The U.S. Preventive Services Task Force recommends a single screening ultrasound for abdominal aortic aneurysm in males age 65 to 75 years who have a history of smoking. There is an estimated number needed to screen of approximately 850 people. It is unclear if screening is useful in women aged 65 to 75 who have smoked and they recommend against screening in women who have never smoked.

Repeat ultrasounds should be carried out in those who have an aortic size greater than 3.0 cm. In those whose aorta is between 3.0 and 3.9 cm this should be every three years, if between 4.0 and 4.4 cm every two year, and if between 4.5 and 5.4 cm every year.

In the United Kingdom one time screening is recommended in all males over 65 years of age. Australia has no guideline on screening.

Screening for an aortic aneurysm so that it may be detected and treated prior to rupture is the best way to reduce the overall mortality of the disease. The most cost-efficient screening test is an abdominal aortic ultrasound study. Noting the results of several large, population-based screening trials, the US Centers for Medicare and Medicaid Services (CMS) now provides payment for one ultrasound study in male or female smokers aged 65 years or older ("SAAAVE Act").

A measurement of blood D-dimer level may be useful in diagnostic evaluation. A level less than 500 ng/ml may be considered evidence against a diagnosis of aortic dissection, although this guideline is only applicable in cases deemed "low risk" and within 24 hours of symptom onset. The American Heart Association does not advise using this test in making the diagnosis, as evidence is still tentative.

Computed tomography angiography is a fast, noninvasive test that gives an accurate three-dimensional view of the aorta. These images are produced by taking rapid, thin-cut slices of the chest and abdomen, and combining them in the computer to create cross-sectional slices. To delineate the aorta to the accuracy necessary to make the proper diagnosis, an iodinated contrast material is injected into a peripheral vein. Contrast is injected and the scan performed using a bolus tracking method. This type of scan is timed to an injection to capture the contrast as it enters the aorta. The scan then follows the contrast as it flows though the vessel. It has a sensitivity of 96 to 100% and a specificity of 96 to 100%. Disadvantages include the need for iodinated contrast material and the inability to diagnose the site of the intimal tear.

Guidelines were issued in March 2010 for early detection of thoracic aortic disease, by the American College of Cardiology, the American Heart Association, and other groups. Among the recommendations:

- First-degree relatives of people with thoracic aortic aneurysm or dissection should have aortic imaging to identify asymptomatic disease.

- People with symptoms suggestive of thoracic aortic dissection should be routinely evaluated "to establish a pretest risk of disease that can then be used to guide diagnostic decisions."

- People diagnosed with Marfan syndrome should immediately have an echocardiogram to measure the aorta, and followed up 6 months later to check for aortic enlargement.

2002 the CT scan was assessed for it reliability for imaging inflammatory aortic aneurysms and to quantitatively evaluate its features. The finding were that CT scan was a reliable means to diagnose IAA.

2008 a study was done to test the effectiveness of MRI and FDG-PET tests to detect, diagnose, and measure inflammatory aortic arch syndrome. The results from the study were that MRI and FDG-PET were unreliable techniques due to giant cell arteritis.

2015 following endovascular repair of an aortic aneurysm the type of the endograft’s material used for repair seems to play a role in the inflammatory response associated with IAA.

Aortic aneurysms are often discovered during an X-ray, ultrasound, or echocardiogram done for other reasons. IAA may also be found during a routine physical exam by feeling for bulges in the abdominal area. If your doctor thinks you might have an aortic aneurysm, you will likely have a medical history and physical exam. You might have further tests to locate the aneurysm.

When an aneurysm is suspected or diagnosed, it is important to:

- Pinpoint the location of the aneurysm.

- Estimate its size.

- Find out how fast it is growing.

- Find out whether other blood vessels are involved.

- See if there are blood clots or inflammation.

Tests to help find out the location, size, and rate of growth of an aneurysm include:

- Abdominal ultrasound - This imaging allows the doctor to observe growth of the aneurysm. If the aneurysm is large, a monitoring ultrasound may need to occur every 6 to 12 months. If the aneurysm is small, monitoring may occur every 2 to 3 years.

