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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.