An aortic aneurysm forms when the wall of the aorta, the body’s largest artery, weakens and bulges outward like a balloon. The underlying cause depends on where the aneurysm develops, but the common thread is damage to the structural layers of the artery wall. That damage can come from a combination of high blood pressure, smoking, genetic conditions, inflammation, infection, or simply aging.
How the Aortic Wall Breaks Down
The aorta has a thick middle layer packed with elastic fibers and smooth muscle cells that allow it to stretch and recoil with every heartbeat. An aneurysm develops when this middle layer degenerates. The smooth muscle cells die off, and enzymes produced during inflammation chew through the elastic fibers that give the wall its strength. Once enough of that structural scaffolding is destroyed, the wall can no longer hold its shape under the force of blood pressure, and it begins to balloon outward.
This process, called medial degeneration, is accompanied by an influx of immune cells: white blood cells, macrophages, and mast cells that drive further tissue breakdown. It can happen slowly over decades, driven by atherosclerosis and high blood pressure, or it can progress more rapidly in someone with a genetic connective tissue disorder.
Smoking Is the Strongest Modifiable Risk Factor
No single lifestyle factor raises the risk of an abdominal aortic aneurysm more than smoking. A large meta-analysis published in Arteriosclerosis, Thrombosis, and Vascular Biology found that men who currently smoke are roughly 5 times more likely to develop an abdominal aortic aneurysm than men who have never smoked. For women, the relative risk is even steeper: current female smokers face about 8 times the risk of women who have never smoked. Even people who quit years ago carry elevated risk compared to lifelong nonsmokers.
Smoking damages the aortic wall through multiple routes. It accelerates atherosclerosis, triggers chronic inflammation in the vessel lining, and impairs the body’s ability to repair elastic tissue. The U.S. Preventive Services Task Force defines an “ever smoker” as someone who has smoked 100 or more cigarettes in their lifetime, and that threshold is enough to qualify for screening.
High Blood Pressure and Abnormal Blood Flow
Chronically elevated blood pressure forces the aortic wall to absorb more mechanical stress with every heartbeat. Over time, that sustained pressure stretches and weakens the elastic fibers in the wall, particularly in areas where blood flow is already turbulent. The frictional force of blood against the inner wall, known as wall shear stress, plays a direct role. Elevated shear stress has been linked to breakdown of the structural matrix in the aortic wall and thinning of elastic fibers.
Abnormal flow patterns matter too. In people born with a bicuspid aortic valve (a valve with two flaps instead of the normal three), blood exits the heart in a jet-like pattern that hits the ascending aorta at an angle. This creates localized zones of high shear stress that activate inflammatory pathways in the vessel wall, promoting dilation even in the absence of other risk factors.
Genetic and Connective Tissue Disorders
About 20% of thoracic aortic aneurysms run in families, and several well-defined genetic conditions dramatically increase the risk.
Marfan syndrome is the most widely recognized. It’s caused by mutations in the gene for fibrillin-1, a protein that forms the structural backbone of elastic tissue throughout the body. More than 1,500 different mutations in this gene have been identified. People with Marfan syndrome develop medial degeneration of the aorta at a young age, often leading to aneurysms of the ascending aorta in their 20s or 30s.
Loeys-Dietz syndrome, caused by mutations in genes involved in a key growth-signaling pathway, produces aggressive aortic aneurysms that can rupture at smaller diameters than those seen in Marfan syndrome. Vascular Ehlers-Danlos syndrome, caused by a deficiency of type III collagen, weakens the aorta and other arteries so severely that rupture or dissection can occur without warning.
Not all genetic cases involve a named syndrome. Familial thoracic aortic aneurysm disease accounts for a significant share, driven by mutations in genes that control the contraction of smooth muscle cells in the artery wall. Mutations in one of these genes, ACTA2, are responsible for about 14% of familial cases.
Bicuspid Aortic Valve
A bicuspid aortic valve is the most common congenital heart defect, affecting roughly 1% to 2% of the population. It carries a substantial risk of ascending aortic aneurysm, with studies reporting prevalence rates of 35% to 68% for dilation of the proximal ascending aorta in people with this condition. The cause is likely a combination of abnormal blood flow patterns and an intrinsic weakness in the aortic wall tissue itself, since the same developmental signals that shape the valve also shape the aorta.
Where the Aneurysm Forms Shapes Its Cause
Thoracic and abdominal aortic aneurysms have overlapping but distinct causes, and understanding the difference matters.
Aneurysms of the ascending thoracic aorta (the portion closest to the heart) most often result from medial degeneration, the slow breakdown of smooth muscle and elastic fibers described above. Atherosclerosis is an infrequent cause in this location. Instead, the main drivers are genetic connective tissue disorders, bicuspid aortic valve disease, and age-related degeneration. These aneurysms tend to appear in younger patients and are more strongly tied to family history.
Aneurysms of the descending thoracic aorta and the abdominal aorta are predominantly driven by atherosclerosis. Cholesterol-laden plaques infiltrate and inflame the vessel wall, weakening it over years. Smoking, high blood pressure, high cholesterol, and older age are the major risk factors here. The abdominal aorta is especially vulnerable because it receives less blood supply to its own wall tissue compared to the thoracic aorta, making it slower to repair damage.
Inflammatory Diseases
Certain inflammatory conditions directly attack the aortic wall. Takayasu arteritis, a form of vasculitis most common in women under 40, causes cycles of inflammation and scarring in the aorta and its major branches. Over time, the weakened wall stretches into an aneurysm that can tear or rupture. Giant cell arteritis, which typically affects adults over 50, can cause similar damage to the thoracic aorta.
These inflammatory aneurysms are less common than those caused by atherosclerosis or genetic disease, but they can be particularly dangerous because they may develop in unusual locations along the aorta and progress unpredictably.
Infection
Infected (mycotic) aortic aneurysms are rare but serious. Bacteria seed the aortic wall through the bloodstream, often lodging in areas already weakened by atherosclerotic plaque. Staphylococcal species, particularly Staphylococcus aureus, now account for 50% to 60% of cases. Salmonella, once the leading cause, still represents 30% to 40% of infected aortic aneurysms and remains especially common in parts of Asia. Tuberculosis can also erode the aortic wall, typically by spreading from an adjacent spinal infection, though this is rare in high-income countries.
Infected aneurysms tend to grow quickly and carry a high risk of rupture, making them surgical emergencies once identified.
Age, Sex, and Other Risk Factors
Age is a major independent risk factor. The aortic wall gradually loses elasticity over decades as elastic fibers fragment and are replaced by stiffer collagen. Most abdominal aortic aneurysms are diagnosed in people over 60.
Men are significantly more likely to develop abdominal aortic aneurysms than women, by a ratio of roughly 4 to 1. However, when women do develop them, the aneurysms tend to rupture at smaller diameters and carry higher mortality. Family history matters regardless of sex: having a first-degree relative with an aortic aneurysm roughly doubles your risk.
Who Gets Screened
The U.S. Preventive Services Task Force recommends a one-time abdominal ultrasound for men aged 65 to 75 who have ever smoked. Men in that age range who have never smoked may still benefit from selective screening based on other risk factors. For women aged 65 to 75 who have smoked or have a family history, the evidence is currently insufficient to make a firm recommendation either way. Women who have never smoked and have no family history are recommended against routine screening, since their risk is very low.
Screening for thoracic aortic aneurysms follows a different path. It’s typically guided by family history, known genetic syndromes, or the presence of a bicuspid aortic valve, and usually involves imaging of the chest rather than a simple ultrasound.