- Computed tomography (CT) and magnetic resonance angiogram (MRA) - These imaging techniques give a more detailed view of the aneurysm. These techniques may be used to gather information about aneurysm's relation to the blood vessels of the kidney or other organs. Your doctor needs this information especially before surgery. CT is used to watch the growth of a thoracic aortic aneurysm.

- Echocardiogram - This ultrasound exam is used to study the heart. A transthoracic echocardiogram (TTE) or a transesophageal echocardiogram (TEE) may also be done to further diagnose thoracic aortic aneurysm.

- Angiogram - An angiogram can help your doctor identify the size of the aneurysm and also examine if there are any aortic dissections, blood clots, or other blood vessel involvement.

Although the current standard of determining rupture risk is based on maximum diameter, it is known that smaller AAAs that fall below this threshold (diameter5.5 cm) may remain stable. In one report, it was shown that 10–24% of ruptured AAAs were less than 5 cm in diameter. It has also been reported that of 473 non-repaired AAAs examined from autopsy reports, there were 118 cases of rupture, 13% of which were less than 5 cm in diameter. This study also showed that 60% of the AAAs greater than 5 cm (including 54% of those AAAs between 7.1 and 10 cm) never experienced rupture. Vorp "et al." later deduced from the findings of Darling "et al." that if the maximum diameter criterion were followed for the 473 subjects, only 7% (34/473) of cases would have succumbed to rupture prior to surgical intervention as the diameter was less than 5 cm, with 25% (116/473) of cases possibly undergoing unnecessary surgery since these AAAs may never have ruptured.

Alternative methods of rupture assessment have been recently reported. The majority of these approaches involve the numerical analysis of AAAs using the common engineering technique of the finite element method (FEM) to determine the wall stress distributions. Recent reports have shown that these stress distributions have been shown to correlate to the overall geometry of the AAA rather than solely to the maximum diameter. It is also known that wall stress alone does not completely govern failure as an AAA will usually rupture when the wall stress exceeds the wall strength. In light of this, rupture assessment may be more accurate if both the patient-specific wall stress is coupled together with patient-specific wall strength. A non-invasive method of determining patient-dependent wall strength was recently reported, with more traditional approaches to strength determination via tensile testing performed by other researchers in the field. Some of the more recently proposed AAA rupture-risk assessment methods include: AAA wall stress; AAA expansion rate; degree of asymmetry; presence of intraluminal thrombus (ILT); a rupture potential index (RPI); a finite element analysis rupture index (FEARI); biomechanical factors coupled with computer analysis; growth of ILT; geometrical parameters of the AAA; and also a method of determining AAA growth and rupture based on mathematical models.

The post-operative mortality for an already ruptured AAA has slowly decreased over several decades but remains higher than 40%. However, if the AAA is surgically repaired before rupture, the post-operative mortality rate is substantially lower: approximately 1-6%.

The risk of aneurysm enlargement may be diminished with attention to the patient's blood pressure, smoking and cholesterol levels. There have been proposals to introduce ultrasound scans as a screening tool for those most at risk: men over the age of 65. The tetracycline antibiotic doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilizing properties. In contrast, fluoroquinolones antibiotics are being investigated as a potential contributor to aortic aneurysms, given their tendency to break down collagen fibrils.

Anacetrapib is a cholesteryl ester transfer protein inhibitor that raises high-density lipoprotein (HDL) cholesterol and reduces low-density lipoprotein (LDL) cholesterol.

Anacetrapib reduces progression of atherosclerosis, mainly by reducing non-HDL-cholesterol, improves lesion stability and adds to the beneficial effects of atorvastatin

Elevating the amount of HDL cholesterol in the abdominal area of the aortic artery in mice both reduced the size of aneurysms that had already grown and prevented abdominal aortic aneurysms from forming at all. In short, raising HDL cholesterol is beneficial because it induces programmed cell death. The walls of a failing aorta are replaced and strengthened. New lesions should not form at all when using this drug.

Mortality from aortic rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.

