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Table 1 Patients demographics and clinical presentation of the aneurysms studied for lipid accumulation and oxidized lipids

From: Lipid accumulation, lipid oxidation, and low plasma levels of acquired antibodies against oxidized lipids associate with degeneration and rupture of the intracranial aneurysm wall

Variables Bleeding status P-value
  Unruptured Ruptured  
(n = 18) (n = 36)
A.Patients    
Age (years) 55y. (42–70) 57y. (34–84) 0.773
Gender (females) 56% (10/18) 72% (26/36) 0.239
Patients with multiple sIAs (≥2) 33% (6/18) 36% (13/36) 1.000
History of prior SAH (from the studied sIA or another sIA) 20% (3/15) 97% (35/36) † <0.001*
Familial background    0.174
    Documented familial background (sIAs) 0% (0/18) 8% (3/36)  
    Possible familial background # 11% (2/18) 11% (4/36)  
    Family history unknown 39% (7/18) 58% (21/36)  
    No familial background (verified cases) 50% (9/18) 22% (8/36)  
Smoking    0.129
    Current smoker 50% (9/18) 39% (14/36)  
    Ex-smoker 17% (3/18) 3% (1/36)  
    Never smoked 17% (3/18) 17% (6/36)  
    Status not known 17% (3/18) 42% (15/36)  
Hypertension 83% (15/18) 36% (13/36) 0.004*
B.Aneurysms    
Neck diameter (mm) 4.5 mm (3–7) 4 mm (1.5-8) 0.273
Width of fundus (mm) 6.0 mm (3–11) 7.0 mm (3–19) 0.624
Lenght of fundus (mm) 6.3 mm (3–11) 6.5 mm (2–27) 0.773
  1. Median and range are given for continuous variables, proportions for categorical variables. Mann–Whitney U-test was used for continous and Fisher’s Exact test for categorical variables. P-values <0.05 are marked with *.
  2. † One of the ruptured aneurysms presented in the operation with old thrombus and hemosiderin surrounding the aneurysm although the patient had not been diagnosed with SAH and had not had any symptomps suggesting SAH.
  3. # When patients had multiple relatives that had been diagnosed with intracranial hemorrhage but the etiology of the hemorrhage was not clear.