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.

Surgery (open or endovascular) is the definite treatment of an aortic aneurysm. Medical therapy is typically reserved for smaller aneurysms or for elderly, frail patients where the risks of surgical repair exceed the risks of non-operative therapy (observation alone).

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.

Conservative management is indicated in people where repair carries a high risk of mortality and in patients where repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smoking cessation.

Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the risk of rupture. As an AAA grows in diameter, the risk of rupture increases. Surveillance until an aneurysm has reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to early intervention.

In an acute dissection, treatment choice depends on its location. For Stanford type A (ascending aortic) dissection, surgical management is superior to medical management. For uncomplicated Stanford type B (distal aortic) dissections (including abdominal aortic dissections), medical management is preferred over surgical.

The risk of death due to aortic dissection is highest in the first few hours after the dissection begins, and decreases afterward. Because of this, the therapeutic strategies differ for the treatment of an acute dissection compared to a chronic dissection. An acute dissection is one in which the individual presents within the first two weeks. If the individual has managed to survive this window period, his prognosis is improved. About 66% of all dissections present in the acute phase. Individuals who present two weeks after the onset of the dissection are said to have chronic aortic dissections. These individuals have been self-selected as survivors of the acute episode and can be treated with medical therapy as long as they are stable.

The size cut off for aortic aneurysm is crucial to its treatment. A thoracic aorta greater than 4.5 cm is generally defined as aneurysmal, while a size greater than 6 cm is the distinction for treatment, which can be either endovascular or surgical, with the former reserved for pathology at the descending aorta.

Indication for surgery may depend upon the size of the aneurysm. Aneurysms in the ascending aorta may require surgery at a smaller size than aneurysms in the descending aorta.

Treatment may be via open or via endovascular means.

The treatment options for asymptomatic AAA are management, surveillance with a view to eventual repair, and immediate repair. Two modes of repair are available for an AAA: open aneurysm repair, and endovascular aneurysm repair (EVAR). An intervention is often recommended if the aneurysm grows more than 1 cm per year or it is bigger than 5.5 cm. Repair is also indicated for symptomatic aneurysms.

Aortic dissection generally presents as a hypertensive emergency, and the prime consideration of medical management is strict blood pressure control. The target blood pressure should be a mean arterial pressure (MAP) of 60 to 75 mmHg, or the lowest blood pressure tolerated. Initial decreases should be by about 20%.

Another factor is to reduce the shear-force dP/dt (force of ejection of blood from the left ventricle). Long-term management of physical, emotional, and psychological stresses are important to controlling blood pressure.

Beta blockers are the first-line treatment for patients with acute and chronic aortic dissection. In acute dissection, fast-acting agents which can be given intravenously and have doses that are easier to adjust (such as esmolol, propranolol, or labetalol) are preferred. Vasodilators such as sodium nitroprusside can be considered for people with ongoing high blood pressure, but they should never be used alone, as they often stimulate a reflexive increase in the heart rate.

Calcium channel blockers can be used in the treatment of aortic dissection, particularly if a contraindication to the use of beta blockers exists. The calcium channel blockers typically used are verapamil and diltiazem, because of their combined vasodilator and negative inotropic effects.

If the individual has refractory hypertension (persistent hypertension on the maximum doses of three different classes of antihypertensive agents), an involvement of the renal arteries in the aortic dissection plane should be considered.

Aortic ruptures can be repaired surgically via open aortic surgery or using endovascular therapy (EVAR), regardless of cause, just as non-ruptured aortic aneurysms are repaired. An aortic occlusion balloon can be placed to stabilize the patient and prevent further blood loss prior to the induction of anesthesia.

Historically, the treatment of arterial aneurysms has been limited to either surgical intervention, or watchful waiting in combination with control of blood pressure. In recent years, endovascular or minimally invasive techniques have been developed for many types of aneurysms. Aneurysm Clips are used for surgical procedure i.e. clipping of aneurysms.

