Aneurysm presentation may range from life-threatening complications of hypovolemic shock to being found incidentally on X-ray. Symptoms will differ by the site of the aneurysm and can include:

Abdominal aneurysms are usually asymptomatic, but rarely can cause lower back pain or lower limb ischemia

Fusiform dolichoectatic aneurysms represent a widening of a segment of an artery around the entire blood vessel, rather than just arising from a side of an artery's wall. They can rupture but usually do not.

A small, unchanging aneurysm will produce few, if any, symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may experience no symptoms at all.

About 96% of individuals with aortic dissection present with severe pain that had a sudden onset. The pain may be described as a tearing, stabbing, or sharp sensation; 17% of individuals feel the pain migrate as the dissection extends down the aorta. The location of pain is associated with the location of the dissection. Anterior chest pain is associated with dissections involving the ascending aorta, while interscapular (back) pain is associated with descending aortic dissections. If the pain is pleuritic in nature, it may suggest acute pericarditis caused by bleeding into the pericardial sac. This is a particularly dangerous eventuality, suggesting that acute pericardial tamponade may be imminent. Pericardial tamponade is the most common cause of death from aortic dissection.

While the pain may be confused with the pain of a myocardial infarction (heart attack), aortic dissection is usually not associated with the other signs that suggest myocardial infarction, including heart failure and ECG changes.

Individuals with aortic dissection who do not present with pain have a chronic dissection.

Less common symptoms that may be seen in the setting of aortic dissection include congestive heart failure (7%), fainting (9%), stroke (6%), ischemic peripheral neuropathy, paraplegia, and cardiac arrest. If the individual had a fainting episode, about half the time it is due to bleeding into the pericardium leading to pericardial tamponade.

Neurological complications of aortic dissection (i.e., stroke and paralysis) are due to the involvement of one or more arteries supplying portions of the central nervous system.

If the aortic dissection involves the abdominal aorta, compromise of the branches of the abdominal aorta is possible. In abdominal aortic dissections, compromise of one or both renal arteries occurs in 5–8% of cases, while mesenteric ischemia (ischemia of the large intestines) occurs 3–5% of the time.

Inflammatory Aortic Aneurysms occur typically in a younger population compared to the typical Abdominal Aortic Aneurysm group. Risk of rupture for the IAA group, due to thinning of anuerysm walls, are also rare due to inflammation and fibrosis

Unruptured inflammatory AAAs are usually symptomatic:

- abdominal or back pain (70 to 80%)

- abdominal tenderness

- fever

- weight loss

- elevated erythrocyte sedimentation rate (90%)

People with an aortic dissection often have a history of high blood pressure; the blood pressure is quite variable at presentation with acute aortic dissection, and tends to be higher in individuals with a distal dissection. In individuals with a proximal aortic dissection, 36% present with hypertension, while 25% present with hypotension. Proximal aortic dissections tend to be more associated with weakening of the vascular wall due to cystic medial degeneration. In those who present with distal (type B) aortic dissections, 60-70% present with high blood pressure, while 2-3% present with low blood pressure.

Severe hypotension at presentation is a grave prognostic indicator. It is usually associated with pericardial tamponade, severe aortic insufficiency, or rupture of the aorta. Accurate measurement of the blood pressure is important. Pseudohypotension (falsely low blood-pressure measurement) may occur due to involvement of the brachiocephalic artery (supplying the right arm) or the left subclavian artery (supplying the left arm).

In medical pathology, a dissection is a tear within the wall of a blood vessel, which allows blood to separate the wall layers. By separating a portion of the wall of the artery (a layer of the tunica intima or tunica media), a dissection creates two lumens or passages within the vessel, the native or true lumen, and the "false lumen" created by the new space within the wall of the artery.

The diagnosis of thoracic aortic aneurysm usually involves patients in their 60s and 70s.

Dissections become threatening to the health of the organism when growth of the false lumen prevents perfusion of the true lumen and the end organs perfused by the true lumen. For example, in an aortic dissection, if the left subclavian artery orifice were distal to the origin of the dissection, then the left subclavian would be said to be perfused by the false lumen, while the left common carotid (and its end organ, the left hemisphere of the brain) if proximal to the dissection, would be perfused by the true lumen proximal to the dissection.

