What Is Aortitis? Causes, Symptoms & Treatment

Aortitis is inflammation of the aorta, the largest artery in your body. The inflammation causes the aortic wall to thicken and stiffen, which can eventually lead to serious complications like aneurysms or blocked blood flow to vital organs. Aortitis has two broad categories: non-infectious (caused by immune system disorders) and infectious (caused by bacteria, fungi, or viruses).

What Causes Aortitis

The most common form is non-infectious aortitis, driven by the immune system attacking the aortic wall. Two conditions account for the majority of cases. Giant cell arteritis is the single most common cause, predominantly affecting women over 50, with an incidence of 15 to 25 per 100,000 people per year in Europe. Takayasu arteritis is rarer, at roughly 2.6 cases per million people per year in the United States, and typically appears in young women during their twenties or thirties, with the highest rates in East Asia.

Other autoimmune and inflammatory conditions linked to aortitis include lupus, rheumatoid arthritis, Behçet disease, and sarcoidosis, though these cause aortic inflammation less frequently.

Infectious aortitis is uncommon but dangerous. Salmonella is the most frequently identified bacterial cause, responsible for more than a third of cases. Staphylococcus aureus is the second most common. Other pathogens include E. coli, Streptococcus, Klebsiella, and, rarely, fungi like Aspergillus or Candida. Syphilis was once a leading cause of infectious aortitis, but it has practically disappeared in modern practice. Infectious aortitis tends to strike older adults or people with weakened immune systems, particularly those who already have some damage or weakening of the aortic wall.

Symptoms and How It Feels

Aortitis can be frustratingly vague in how it presents. The inflammation itself produces systemic symptoms: fever, fatigue, malaise, and a general feeling of being unwell. These overlap with dozens of other conditions, which is one reason diagnosis is often delayed. In Takayasu arteritis, the gap between when symptoms start and when the disease is formally identified can stretch anywhere from 2 to 11 years.

When blood flow to specific organs is compromised, symptoms become more localized. Back pain or abdominal pain can occur, particularly in infectious aortitis. Giant cell arteritis often drives patients to seek help because of new, persistent headaches and vision problems caused by inflammation affecting the blood supply to the optic nerve. Jaw pain while chewing, a symptom called jaw claudication, is a hallmark sign of giant cell arteritis that points to involvement of the external carotid artery.

Weight loss and night sweats may also appear, especially in chronic cases. Because these symptoms are so nonspecific, aortitis is often discovered incidentally on imaging ordered for another reason.

How Aortitis Is Diagnosed

Blood tests are the first step. Two markers of inflammation, the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are typically elevated well above normal. In patients with biopsy-confirmed giant cell arteritis, the median ESR is around 62 mm/hour (normal is under 22 for men and under 29 for women), and the median CRP is around 52 mg/L (normal is under 8). These numbers don’t diagnose aortitis on their own, but they signal that significant inflammation is happening somewhere in the body.

Imaging confirms the diagnosis and maps how far the inflammation extends. On CT, aortic wall thickness of 2 to 3 mm or more is considered diagnostic. CT angiography and MRI angiography provide detailed views of where the aorta has narrowed or bulged. MRI is particularly useful because different imaging sequences can distinguish active swelling from older scarring, helping gauge whether the disease is currently flaring.

PET-CT, which highlights areas of high metabolic activity, is the most sensitive imaging tool for detecting aortitis. A meta-analysis found it has a sensitivity of about 80% and specificity of 89%, with some individual studies reporting sensitivity as high as 92 to 100%. It is especially valuable for picking up inflammation before structural damage is visible on other scans. When giant cell arteritis is suspected, a biopsy of the temporal artery (a small artery near the temple) is recommended, though treatment should not be delayed while waiting for the result.

Potential Complications

Left untreated or poorly controlled, aortitis weakens the aortic wall over time. The most concerning complication is aortic aneurysm, a ballooning of the vessel that can eventually rupture. In a large study of patients with non-infectious thoracic aortitis who needed surgery, 70% had surgery for an aneurysm that had grown to a critical size, 14% for a symptomatic aneurysm, and 13% for aortic dissection, a tear in the wall layers that is a medical emergency.

Aortic dissection in particular carries a high risk of needing repeat procedures. In that same study, having a dissection nearly tripled the likelihood of requiring a second vascular surgery. Inflammation in the descending thoracic aorta (the section running down the back of the chest) also independently raised that risk. Stroke and blood clots are additional concerns, especially in Takayasu arteritis. In one study, patients with Takayasu arteritis who had aortitis at diagnosis had a five-year relapse rate of nearly 63%, and about a quarter experienced a serious vascular event within ten years, most commonly a thoracic aortic aneurysm or stroke.

Treatment Approach

For non-infectious aortitis, the cornerstone of treatment is high-dose steroids to rapidly suppress inflammation. Guidelines recommend starting at a dose of about 1 mg per kilogram of body weight per day, up to a maximum of 60 mg daily. This high dose is maintained for roughly a month, then gradually tapered. By three months, the goal is to be down to 10 to 15 mg per day. The taper needs to be steady and consistent; alternating between high and low doses on different days increases the risk of relapse.

Because long-term steroid use carries its own serious side effects (bone thinning, high blood sugar, weight gain, elevated blood pressure), doctors often add a second medication to help lower the steroid dose sooner. Methotrexate, taken once a week, is the most studied option. A pooled analysis of multiple trials found it modestly reduces relapse rates and lowers the total amount of steroids a patient needs over time. It is especially worth considering early if you have conditions that make prolonged steroid use risky, like osteoporosis or diabetes.

A newer option targets a specific inflammatory signal called IL-6. This biologic medication has shown promising results in reducing symptoms and inflammation markers in both case series and early trials, and it is increasingly used when steroids alone are not enough or when relapses keep occurring. Low-dose aspirin is also recommended for all patients with giant cell arteritis to reduce the risk of stroke and other blood clot-related events.

Infectious aortitis follows a completely different path. The priority is identifying the specific organism through blood cultures and then treating with targeted antibiotics or antifungals. Surgery may be needed to repair or replace a damaged section of the aorta, especially if an aneurysm has formed. For Takayasu arteritis, any reconstructive surgery on the aorta should ideally wait until the disease is in a quiet phase and be performed at a specialized center.

Long-Term Outlook

Aortitis is a chronic condition for most people. Even with appropriate treatment, relapses are common, particularly in Takayasu arteritis. The high five-year relapse rate means that ongoing monitoring is essential. Follow-up typically involves regular blood tests to track inflammation levels, combined with periodic imaging to watch for new or worsening aneurysms or narrowing.

The good news is that aggressive early treatment significantly improves outcomes. Statin use after an aortitis diagnosis has been associated with roughly halving the risk of needing additional vascular procedures, likely because statins have anti-inflammatory properties on top of their cholesterol-lowering effects. Patients who respond well to initial therapy and maintain low inflammation levels long-term have a substantially better prognosis than those who experience repeated flares or develop structural complications early on.