Diagnosis is often suspected in patients "in extremis" (close to death) with abdominal trauma or with relevant risk-factors. Diagnosis is confirmed quickly in the Emergency room by ultrasound or CT scan.

Thoracic abdominal aneurysm is defined as a diameter exceeding the following cutoff:

- 4.5 cm in the United States

- 4.0 cm in South Korea

A diameter of 3.5 cm is generally considered dilated. However, average values vary with age and size of the reference population, as well as different segments of the aorta.

Diagnosis of a ruptured cerebral aneurysm is commonly made by finding signs of subarachnoid hemorrhage on a computed tomography (CT) scan. If the CT scan is negative but a ruptured aneurysm is still suspected based on clinical findings, a lumbar puncture can be performed to detect blood in the cerebrospinal fluid. Computed tomography angiography (CTA) is an alternative to traditional angiography and can be performed without the need for arterial catheterization. This test combines a regular CT scan with a contrast dye injected into a vein. Once the dye is injected into a vein, it travels to the cerebral arteries, and images are created using a CT scan. These images show exactly how blood flows into the brain arteries.

Due to the acute hemodynamic deterioration associated with myocardial rupture, the diagnosis is generally made based on physical examination, changes in the vital signs, and clinical suspicion. The diagnosis can be confirmed with echocardiography. The diagnosis is ultimately made at autopsy.

Since the cause of FAD has not been genetically pinpointed, the only way to diagnose FAD is through the examination of phenotypic variations in the aorta. Usually echocardiography is used to take measurements of the aortic root as well as transesophageal echocardiography. Biomarkers lend a quick way to diagnose dissection when time is of the essence. These have the ability to relay the levels of smooth muscle mysosin heavy chain protein present, which is released from damaged aortic tissue.

There are two types of FAD; groups A and B. Normally if any area of the ascending aorta is involved in the dissection this is considered group A. If the dissection occurs within the descending aorta this is classified in group B. These two groups can than be broken down into three classes of FAD: Type 1, Type 2 and Type 3. Group A consists of Types 1 and 2, whereas Group B consists only of Type 3. Type 1 encompasses dissection in the distal ascending aorta closest to the heart, not including the aortic arch. Type 2 refers to dissection of the ascending aorta, closer to and including the aortic arch. Type 3 refers to the descending thoracic and abdominal aorta.

Group A dissections are the more serious of the two due to the location of the dissection in the ascending aorta, which leads to a higher risk of congestive heart failure and pericardium and/or aortic valve rupture. Individuals also tend to be predisposed to type A if they do have Marfans or Elhers-Danlos syndromes. These contribute to a higher fatality rate in group A dissection if immediate surgery is not performed. The most common corrective surgeries are actual aortic valve replacement and coronary artery bypass. The five year survival rate after surgery is a successful 70.4% due to vigilant monthly physical exams and chest x-rays to monitor progress. Group B dissections typically have a higher surgery mortality rate and are therefore not good candidates. Instead medical management is the common response to treating and keeping dissections of the descending aorta under control.

The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial infarction. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction. On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered. The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.

The condition is difficult to detect and may go unnoticed, because many patients have no specific symptoms. Diagnosis is further complicated by the fact that many patients with the injury experienced multiple other serious injuries as well, so the attention of hospital staff may be distracted from the possibility of aortic rupture. In fact most cases occur along with other injuries.

A common symptom is unusually high blood pressure in the upper body and very low blood pressure in lower limbs. Another symptom is renal failure where the creatinine level shoots very high and urine output becomes negligible. In most cases, however, the doctors would misinterpret renal failure as due to issues with the kidney itself and may recommend dialysis.

Though not completely reliable, chest X-rays are the first-line treatment, initially used to diagnose this condition when the patient is unstable and cannot be sent to the CT bay. The preferred method of diagnosis used to be CT angiogram until it was found to cause complications in some people; now it is reserved for when CT scans are inconclusive.

