Between 70 and 80 percent of people who develop brain aneurysms are smokers. According to a study published in August in the Journal of Neurology, Neurosurgery and Psychiatry , smokers who had a brain aneurysm were three times more likely than nonsmokers to have a subarachnoid hemorrhage SAH. Another study, published in April in the Journal of Neurosurgery , found people who suffered a brain aneurysm, underwent endovascular EVAR repair — a procedure that uses a catheter inserted into the artery to place a stent graph — and continued to smoke had a nearly threefold increase for risk of recurrence.
Former and current smokers had an about 26 percent rate of recurrence, while newer smokers had an about 17 percent rate of recurrence. According to a study published in November in the journal Arteriosclerosis, Thrombosis and Vascular Biology , 1 in 17 people who are current or former smokers have a lifetime risk for developing an aortic abdominal aneurysm, a condition in which a bulge forms in the section of the aorta, the main artery in the body. People who already have abdominal aortic aneurysms and continue to smoke are at an increased risk for the aneurysm expanding and rupturing.
According to a meta-analysis published in May in The British Journal of Surgery, 35 percent of smokers who had a small abdominal aortic aneurysm between 3 and 5. Smokers who quit are also at risk. According to a study published in the journal Circulation , people who stopped smoking 10 to 19 years earlier were still nearly three times as likely as nonsmokers to develop abdominal aortic aneurysms.
The risk for abdominal aortic aneurysms is higher in smokers who are women than in those who are men. Women who were current smokers had nine times the risk of women who had never smoked, the same study found.
There is no theory or research to support why this disparity exists, says George P. But regardless of sex, the length of time spent smoking and the number of cigarettes are factors directly related to the risk for aneurysm. In some people, the combination of genetics and smoking can significantly increase the risk of a brain aneurysm. According to research presented at the American Stroke Association's International Stroke Conference in , those people who carried a copy of a risky gene variation were between 37 and 48 percent more likely to develop an aneurysm than those without the gene variant.
Those who had the gene variant and also smoked the equivalent of one pack of cigarettes a day for 20 years had a nearly fivefold risk. Those with two copies of the gene variant had an even higher risk. Another study published in the journal Neurology found smokers who have a family history of brain aneurysm are significantly more likely to suffer a stroke from a brain aneurysm themselves.
One of the best ways to reduce your risk for an aneurysm is to stop smoking. According to the study in the journal Arteriosclerosis, Thrombosis, and Vascular Biology , middle-aged smokers who had a 1 in 9 chance of developing an abdominal aortic aneurysm reduced their risk of an aneurysm by 29 percent if they quit during the study period.
The study in Neurology, Neurosurgery and Psychiatry showed people who quit smoking for five or fewer years were 59 percent less likely afterward to suffer a subarachnoid hemorrhage. Because nicotine is so addictive, quitting smoking is one of the hardest things to do, but the good news is that there are more former smokers today than current smokers.
There are also effective treatments and resources available, such as prescription medication and over-the-counter products, like nicotine gum , patches, and lozenges. The point estimates for the ORs were Figure 2.
Distribution of daily cigarette intake in cases and controls. CPD, number of cigarettes smoked per day. Figure 3. Table 3. Conditional logistic regression analysis related to intracranial aneurysm rupture.
In the conditional logistic regression models, bifurcation location significantly increased the risk of IAR OR, The results were showed in Table 3. Furthermore, compared with former smokers who had quit at least 1 year before evaluation, current smokers were more predisposed to IAR, suggesting the importance of smoking cessation in patients with an IA. One possible explanation is that most smoking-induced changes are reversible after quitting, although previous studies suggested that former smokers demonstrate an ongoing low-grade inflammatory response that persists long after smoking cessation Cigarette smoke is an aerosol containing thousands of chemicals, including nicotine, carbon monoxide, and oxidant compounds 14 , and chronic exposure induces multiple pathological effects in the vascular endothelium and facilitates inflammation.
This process consistently weakens the UIA wall making it more vulnerable to trigger factors and eventually leads to rupture. Aneurysm growth has also been shown to be increased by current smoking supporting the concept that smoking increases SAH particularly by increasing aneurysm size and possibility of rupture 16 , However, some authors have proposed that smoking may not be a trigger for aneurismal rupture These contradicting results are probably explained by the lack of standard in design in which no details on the amount of cigarettes consumed were available.
As we asked a detailed question with regards to the CPD, we were able to assess the precise consumption, which is strength of this study. In smokers, an accumulation of smoke-induced chemical mediators has been positively correlated within creased impairment of the endothelial capacity and, therefore, an increased risk of IAR Although the CPD was a strong and independent risk factor for UIAs in our study, it should be noted that this straightforward index of cumulative exposure does not take the duration of smoking into account.