Vessels and organs that are perfused from a false lumen may be well-perfused to varying degrees, from normal perfusion to no perfusion. In some cases, little to no end-organ damage or failure may be seen. Similarly, vessels and organs perfused from the true lumen but distal to the dissection may be perfused to varying degrees. In the above example, if the aortic dissection extended from proximal to the left subclavian artery takeoff to the mid descending aorta, the common iliac arteries would be perfused from the true lumen distal to the dissection but would be at risk for malperfusion due to occlusion of the true lumen of the aorta by the false lumen.

A thoracic aortic aneurysm is an aortic aneurysm that presents primarily in the thorax.

A thoracic aortic aneurysm is the "ballooning" of the upper aspect of the aorta, above the diaphragm. Untreated or unrecognized they can be fatal due to dissection or "popping" of the aneurysm leading to nearly instant death. Thoracic aneurysms are less common than an abdominal aortic aneurysm. However, a syphilitic aneurysm is more likely to be a thoracic aortic aneurysm than an abdominal aortic aneurysm.

The symptoms are often very similar to those of myocardial infarction (heart attack), with the most common being persistent chest pain.

Aortic rupture is the rupture or breakage of the aorta, the largest artery in the body. Aortic rupture is a rare, extremely dangerous condition. The most common cause is an abdominal aortic aneurysm that has ruptured spontaneously. Aortic rupture is distinct from aortic dissection, which is a tear through the inner wall of the aorta that can block the flow of blood through the aorta to the heart or abdominal organs.

An aortic rupture can be classified according to its cause into one of the following main types:

- Traumatic aortic rupture

- Aortic rupture secondary to an aortic aneurysm

Generally, it has a good prognosis. In Kawasaki's disease, untreated, there is a 1–2% death rate, from cardiac causes.

Head pain occurs in 50–75% of all cases of vertebral artery dissection. It tends to be located at the back of the head, either on the affected side or in the middle, and develops gradually. It is either dull or pressure-like in character or throbbing. About half of those with VAD consider the headache distinct, while the remainder have had a similar headache before. It is suspected that VAD with headache as the only symptom is fairly common; 8% of all cases of vertebral and carotid dissection are diagnosed on the basis of pain alone.

Obstruction of blood flow through the affected vessel may lead to dysfunction of part of the brain supplied by the artery. This happens in 77–96% of cases. This may be temporary ("transient ischemic attack") in 10–16% of cases, but many (67–85% of cases) end up with a permanent deficit or a stroke. The vertebral artery supplies the part of the brain that lies in the posterior fossa of the skull, and this type of stroke is therefore called a posterior circulation infarct. Problems may include difficulty speaking or swallowing (lateral medullary syndrome); this occurs in less than a fifth of cases and occurs due to dysfunction of the brainstem. Others may experience unsteadiness or lack of coordination due to involvement of the cerebellum, and still others may develop visual loss (on one side of the visual field) due to involvement of the visual cortex in the occipital lobe. In the event of involvement of the sympathetic tracts in the brainstem, a partial Horner's syndrome may develop; this is the combination of a drooping eyelid, constricted pupil, and an apparently sunken eye on one side of the face.

If the dissection of the artery extends to the part of the artery that lies inside the skull, subarachnoid hemorrhage may occur (1% of cases). This arises due to rupture of the artery and accumulation of blood in the subarachnoid space. It may be characterized by a different, usually severe headache; it may also cause a range of additional neurological symptoms.

13–16% of all people with vertebral or carotid dissection have dissection in another cervical artery. It is therefore possible for the symptoms to occur on both sides, or for symptoms of carotid artery dissection to occur at the same time as those of vertebral artery dissection. Some give a figure of multiple vessel dissection as high as 30%.

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

Acquired causes include atherosclerosis, Kawasaki disease and coronary catheterization.

It can also be congenital.