Hypertension and cigarette smoking are the most important risk factors, though the importance of genetic factors has been increasingly recognized. Approximately 10% of patients may have other family members who have aortic aneurysms. It is also important to note that individuals with a history of aneurysms in other parts of the body have a higher chance of developing a thoracic aortic aneurysm.

There are currently two treatment options for brain aneurysms: surgical clipping or endovascular coiling. There is currently debate in the medical literature about which treatment is most appropriate given particular situations.

Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. It consists of a craniotomy to expose the aneurysm and closing the base or neck of the aneurysm with a clip. The surgical technique has been modified and improved over the years.

Endovascular coiling was introduced by Guido Guglielmi at UCLA in 1991. It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Platinum coils initiate a clotting reaction within the aneurysm that, if successful fill the aneurysm dome and prevent its rupture. Flow diverter can be used but not without complications sometimes.

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.

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.

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for securing intracranial aneurysms: surgical clipping or endovascular coiling. If possible, either surgical clipping or endovascular coiling is usually performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of rebleeding.

While a large meta-analysis found the outcomes and risks of surgical clipping and endovascular coiling to be statistically similar, no consensus has been reached. In particular, the large randomised control trial International Subarachnoid Aneurysm Trial appears to indicate a higher rate of recurrence when intracerebral aneurysms are treated using endovascular coiling. Analysis of data from this trial has indicated a 7% lower eight-year mortality rate with coiling, a high rate of aneurysm recurrence in aneurysms treated with coiling—from 28.6-33.6% within a year, a 6.9 times greater rate of late retreatment for coiled aneurysms, and a rate of rebleeding 8 times higher than surgically-clipped aneurysms.

Inflammatory aortic aneurysm (IAA), also known as Inflammatory abdominal aortic aneurysm (IAAA), is a type of abdominal aortic aneurysm (AAA) where the walls of the aneurysm become thick and inflamed. Similar to AAA, IAA occurs in the abdominal region. IAA is closely associated and believed to be a response to and extensive peri-anuerysmal fibrosis, which is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process IAA accounts for 5-10% of aortic aneurysms. IAA is occurs mainly in a population that is on average younger by 10 years than most AAA patients. Some common symptoms of IAA may include back pain, abdominal tenderness, fevers, weight loss or elevated Erythrocyte sedimentation rate (ESR) levels. Corticosteroids and other immunosuppressive drugs have been found to decrease symptoms and the degree of peri-aortic inflammation and fibrosis

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).

Although the exact cause is unknown, some risk factors associated with individuals with IAA are:

Tobacco Use: Cigarette smoking and other forms of tobacco use appear to increase your risk of aortic aneurysms. In addition to the damaging effects that smoking causes directly to the arteries, smoking contributes to the buildup of fatty plaques in your arteries (atherosclerosis) and high blood pressure. Smoking can also cause your aneurysm to grow faster by further damaging your aorta.

Hardening of the arteries (atherosclerosis). Atherosclerosis occurs when fat and other substances build up on the lining of a blood vessel, increasing your risk of an aneurysm.

Infection in the aorta (vasculitis). In rare cases, abdominal aortic aneurysm may be caused by an infection or inflammation that weakens a section of the aortic wall.

Aneurysms can be treated by clipping the base of the aneurysm with a specially-designed clip. Whilst this is typically carried out by craniotomy, a new endoscopic endonasal approach is being trialled. Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937

After clipping, a catheter angiogram or CTA can be performed to confirm complete clipping.

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.