Therefore, we used the smoking index to investigate whether the increased risk of IAR due to smoking is modifiable. This index can make strong assumptions regarding the equivalence of the roles of intensity and duration We found a significant association between the smoking index and the risk of IAR Figure 3.
Our results are congruent with the basic research findings that the effects of cigarette smoke on endothelial cells are only functional initially, while the endothelial-cell layer exhibits physical damage and can even be completely destroyed by chronic exposure of cigarette smoke increase of smoking index Moreover, increasing degrees of smoking may be more permissive to accelerate morphological changes of aneurysms These changes, in turn, may increase the eventual rupture risk of the aneurysm.
We confirmed this association using a conditional logistic regression model. However, the association between a smoking index of — and the risk of IAR did not reach statistical significance in our study.
This result may be due to our retrospective study design and limited sample size. In our study, This finding is consistent with previous reports The arterial wall is consistently weakened, where it bifurcates because this area correlates with increased hemodynamic stress and higher blood flow.
Thus, IAs in bifurcation locations have a higher risk of rupture than those in other locations Our results showed that the bifurcation risk increased for smokers and nonsmokers. The risk of IAR in female smokers might be greater than the rupture risk in male smokers.
This hypothesis is supported by several studies reporting a dramatic sex-based difference in risk at a given level of cigarette consumption 24 , In their community-based case—control analysis, Bonita et al. Age is an important independent risk factor for acute aneurysm rupture 18 , 25 , and one of the most important factors affecting cigarette consumption duration.
Our study showed that hyperlipidemia independently decreased the risk of IAR. Recently, several studies reported similar results 5 , Interestingly, a recent study reported an association between the administration of statins and reduced UIA formation in rats It may be that hypercholesterolemic patients treated with statins gain a similar protective benefit. In their study of patients with SAH, Hughes et al.
However, few other studies demonstrating an association between BMI and aneurysm rupture are available. We also found that diabetes mellitus was associated with a decreased risk of IAR. It has been hypothesized that many patients had presented for evaluation of their diabetes mellitus, allowing some IAs to be diagnosed before they ruptured or altering lifestyle factors and continuing medical care to reduce the risk of SAH.
However, the biological foundation of this inverse correlation needs further investigation. It should be noted that various factors, such as previous SAH, hypertension, location in the posterior circulation, larger AR, and larger size have been reported to increase the risk of IAR 27 — However, in this study, these factors were not significantly related to rupture. These inconsistencies might be attributed to the instability of the factors, limited sample of our study and design of matched cases.
Although the case group included more patients with at least an education level of high school than the control group Our study has several strengths. First, this study has avoided concerns of previous retrospective studies by use of sex- and age-matched controls for patients with ruptured IAs. As all study patients came from the same hospital within 2 years, we were able to perform our analysis in a defined population.
Second, the rigorous measurement of aneurysm characteristics by two experienced neurosurgeons ensured a representative and fair comparison between cases and controls.
Finally, to minimize recall bias, we included only patients evaluated or treated at our institution within 2 years of our study start date. However, the study had several limitations. First, it was a retrospective study from a single center, suggesting that the collection of data was potentially biased.
Second, the aneurysm features, such as size, AR, and SR, might change after rupture, and these changes could cause bias. Finally, we did not take passive smoking into account, because it is difficult to determine the intensity and duration of passive smoking, and most smokers were also passive smokers. Further study of the effects of passive smoking on IAs is needed. All in all, your aorta is approximately two feet long and a little larger than an inch in diameter.
However, it supplies blood to:. When you have an aneurysm, part of an artery wall weakens, causing an abnormal bulge or balloon. As the tissue continues to weaken or become more damaged, your risk of a serious tear or rupture in the artery wall increases. You can develop an aortic aneurysm anywhere in this major vessel, but the most common occurs in the abdomen. This includes smoking, smokeless chewing tobacco, and e-cigarettes.
Over time, the walls of your aorta naturally lose their elasticity, which can increase your chances of an aneurysm forming.
However, tobacco use can further weaken the aorta walls. Not only does this increase the possibility of developing an aneurysm, but it also makes it more likely that the aneurysm could rupture. Studies also indicate that smoking could lead to biological changes in your DNA that impact your offspring, putting them at higher risk of an aneurysm in the future. Other factors that increase your risk of aortic aneurysms include being white, male, over age 65, and having a family history of aneurysms.
First and foremost, quit smoking or using other tobacco products and avoid exposure to secondhand smoke. Next, follow a healthy lifestyle by getting regular exercise and eating a diet with whole grains, fruits and vegetables, and lean proteins. You should also watch your heart health by keeping your blood pressure and cholesterol under control and avoiding saturated and trans fats.
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