CI −0.24 to −0.04; p = 0.006) of angiographic CV and development of DIND (aOR 0.76; 95% CI 0.59–0.98; p = 0.034). Only the duration (in days: RC −0.43; 95% CI −0.77 to −0.10; p = 0.010) but not the presence (aOR 0.87; 95% CI 0.68 to 1.11; p = 0.265) and severity (cerebral blood flow, in cm/s: RC +1.57; 95% CI −7.45 to +10.58; p = 0.731) of TCD CV was associated with CSC. Finally, the increasing levels of CSC were related to poorer 6-month functional outcome (RC +0.12; 95% CI +0.05 to +0.18; p < 0.001). Conclusions: CSC appears to be protective against angiographic CV and DIND, but correlates with worse overall outcome, suggesting that atherosclerosis, represented by CSC, affects cerebrovascular regulation and overall prognosis. We suggest careful evaluation of primary imaging studies for markers of atherosclerosis to identify patients at risk for CV and patients with low risk for CV but still at high risk for poor outcome.