Morphological Effect on Wall Shear Stress in Intracranial Aneurysms.

BACKGROUND AND STUDY AIMS: Both high and low wall shear stress (WSS) play important roles in the development and rupture of intracranial aneurysms (IAs). This study aimed to determine the morphological factors that affect WSS in the IA and the parent artery. MATERIAL AND METHODS: We studied a total of 66 IAs with three-dimensional imaging. Computational fluid dynamics (CFD) models were constructed and used to characterize the hemodynamics quantitatively. Aneurysms were grouped according to the mean neck width. The associations among hemodynamics and morphology were analyzed. RESULTS: Aspect ratio was correlated to lowest WSS (r = - 0.576), aneurysm-to-parent vessel (A-P) WSS ratio (r = - 0.500), and lowest-parent vessel (L-P) WSS ratio (r = - 0.575). Height-to-width ratio and height were correlated to WSS. Mean aneurysm WSS (p = 0.023), lowest WSS (p < 0.0001), highest-to-lowest WSS ratio (p = 0.004), L-P WSS ratio (p < 0.0001), highest-parent vessel (H-P) WSS ratio (p = 0.008), A-P WSS ratio (p < 0.001), and height (p < 0.001) were different between the two groups of aneurysms that were divided by the relationship between the diameters of the aneurysms and the necks. Multivariable analysis showed that the lowest WSS (p = 0.028) and A-P WSS ratio (p = 0.001) were independently associated with neck width. CONCLUSION: Morphological characteristics are associated with IA and parent vessel WSS. Aneurysms with different neck widths have different hemodynamics. These results could help in understanding the progression of IA and in building predictive models for IA rupture.

Serum caspase-cleaved cytokeratin-18 levels and outcomes after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Cell apoptosis is involved in acute brain injury after aneurysmal subarachnoid hemorrhage (aSAH). The protein cytokeratin-18 (CK-18) is cleaved by the action of caspases during apoptosis, and the resulting fragments are released into the blood as caspase-cleaved CK (CCCK)-18. Our study examined the relationship between circulating CCCK-18 levels and long-term clinical outcomes among aSAH patients. METHODS: We recruited 128 aSAH patients and 128 controls (matched on age and sex). Serum was collected at admission to the emergency department. Unfavorable outcome was defined as the Glasgow Outcome Score scores of 1-3. After a 6-month follow-up period, outcomes were assessed using a logistic regression analyses. The prognostic predictive values were evaluated according to receiver operating curves analysis. RESULTS: aSAH patients had higher plasma CCCK-18 levels compared to controls (235.1 ± 86.8 U/L vs. 25.6 ± 23.4 U/L, P<0.001). CCCK-18 was independently associated with World Federation of Neurological Surgeons (WFNS) scores (t=4.460, P<0.001) and modified Fisher scores (t=3.781, P<0.001). Furthermore, CCCK-18 levels were markedly higher among patients with an unfavorable outcome and among non-survivors. CCCK-18 was yet identified as an independent prognostic predictor for mortality (odds ratio, 5.769; 95% confidence interval, 1.196-27.832; P=0.029) and unfavorable outcome (odds ratio, 4.909; 95% confidence interval, 1.521-15.838; P=0.008), as well as had similar predictive values for them compared with WFNS scores and modified Fisher scores. CONCLUSIONS: High circulating CCCK-18 levels were associated with injury severity and a poor clinical outcome after aSAH and CCCK-18 had the potential to be a good prognostic biomarker for aSAH.

[Correlative factors of traumatic embolism in superficial cerebral vein].

OBJECTIVE: To analyze the correlative factors of traumatic embolism in superficial cerebral vein and explore their corresponding treatments. METHODS: A total of 74 cases were divided into 3 groups according to their injury mechanisms. Group A: traumatic brain injury in superficial cerebral vein with cerebral contusion, acute intracerebral hematoma and subdural hematoma in the same place; Group B: traumatic brain injury in superficial cerebral vein with acute intracerebral hematoma, subdural hematoma and skull fracture in the same place; Group C: traumatic brain injury in superficial cerebral vein with acute subdural hematoma and skull fracture in the same place, without cerebral contusion or acute intracerebral hematoma. They were divided into different groups according to gender, age, pre-operative GCS and cerebral hernia. RESULTS: Among 74 cases, 28, 39 and 7 cases belonged to groups A, B and C respectively. There was significant difference among injured veins in three groups (P < 0.01). Cerebral infarction was found in 37 cases in groups A and B while only 2 cases in group C. Cerebral infarction had no correlation with sex, age, pre-operative GCS and cerebral hernia. CONCLUSION: Injuries in superficial cerebral vein are mainly caused by skull fracture, contre-coup injury and shearing force. Cerebral infarction often exists if there is cerebral contusion. It is necessary to protect injured primary superficial cerebral veins and ambient venous network, remove intracranial hematoma and large bone flap to reduce intracranial hypertension and dilute blood post-operatively to prevent venous embolism.