The main cause of an aneurysm is the gradual weakening of an artery wall, most often driven by high blood pressure and smoking. These two factors damage the structural proteins that keep arteries strong and flexible, eventually allowing a section of the vessel to balloon outward. While no single cause applies to every case, the combination of sustained blood pressure stress and lifestyle factors accounts for the majority of aneurysms.
How an Artery Wall Breaks Down
Arteries are built from layers of elastic fibers and collagen that let them stretch with every heartbeat and snap back into shape. An aneurysm forms when those fibers degrade faster than the body can repair them. The elastic tissue fragments, the collagen scaffolding weakens, and the wall thins out in one spot. Blood pressure pushes against that weakened area, causing it to bulge like a worn section of a garden hose.
This breakdown is closely tied to inflammation. Immune cells infiltrate the artery wall and release enzymes called matrix metalloproteinases that actively chew through elastic fibers. Once that cycle of inflammation and tissue destruction takes hold, it tends to feed on itself. The wall loses its ability to resist the constant force of blood flow, and the bulge slowly grows.
High Blood Pressure: The Constant Force
Chronic high blood pressure is the single most consistent risk factor across all aneurysm types, whether in the brain, the chest, or the abdomen. Every heartbeat pushes blood against the artery wall, and when that pressure stays elevated for years, the wall remodels in damaging ways. Research on aortic tissue shows that sustained hypertension roughly halves the stiffness of elastic fibers compared to normal blood pressure, meaning the wall becomes far less resilient.
High blood pressure also weakens the bond between the layers of the artery wall. Studies measuring how much force it takes to peel apart aortic wall layers found that hypertension reduced that force by about 27%, and blood pressure that swings unpredictably (unstable hypertension) reduced it even further. This creates a vicious cycle: as the wall loses elasticity, it becomes less able to absorb pressure, which raises the effective stress on the wall, which accelerates the damage.
Smoking Is the Strongest Modifiable Risk
Smoking stands out as the most powerful lifestyle risk factor, especially for abdominal aortic aneurysms. A large UK Biobank study found that current smokers had roughly 4.3 times the risk of developing an aortic aneurysm compared to people who never smoked. For abdominal aortic aneurysms specifically, the risk jumped to nearly 9 times higher. Even former smokers carried about 1.7 times the risk, meaning the damage persists after quitting.
The biology behind this is well understood. Chemicals in tobacco smoke trigger immune cells in the artery wall to release the same destructive enzymes that break down elastic tissue. Compounds in cigarette smoke also promote cell death in the smooth muscle of the aorta and amplify inflammatory signaling. Human aortic tissue from smokers consistently shows significant reductions in the elastic fiber network compared to nonsmokers. Smoking essentially accelerates the same wall-degradation process that high blood pressure sets in motion.
Genetic Conditions That Weaken Arteries
Some people are born with connective tissue that is structurally weaker than normal, making them vulnerable to aneurysms at a much younger age. The best-known example is Marfan syndrome, which affects roughly 2 to 3 in every 10,000 people. Marfan syndrome is caused by mutations in the gene that produces fibrillin, a protein essential to elastic fiber structure. About 70 to 93% of people meeting diagnostic criteria carry this mutation. The hallmark cardiovascular problem is progressive widening of the aortic root, which can lead to aneurysm, dissection, or rupture if not monitored.
Vascular Ehlers-Danlos syndrome is rarer (about 1 in 100,000 to 200,000 people) but more dangerous in some ways. It involves defective type III collagen, which makes arteries fragile enough to rupture, often in the third or fourth decade of life. Loeys-Dietz syndrome, bicuspid aortic valve disease, and familial patterns of thoracic aortic aneurysm are other inherited conditions that significantly raise risk. If a close family member had an aneurysm, particularly at a young age, genetic factors are worth discussing with a doctor.
Atherosclerosis and Arterial Remodeling
The relationship between atherosclerosis (plaque buildup in arteries) and aneurysms has been debated for decades. The two conditions share many of the same risk factors: smoking, high blood pressure, high cholesterol, and age. But there’s a plausible direct link as well. When plaque narrows an artery, the vessel tries to compensate by remodeling and expanding outward to maintain blood flow. This compensatory remodeling thins the middle layer of the artery wall. If that process goes too far, the thinned wall can develop into an aneurysm.
Plaque also drives chronic inflammation. Inflammatory cells within the plaque release signaling molecules that break down elastic fibers in deeper layers of the wall. This combination of structural thinning and inflammatory destruction helps explain why abdominal aortic aneurysms are so strongly associated with atherosclerotic disease, while thoracic and brain aneurysms often are not.
Brain Aneurysms Have a Different Profile
Intracranial (brain) aneurysms share some risk factors with aortic aneurysms, particularly high blood pressure and smoking, but they differ in important ways. Brain aneurysms are generally not considered atherosclerotic. They tend to form at branching points of arteries where blood flow creates turbulence and stress on the wall.
Female sex plays a larger role in brain aneurysms than in aortic ones. Women have roughly twice the odds of having a brain aneurysm compared to men. Researchers have noted that intracranial arteries and the aorta both develop from the same embryonic cells (neural crest cells), which may explain why some people develop aneurysms in both locations. Among people with thoracic aortic aneurysms, those who also smoked had about 3.9 times the odds of harboring a brain aneurysm as well.
Less Common Causes
Infections can, in rare cases, cause aneurysms. These are called mycotic aneurysms and develop when bacteria or fungi invade the artery wall, usually during a bloodstream infection. The most common culprits are Staphylococcus aureus and Salmonella. The infection triggers intense local inflammation, attracting immune cells that break down the vessel wall from within. People with weakened immune systems, those who use intravenous drugs, or those with heart valve infections are most at risk.
Physical trauma can also create a type of aneurysm called a pseudoaneurysm, or false aneurysm. Unlike a true aneurysm where the wall stretches outward, a pseudoaneurysm involves a tear in the inner layer of the vessel that allows blood to collect between the wall’s layers. This can happen after surgery, catheter-based procedures, or blunt injury to areas like the hip or lower back.
Who Gets Screened
Because most aneurysms grow silently without symptoms, screening matters for people at higher risk. The U.S. Preventive Services Task Force recommends a one-time ultrasound screening for abdominal aortic aneurysm in men aged 65 to 75 who have ever smoked (defined as 100 or more cigarettes in a lifetime). Men in that age range who have never smoked may still be offered screening on a case-by-case basis. The Task Force recommends against routine screening for women who have never smoked and have no family history, though the evidence for women who have smoked remains inconclusive.
These guidelines reflect the reality that abdominal aortic aneurysms are overwhelmingly concentrated in older men with smoking histories. Screening with ultrasound is quick, painless, and highly accurate, and catching an aneurysm before it ruptures dramatically changes outcomes.