Most intact aortic aneurysms do not produce symptoms. As they enlarge, symptoms such as abdominal pain and back pain may develop. Compression of nerve roots may cause leg pain or numbness. Untreated, aneurysms tend to become progressively larger, although the rate of enlargement is unpredictable for any individual. Rarely, clotted blood which lines most aortic aneurysms can break off and result in an embolus.

Aneurysms can be found on physical examination. Medical imaging is necessary to confirm the diagnosis and to determine the anatomic extent of the aneurysm. In patients presenting with aneurysm of the arch of the aorta, a common sign is a hoarse voice from stretching of the left recurrent laryngeal nerve, a branch of the vagus nerve that winds around the aortic arch to supply the muscles of the larynx.

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.

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).

Aortic aneurysms are classified by their location on the aorta.

- An aortic root aneurysm, or aneurysm of the sinus of Valsalva.

- Thoracic aortic aneurysms are found within the chest; these are further classified as ascending, aortic arch, or descending aneurysms.

- Abdominal aortic aneurysms, "AAA" or "Triple A," the most common form of aortic aneurysm, involve that segment of the aorta within the abdominal cavity. Thoracoabdominal aortic aneurysms involve both the thoracic and abdominal aorta.

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

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.

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

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:

The vast majority of aneurysms are asymptomatic. However, as abdominal aortic aneurysms expand, they may become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, or scrotum. The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery. The complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable and pulsatile abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.

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

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%)

The signs and symptoms of a ruptured AAA may include severe pain in the lower back, flank, abdomen or groin. A mass that pulses with the heart beat may also be felt. The bleeding can lead to a hypovolemic shock with low blood pressure and a fast heart rate. This may lead to brief passing out.

The mortality of AAA rupture is as high as 90 percent. 65 to 75 percent of patients die before they arrive at the hospital and up to 90 percent die before they reach the operating room. The bleeding can be or into the abdominal cavity. Rupture can also create a connection between the aorta and intestine or inferior vena cava. Flank ecchymosis (appearance of a bruise) is a sign of retroperitoneal bleeding, and is also called Grey Turner's sign.

Aortic aneurysm rupture may be mistaken for the pain of kidney stones, or muscle related back pain.

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

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.

If unruptured, this type of aneurysm may be asymptomatic and therefore go undetected until symptoms appear or medical imaging is performed for other reasons. A ruptured aneurysm typically leads to an aortocardiac shunt and progressively worsening heart failure.

An aneurysm of the aortic sinus may rupture due to infective endocarditis involving the aortic wall and tertiary-stage syphilis.

The manifestations appear depending on the site where the sinus has ruptured. For example, if the sinus ruptures in a low pressure area like the right atrium or right ventricle then a continuous type of murmur is heard. The murmur is located in the left parasternal region mainly confined to the lower sternum. It is also accompanied by a superficial thrill. A ruptured Sinus of Valsalva abscess represents a surgical emergency.

Familial aortic dissection or FAD refers to the splitting of the wall of the aorta in either the arch, ascending or descending portions. FAD is thought to be passed down as an autosomal dominant disease and once inherited will result in dissection of the aorta, and dissecting aneurysm of the aorta, or rarely aortic or arterial dilation at a young age. Dissection refers to the actual tearing open of the aorta. However, the exact gene(s) involved has not yet been identified. It can occur in the absence of clinical features of Marfan syndrome and of systemic hypertension. Over time this weakness, along with systolic pressure, results in a tear in the aortic intima layer thus allowing blood to enter between the layers of tissue and cause further tearing. Eventually complete rupture of the aorta occurs and the pleural cavity fills with blood. Warning signs include chest pain, ischemia, and hemorrhaging in the chest cavity. This condition, unless found and treated early, usually results in death. Immediate surgery is the best prognosis in most cases. FAD is not to be confused with PAU (penetrating atherosclerotic ulcers) and IMH (intramural hematoma), both of which present in ways similar to that of familial aortic dissection.

This type of aneurysm is typically congenital and may be associated with heart defects. It is sometimes associated with Marfan syndrome or Loeys–Dietz syndrome, but may also result from Ehlers–Danlos syndrome, bicuspid aortic valve, atherosclerosis, hypoplastic left heart syndrome, syphilis, cystic medial necrosis, chest injury, or infective endocarditis.

It is unclear whether stenting or open surgery is a better for those with aneurysms that are not causing symptoms.

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.

Symptoms related to aortic stenosis depend on the degree of stenosis. Most people with mild to moderate aortic stenosis do not have symptoms. Symptoms usually present in individuals with severe aortic stenosis, though they may occur in those with mild to moderate aortic stenosis as well. The three main symptoms of aortic stenosis are loss of consciousness, anginal chest pain and shortness of breath with activity or other symptoms of heart failure such as shortness of breath while lying flat, episodes of shortness of breath at night, or swollen legs and feet. It may also be accompanied by the characteristic "Dresden china" appearance of pallor with a light flush.

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.

Annuloaortic ectasia is a dilation of the proximal ascending aorta and aortic annulus. It may cause aortic regurgitation, thoracic aortic dissection, aneurysm and rupture. It is often associated with connective tissue diseases like Marfan syndrome and Ehlers Danlos Syndrome. It can also be a complication due to tertiary syphilis. In tertiary syphilis the aortic root becomes so dilated that the aortic valve becomes incompetent and cor bovinum results.

The term was first coined by the American heart surgeon Denton Cooley in 1961.

Traumatic aortic rupture, also called traumatic aortic disruption or transection, is a condition in which the aorta, the largest artery in the body, is torn or ruptured as a result of trauma to the body. The condition is frequently fatal due to the profuse bleeding that results from the rupture. Since the aorta branches directly from the heart to supply blood to the rest of the body, the pressure within it is very great, and blood may be pumped out of a tear in the blood vessel very rapidly. This can quickly result in shock and death. Thus traumatic aortic rupture is a common killer in automotive accidents and other traumas, with up to 18% of deaths that occur in automobile collisions being related to the injury. In fact, aortic disruption due to blunt chest trauma is the second leading cause of injury death behind traumatic brain injury.

Aortic rupture can also be caused by non-traumatic mechanisms, particularly abdominal aortic aneurysm rupture.

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%.

Angina in setting of heart failure also increases the risk of death. In people with angina, the 5-year mortality rate is 50% if the aortic valve is not replaced.

Angina in the setting of AS occurs due to left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement. This ischemia may first be evident during exercise when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of anginal chest pain with exertion. At this stage, a cardiac stress test with imaging may be suggestive of ischemia.

Eventually, however, the heart muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of "ventricular strain pattern" (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that is most susceptible to ischemia because it is the most distant from the epicardial coronary arteries.