Vertebral artery dissection is one of the two types of dissection of the arteries in the neck. The other type, carotid artery dissection, involves the carotid arteries. Vertebral artery dissection is further classified as being either traumatic (caused by mechanical trauma to the neck) or spontaneous, and it may also be classified by the part of the artery involved: extracranial (the part outside the skull) and intracranial (the part inside the skull).

A spontaneous coronary artery dissection (SCAD) (occasionally coronary artery dissection) is a rare, sometimes fatal traumatic condition, with eighty percent of cases affecting women. One of the coronary arteries develops a tear, causing blood to flow between the layers which forces them apart. Studies of the disease place the mortality rate at around 70%.

SCAD is a primary cause of myocardial infarction (MI) in young, fit, healthy women (and some men) with no obvious risk factors. These can often occur during late pregnancy, postpartum and peri-menopausal periods.

Coronary artery ectasia is a rare disease that occurs in only 0.3-4.9% of people in North America. Coronary artery ectasia is characterized by the enlargement of a coronary artery to 1.5 times or more than its normal diameter. The disease is commonly asymptomatic and is normally discovered when performing tests for other conditions such as coronary artery disease, stable angina and other acute coronary syndromes. Coronary artery ectasia occurs 4 times more frequently in males than in females and in people who have risk factors for heart disease such as smokers. While the disease is commonly found in patients with atherosclerosis and coronary artery disease, it can occur by itself and in both cases it can cause health problems. The disease can cause the heart tissue to be deprived of blood and die due to decreased blood flow, and blockages due to blood clots or spasms of the blood vessel. This blood flow disruption can cause permanent damage to the muscle if the deprivation is prolonged. Coronary artery ectasia also increases the chance of developing large weak spots in the affected coronary arteries, or aneurysms that can rupture and result in death. The damage can result in angina which is pain in the chest and is a common complaint in these patients.

Subclavian steal syndrome (SSS), also called subclavian steal phenomenon or subclavian steal steno-occlusive disease, is a constellation of signs and symptoms that arise from retrograde (reversed) blood flow in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. The arm may be supplied by blood flowing in a retrograde direction down the vertebral artery at the expense of the vertebrobasilar circulation. This is called the "subclavian steal". It is more severe than typical vertebrobasilar insufficiency.

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.

For most people, the first symptoms result from atheroma progression within the heart arteries, most commonly resulting in a heart attack and ensuing debility. However, the heart arteries, because (a) they are small (from about 5 mm down to microscopic), (b) they are hidden deep within the chest and (c) they never stop moving, have been a difficult target organ to track, especially clinically in individuals who are still asymptomatic. Additionally, all mass-applied clinical strategies focus on both (a) minimal cost and (b) the overall safety of the procedure. Therefore, existing diagnostic strategies for detecting atheroma and tracking response to treatment have been extremely limited. The methods most commonly relied upon, patient symptoms and cardiac stress testing, do not detect any symptoms of the problem until atheromatous disease is very advanced because arteries enlarge, not constrict in response to increasing atheroma. It is plaque ruptures, producing debris and clots which obstruct blood flow downstream, sometimes also locally (as seen on angiograms), which reduce/stop blood flow. Yet these events occur suddenly and are not revealed in advance by either stress testing, stress tests or angiograms.

Many patients with unruptured IIA may have no symptoms. In patients who do have symptoms these are often related to rupture of the aneurysm and to its cause. Rupture of an IIA results in subarachnoid hemorrhage, symptoms of which include headache, dizziness, seizures, altered mental status and focal neurological deficits.

In contrast to other cerebral aneurysms, large aneurysm size does not increase the chance of rupture. Small IIAs

tend to have high rupture rates, while larger IIAs more commonly cause symptoms due to pressure on the surrounding brain tissue.

Ventricular aneurysms are usually complications resulting from a heart attack. When the heart muscle (cardiac muscle) partially dies during a heart attack, a layer of muscle may survive, and, being severely weakened, start to become an aneurysm. Blood may flow into the surrounding dead muscle and inflate the weakened flap of muscle into a bubble. It may also be congenital.