Atherosclerosis is the most common cause of abdominal aortic aneurysm (AAA). For decades, the condition was actually called “atherosclerotic aneurysm” because the link between fatty plaque buildup in the arteries and weakening of the aortic wall is so well established. But atherosclerosis doesn’t act alone. It sets the stage while other forces, especially smoking, high blood pressure, and genetic vulnerability, accelerate the damage that causes the aorta to balloon outward.
How Atherosclerosis Weakens the Aorta
The abdominal aorta is the largest artery in your body, running through your midsection to supply blood to your legs and organs. Its wall contains layers of elastic fibers and collagen that keep it strong and flexible under constant pressure. An aneurysm forms when those structural proteins break down faster than the body can repair them, and the wall stretches outward like a weak spot on a tire.
Atherosclerosis triggers this process by depositing fatty plaques along the inner lining of the artery. These plaques cause chronic inflammation in the vessel wall, which attracts immune cells, particularly white blood cells called neutrophils and macrophages. Those immune cells release a family of enzymes that chew through the structural proteins holding the wall together. The most important of these enzymes target elastin first, then collagen. Once elastin fibers fragment, the wall loses its ability to snap back after each heartbeat. As collagen breaks down next, the wall loses its tensile strength entirely. The result is progressive, irreversible dilation.
This enzymatic destruction is self-reinforcing. Some of the enzymes activate other dormant enzymes in the wall, creating a cascade of protein breakdown. Oxidative stress and inflammatory signaling molecules keep the cycle going even after the initial plaque damage. That’s why an aneurysm, once started, tends to keep growing.
Why Smoking Is the Strongest Risk Factor
While atherosclerosis is the underlying cause, smoking is the single most powerful modifiable factor driving AAA development. A large meta-analysis published in a major American Heart Association journal found that male smokers are nearly 5 times more likely to develop an AAA than men who have never smoked. For women, the risk is even more dramatic: female smokers face roughly 8.4 times the risk of never-smokers. A separate analysis of over 500,000 people in the UK Biobank confirmed these findings, with similar hazard ratios of 3.78 for men and 6.60 for women.
Tobacco smoke damages blood vessel walls directly, accelerates plaque formation, and amplifies the inflammatory processes that degrade elastin and collagen. The relative risk that smoking confers for AAA is actually higher than its risk for other cardiovascular diseases like heart attack, which underscores just how toxic smoking is to the aortic wall specifically. The U.S. Preventive Services Task Force defines “ever smoker” as someone who has smoked 100 or more cigarettes in their lifetime, a threshold that captures even people who consider themselves light or former smokers.
Other Risk Factors That Contribute
Several additional factors raise your likelihood of developing an AAA, often working alongside atherosclerosis and smoking:
- Age and sex: AAA is 3 to 4 times more common in men than women. Prevalence in men over 65 ranges from 1.7% to 4.5%, compared with 0.5% to 1.3% in women of the same age. The condition is rare before age 60.
- Family history: Having a first-degree relative with AAA increases your risk roughly eightfold compared to the general population. Two genes with the strongest evidence of contributing to inherited risk are involved in regulating cell growth and survival, though specific mutations account for only a small fraction of cases. Family history likely influences how efficiently your body repairs its blood vessel walls over time.
- High blood pressure: Chronic hypertension puts constant mechanical stress on the aortic wall, accelerating dilation once weakening has begun.
- High cholesterol: Elevated levels of triglyceride-rich particles promote continued growth of existing aneurysms in addition to fueling the atherosclerotic plaque that starts the process.
Less Common Causes
A small number of AAAs have nothing to do with atherosclerosis. Inflammation of the aortic wall, called aortitis, can result from autoimmune diseases like giant cell arteritis or Takayasu’s arteritis, both of which target large blood vessels. Rarer inflammatory causes include lupus, rheumatoid arthritis, and Behçet’s disease.
Infections can also weaken the aorta, though this is uncommon in developed countries. Bacterial infections from Staphylococcus or Salmonella, sometimes related to intravenous drug use or prior vascular procedures, can create what’s known as a mycotic aneurysm. Syphilis was historically a notable cause of aortic aneurysms but is now rare and tends to affect the chest portion of the aorta rather than the abdomen.
Size, Rupture Risk, and Why It Matters
Most AAAs produce no symptoms at all. They’re often discovered incidentally during imaging for something else, or through screening. The danger lies almost entirely in rupture, which is frequently fatal. In one long-term surgical series, nearly half of patients who made it to the operating room after a rupture did not survive, and many others die before reaching a hospital.
Rupture risk climbs steeply with size. An aneurysm under 4 cm has essentially no annual rupture risk. At 5 to 5.9 cm, the risk rises to 3% to 15% per year. At 7 cm or larger, the annual risk reaches 20% to 40%. Surgeons generally recommend elective repair once an aneurysm exceeds 5.0 to 5.5 cm, because the risk of rupture at that point begins to outweigh the risk of surgery.
Who Should Be Screened
Because AAAs grow silently, screening with a simple abdominal ultrasound can be lifesaving. The U.S. Preventive Services Task Force recommends a one-time screening ultrasound for men aged 65 to 75 who have ever smoked. For men in that age range who have never smoked, screening is offered selectively based on other risk factors like family history, because the overall benefit in that group is smaller. There is currently no routine screening recommendation for women, though women with significant risk factors may still benefit from discussion with a clinician.
The screening itself takes about 15 minutes, involves no radiation, and requires no preparation beyond a period of fasting. A single normal result is generally sufficient, as new aneurysms rarely develop after a negative screen at age 65 or older.