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Are cerebral aneurysms atherosclerotic?
J Adamson1, S E Humphries, J R Ostergaard
1Department of Surgery, Charing Cross & Westminster Medical School, London, England.
Insights
Smoking and high cholesterol levels significantly increase the risk of ruptured cerebral aneurysms. Genetic factors related to collagen were not found to be a common cause for these dangerous vascular events.
Area of Science:
- Neuroscience
- Cardiovascular Research
- Genetics
Background:
- Cerebral aneurysms pose a significant health risk.
- Identifying risk factors is crucial for prevention and treatment.
Purpose of the Study:
- To investigate plasma and genetic risk factors associated with the rupture of cerebral aneurysms.
Main Methods:
- A case-control study was conducted with patients who experienced ruptured cerebral aneurysms.
- Plasma lipid profiles, apolipoprotein levels, and genetic polymorphisms were analyzed.
- Data from London and Arhus cohorts were combined for comprehensive analysis.
Main Results:
- A history of smoking (over 10 pack years) was strongly associated with increased risk (OR, 9.1).
- Elevated total cholesterol (highest tertile, OR, 10.2) and apolipoprotein B (highest tertile, OR, 6.4) were significant risk factors.
- Low HDL cholesterol (lowest tertile, OR, 3.6) and hypertension (OR, 4.0) also showed associations.
Conclusions:
- An atherosclerotic profile, characterized by high cholesterol and extensive smoking history, contributes to cerebral aneurysm rupture.
- No evidence was found to support inherited type III collagen abnormalities as a common cause of cerebral aneurysms.
Background And Purpose:
The aim of our study was to investigate plasma and genetic risk factors for rupture of cerebral aneurysms.
Methods:
In London, a case-control study was made of 56 consecutive patients admitted to a regional neurosurgical service for treatment of ruptured cerebral aneurysm and of 93 control subjects. A further 40 consecutive patients admitted in Arhus with ruptured cerebral aneurysm also were studied.
Results:
The British case-control study showed that smoking was associated with an increased risk of ruptured cerebral aneurysm (odds ratio, 9.1; 95% confidence interval [CI], 3.4 to 23.8; P < .001 for a history of > 10 pack years). After age and sex adjustment, factors associated with ruptured cerebral aneurysm included a cholesterol concentration in the highest tertile (> or = 6.3 mmol/L; odds ratio, 10.2; 95% CI, 3.9 to 26.7; P < .001), an apolipoprotein B concentration in the highest tertile (> or = 0.84 g/L; odds ratio, 6.4; 95% CI, 2.5 to 16.3; P < .001), and concentrations of HDL cholesterol in the lowest tertile (< 1.1 mmol/L; odds ratio, 3.6; 95% CI, 1.4 to 8.2; P < .01). History of hypertension was of less importance (odds ratio, 4.0; 95% CI, 1.41 to 11.7; P < .01). Smoking history (P < .001) and increased concentrations of cholesterol (P < .0001) were the most important independent risk factors associated with ruptured cerebral aneurysm on multivariate analysis. The histories of hypertension and smoking, together with apolipoprotein B levels, in the Danish patients were similar to those in the British patients. In the entire patient group, the frequencies of two polymorphic variations in the type III collagen gene and polymorphisms at the apolipoprotein B, apolipoprotein C-III, and haptoglobin gene loci were not different from control subjects or the normal population; allele frequencies in British and Danish patients were similar.
Conclusions:
An atherosclerotic profile including increased total cholesterol concentration and a long smoking history may contribute to the rupture of cerebral aneurysms. This study provides no support for the hypothesis that inherited abnormalities of type III collagen are a common cause of cerebral aneurysms.