An aortic aneurysm forms when the wall of the aorta, your body’s largest artery, weakens and bulges outward. The causes range from gradual wear driven by high blood pressure and smoking to inherited conditions that make the aortic wall fragile from birth. In most cases, multiple factors overlap: the biological process is always the same (the wall loses its structural integrity), but what triggers that process varies from person to person.
How the Aortic Wall Breaks Down
The aorta is built in layers. The middle layer, called the media, contains elastic fibers and collagen that allow the artery to stretch with each heartbeat and snap back into shape. An aneurysm develops when this middle layer degrades faster than the body can repair it.
The key players in this breakdown are enzymes called matrix metalloproteinases, or MMPs. These enzymes normally help remodel tissue, but when they’re overproduced or not kept in check by their natural inhibitors, they chew through the elastic fibers that give the aorta its strength. Studies in mice have irrevocably confirmed that an imbalance between these enzymes and their inhibitors is central to how aneurysms start and grow. Once elastic fibers are lost, the aorta gradually stretches under the force of blood pressure, and the bulge slowly expands.
Inflammatory cells also flood into the weakened wall. This chronic inflammation accelerates the destruction by releasing chemical signals that recruit even more immune cells and stimulate more enzyme production. The result is a self-reinforcing cycle: damage attracts inflammation, inflammation causes more damage.
Atherosclerosis and Chronic Inflammation
For decades, doctors assumed that atherosclerosis (the buildup of fatty plaques inside arteries) directly caused abdominal aortic aneurysms because the two conditions share so many risk factors. The relationship turns out to be more nuanced. Fatty plaques don’t simply block the artery and cause a bulge. Instead, the inflammatory cells living inside those plaques release destructive enzymes and chemical signals that diffuse into the deeper layers of the aortic wall. This triggers a secondary wave of tissue breakdown in the media, weakening its structure from the inside out.
Blood clots that form on the inner surface of damaged plaques add fuel. As those clots organize and break down, they release additional inflammatory molecules that push the remodeling process further. So atherosclerosis doesn’t cause aneurysms the way it causes heart attacks, but the chronic, low-grade inflammation it creates in the aortic wall sets the stage for one.
Smoking
Smoking is the single strongest modifiable risk factor for abdominal aortic aneurysms. It both raises the likelihood of developing one and speeds up the growth of aneurysms that already exist. In a Lancet study tracking small aneurysms over time, people who continued smoking saw their aneurysms grow at 0.16 cm per year, compared to 0.09 cm per year in those who had quit. Growth rates also correlated directly with cotinine levels, a blood marker of nicotine exposure, meaning heavier smokers faced faster expansion.
The damage from smoking is twofold. Chemicals in tobacco smoke increase the activity of wall-degrading enzymes in the aorta and reduce the body’s ability to repair elastic fibers. Smoking also promotes inflammation throughout the cardiovascular system, compounding the destructive cycle already described.
High Blood Pressure
Every time your heart beats, it sends a pressure wave through the aorta. Chronically elevated blood pressure means the aortic wall absorbs more mechanical force with every pulse, thousands of times a day, year after year. This repeated stretching triggers changes in the structural proteins of the wall. Specifically, the exaggerated cyclic stress alters the balance of collagen and elastic fibers, making the wall stiffer in some spots and weaker in others.
Pulse pressure, the difference between the top and bottom numbers of a blood pressure reading, appears particularly important. A wide pulse pressure means the aorta is being slammed open and allowed to recoil more dramatically with each beat, increasing the mechanical strain on an already vulnerable wall.
Genetic and Inherited Conditions
Some people are born with connective tissue that can’t hold up to normal aortic forces. These inherited conditions primarily affect the thoracic aorta (the portion in the chest) and tend to cause aneurysms at a younger age.
Marfan syndrome is the most widely recognized. It’s caused by mutations in the gene for fibrillin-1, a protein that forms the scaffolding for elastic fibers. More than 1,500 different mutations in this gene have been identified, which is why the severity of Marfan syndrome varies so widely between individuals. Without normal fibrillin, the aortic wall is structurally weaker from birth, and the signaling pathways that regulate wall repair go haywire.