The classical findings on a chest X-ray will be widened mediastinum, apical cap, and displacement of the trachea, left main bronchus, or nasogastric tube. A normal chest x-ray does not exclude transection, but will diagnose conditions such as pneumothorax or hydrothorax. The aorta may also be torn at the point where it is connected to the heart. The aorta may be completely torn away from the heart, but patients with such injuries rarely survive very long after the injury; thus it is much more common for hospital staff to treat patients with partially torn aortas. When the aorta is partially torn, it may form a "pseudoaneurysm". In patients who do live long enough to be seen in a hospital, a majority have only a partially torn blood vessel, with the outermost adventitial layer still intact. In some of these patients, the adventitia and nearby structures within the chest may serve to prevent severe bleeding. After trauma, the aorta can be assessed by a CT angiogram or a direct angiogram, in which contrast is introduced into the aorta via a catheter.

Renal aneurysms are very rare consisting of only 0.1–0.09% while rupture is even more rare. Conservative treatment with control of concomitant hypertension being the primary option with aneurysms smaller than 3 cm. If symptoms occur, or enlargement of the aneurysm, then endovascular or open repair should be considered. Pregnant women (due to high rupture risk of up to 80%) should be treated surgically.

Death occurs immediately after traumatic rupture of the thoracic aorta 75%–90% of the time since bleeding is so severe, and 80–85% of patients die before arriving at a hospital. Of those who live to reach a hospital, 23% die at the time of or shortly after arrival. In the US, an estimated 7,500–8,000 cases occur yearly, of which 1,000–1,500 make it to a hospital alive; these low numbers make it difficult to estimate the efficacy of surgical options. However, if surgery is performed in time, it can offer a chance of survival.

Though there is a concern that a small, stable tear in the aorta could enlarge and cause complete rupture of the aorta and heavy bleeding, this may be less common than previously believed as long as the patient's blood pressure does not get too high.

Currently, there is controversy over whether or not inheritance truly plays a role in FAD, and if so which gene it acts upon. FAD does not come from strictly one predisposing factor, such as hypertension. It is suggested that the combination of environmental factors along with genetics may contribute to causing FAD. Before newer and more effective cures and therapies can be developed, first the specific gene mutation must be identified. Until such a gene is determined, scientists say patient education, and physician awareness is vital. Currently scientists have found animal models to be beneficial in understanding the pathology behind FAD. In the future there is hope to develop drugs that will better support and strengthen the aortic wall. Endovascular methods of treatment are becoming increasingly popular, and scientists hope to use this technique in both acute and chronic cases.

Medical therapy of aneurysm of the aortic sinus includes blood pressure control through the use of drugs, such as beta blockers.

Another approach is surgical repair. The determination to perform surgery is usually based upon the diameter of the aortic root (with 5 centimeters being a rule of thumb - a normal size is 2-3 centimeters) and the rate of increase in its size (as determined through repeated echocardiography).

A chest X-ray can also assist in the diagnosis and provide clues as to the severity of the disease, showing the degree of calcification of the valve, and in a chronic condition, an enlarged left ventricle and atrium.

Cardiac chamber catheterization provides a definitive diagnosis, indicating severe stenosis in valve area of <1.0 cm (normally about 3 cm). It can directly measure the pressure on both sides of the aortic valve. The pressure gradient may be used as a decision point for treatment. It is useful in symptomatic people before surgery. The standard for diagnosis of aortic stenosis is noninvasive testing with echocardiography. Cardiac catheterization is reserved for cases in which there is discrepancy between the clinical picture and non-invasive testing, due to risks inherent to crossing the aortic valve such as stroke.

Hemopericardium can be diagnosed using echocardiography, a cardiac ultrasound. Chest X-rays are also often taken when hemopericardium is suspected and would reveal an enlarged heart. Other observable signs include rapid heart rate, jugular venous distension, low blood pressure, and pulsus paradoxus.

Unfortunately, coarctations can not be prevented because they are usually present at birth. The best thing for patients who are affected by coarctations is early detection. Some signs that can lead to a coarctation have been linked to pathologies such as Turner syndrome, bicuspid aortic valve, and other family heart conditions.