Type 1 and Type 2 FAD call for the same treatment: immediate surgery to replace the aorta. Surgery is required due to the high risk of mortality. Type 3 is less severe and requires the maintenance of blood pressure through diet and exercise. Upon diagnosing someone with FAD intravenous antihypertensive treatment is frequently used. Often intravenous sodium nitroprusside is used for its efficiency in lessening the pulsatile load thus reducing blood pressure. Reducing this force slows the progression of the dissection. Surgical success depends on age, severity of symptoms, postoperative organ dysfunction and stroke. Surgical intervention is always indicated in Type 1 cases. Aortic surgery is palliative, not curative. The goal is to merely to prevent rupture, restore blood flow, and fix any aortic valve dysfunction. Post operative protocols include frequent monitoring of the aorta diameter. Statins and beta blockers are also popular treatments used to reduce future plaque build up and blockage of epinephrine receptors as a way to control heart rate and blood pressure.

Long term treatment should also include regular check ups every 3 to 6 months. A CT scan or MRI is recommended, along with required chest x-rays. Antihypertensive therapy with beta adrenergic antagonists is required regardless of medical versus surgical treatment. Ten to twenty percent of those who choose surgical intervention are re-operated on due to compression, aneurysm development or blood leakage.

Traumatic aortic rupture is treated with surgery. However, morbidity and mortality rates for surgical repair of the aorta for this condition are among the highest of any cardiovascular surgery. For example, surgery is associated with a high rate of paraplegia, because the spinal cord is very sensitive to ischemia (lack of blood supply), and the nerve tissue can be damaged or killed by the interruption of the blood supply during surgery.

A less invasive option for treatment is endovascular repair, which does not require open thoracotomy and can be safer for people with other injuries to organs.

Since high blood pressure could exacerbate an incomplete tear in the aorta or even separate it completely from the heart, which would almost inevitably kill the patient, hospital staff take measures to keep the blood pressure low. Such measures include giving pain medication, keeping the patient calm, and avoiding procedures that could cause gagging or vomiting. Beta blockers and vasodilators can be given to lower the blood pressure, and intravenous fluids that might normally be given are foregone to avoid raising it.

From analysis of the existing small treatment trials of cervical artery dissection (carotid and vertebral) it appears that aspirin and anticoagulation (heparin followed by warfarin) are equally effective in reducing the risk of further stroke or death. Anticoagulation is regarded as more powerful than antiplatelet therapy, but anticoagulants may increase the size of the hematoma and worsen obstruction of the affected artery. Anticoagulation may be relatively unsafe if a large stroke has already occurred, as hemorrhagic transformation is relatively common, and if the dissection extends into V4 (carrying a risk of subarachnoid hemorrhage). Anticoagulation may be appropriate if there is rapid blood flow (through a severely narrowed vessel) on transcranial doppler despite the use of aspirin, if there is a completely occluded vessel, if there are recurrent stroke-like episodes, or if free-floating blood clot is visible on scans. Warfarin is typically continued for 3–6 months, as during this time the flow through the artery usually improves, and most strokes happen within the first 6 months after the development of the dissection. Some regard 3 months as sufficient.

Professional guidelines in the UK recommend that patients with VA dissection should be enrolled in a clinical trial comparing aspirin and anticoagulation if possible. American guidelines state that the benefit of anticoagulation is not currently established.

Treatment is focused on reducing stroke episodes and damage from a distending artery. Four treatment modalities have been reported in the treatment of vertebral artery dissection. The two main treatments involve medication: anticoagulation (using heparin and warfarin) and antiplatelet drugs (usually aspirin). More rarely, thrombolysis (medication that dissolves blood clots) may be administered, and occasionally obstruction may be treated with angioplasty and stenting. No randomized controlled trials have been performed to compare the different treatment modalities. Surgery is only used in exceptional cases.

Some people live with this type of aneurysm for many years without any specific treatment. Treatment is limited to surgery (ventricular reduction) for this defect of the heart. However, surgery is not required in most cases but, limiting the patient's physical activity levels to lower the risk of making the aneurysm bigger is advised. Also ACE Inhibitors seem to prevent Left Ventricular remodeling and aneurysm formation.

Blood thinning agents may be given to help reduce the likelihood of blood thickening and clots forming, along with the use of drugs to correct the irregular rhythm of the heart (seen on the electrocardiogram)