Loeys-Dietz syndrome involves mutations in genes that control a growth factor signaling pathway critical for maintaining the aortic wall. Several subtypes exist, each tied to a different gene in the same pathway. People with Loeys-Dietz syndrome can develop aneurysms at smaller aortic sizes and at younger ages than those with Marfan syndrome, making early detection especially important.
Vascular Ehlers-Danlos syndrome results from a deficiency of type III collagen, one of the main structural proteins in blood vessel walls. This form is particularly dangerous because the aorta and other arteries can tear or rupture with little warning, sometimes before an aneurysm is even detected on imaging.
Even without a named syndrome, family history matters. About 20% of people with thoracic aortic aneurysms have a close relative with the same condition. Familial thoracic aortic aneurysm and dissection can be caused by mutations in the same signaling pathway genes as Loeys-Dietz syndrome, suggesting a shared biological mechanism.
Bicuspid Aortic Valve
A normal aortic valve has three flaps. Roughly 1 to 2% of the population is born with only two, a condition called bicuspid aortic valve. About half of people with this valve abnormality develop a thoracic aortic aneurysm, and they face an eightfold higher risk of aortic dissection (a life-threatening tear) compared to the general population.
Two mechanisms likely work together. First, a two-flap valve creates an asymmetric jet of blood that hits certain regions of the ascending aorta with unusually high force, accelerating wear on the wall. Second, the same developmental process that produced the abnormal valve may have left the aortic wall itself with subtle structural weaknesses. Research confirms that people with bicuspid valves have stiffer, less elastic aortas even before any aneurysm appears, supporting the idea that the wall is inherently more vulnerable.
Inflammatory and Infectious Causes
Certain autoimmune conditions attack the aortic wall directly. Giant cell arteritis and Takayasu arteritis are both classified as large-vessel vasculitis, meaning they cause widespread inflammation in the aorta and its major branches. Over time, this inflammation can weaken segments of the wall enough to produce aneurysms, or narrow them enough to restrict blood flow. Giant cell arteritis typically affects people over 50, while Takayasu arteritis tends to appear in younger adults.
Infected (mycotic) aneurysms are rare but serious. Bacteria or fungi seed the aortic wall, usually through the bloodstream during an infection elsewhere in the body. Among people who develop these aneurysms in the setting of heart valve infections, Streptococcus species are the most common organisms found (about 37% of cases), followed by Staphylococcus aureus (28%). Candida, a type of fungus, is uncommon overall but carries nearly five times the odds of producing an infected aneurysm compared to other organisms.
Age and Sex
Aortic aneurysms are overwhelmingly a condition of older adults. In a screening study of people over 50, the average age of those found to have an abdominal aortic aneurysm was nearly 69. Men are far more likely to be affected: 8.2% of men screened had an aneurysm compared to 1.3% of women. Among men aged 50 to 64, the prevalence was already 5.4%.
This disparity is partly why screening guidelines in most countries target older men, particularly those who have ever smoked. Women develop aneurysms less often, but when they do, the aneurysms tend to rupture at smaller sizes, making detection no less important.
When Size Determines Risk
An aneurysm’s danger is tied to its size. Small aneurysms are monitored with periodic imaging, while larger ones are considered for surgical repair. Current guidelines recommend considering surgery for thoracic aortic aneurysms at 5.0 cm in experienced centers, lowered from the previous threshold of 5.5 cm. For people with genetic conditions like Marfan or Loeys-Dietz syndrome, thresholds are adjusted even lower based on the specific mutation, sex, and body size. One common formula divides the aorta’s cross-sectional area by the patient’s height to standardize risk across different body types.
For abdominal aortic aneurysms, the typical surgical threshold is 5.5 cm for men and 5.0 cm for women, or any aneurysm growing faster than 0.5 cm in six months. Below those sizes, the risk of the surgery itself generally outweighs the risk of rupture, so the strategy is regular surveillance and aggressive management of blood pressure and smoking.