The incidence of VBI increases with age and typically occurs in the seventh or eighth decade of life. Reflecting atherosclerosis, which is the most common cause of VBI, it affects men twice as often as women and patients with hypertension, diabetes, smoking, and dyslipidemias have a higher risk of developing VBI.

VBI, often provoked by sudden and temporary drops in blood pressure, can cause transient ischemic attacks. Postural changes (see orthostatic hypotension), such as getting out of bed too quickly or standing up after sitting for extended periods of time, often provoke these attacks. Exercise of the legs, or the sudden cessation of leg exercises, may also bring on the symptoms of VBI. For the sedentary older subject, going up a flight of stairs or walking the dog may be enough to cause pooling of blood in the legs and a drop in blood pressure in the distal arteries of the head. Heat and dehydration may also be contributing causes.

Mechanical forces acting upon the neck at any age can cause VBI by exacerbating arterial insufficiency or outright occluding one or both vertebrobasilar arteries. Internal forces include those caused by turning the head to an extreme angle to the side, especially with the neck extended. The patient can create this condition while driving a vehicle in reverse, shooting a bow and arrow, bird watching, or stargazing. There was a study demonstrating the relationship between VBI and yoga practice, though this subject is in need of updated research. External forces include those caused by sports or other physical contact.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

Patients should discuss with their physician possible causes for their VBI symptoms. As discussed above, postural changes, exercise, and dehydration are some of the likely culprits. Treatment usually involves lifestyle modifications. For example, if VBI is attributed mainly to postural changes, patients are advised to slowly rise to standing position after sitting for a long period of time. An appropriate exercise regimen for each patient can also be designed in order to avoid the excessive pooling of blood in the legs. Dehydrated patients are often advised to increase their water intake, especially in hot, dry climates. Finally, when applicable, patients are often advised to stop smoking and to control their hypertension, diabetes, and cholesterol level.

In the event that a patient suffers a “drop attack,” and especially for the elderly population, the most important action is to be evaluated for associated head or other injuries. To prevent drop attacks, patients are advised to “go to the ground” before the knees buckle and shortly after feeling dizzy or experiencing changes in vision. Patients should not be concerned about the social consequences of suddenly sitting on the floor, whether in the mall or sidewalk, as such actions are important in preventing serious injuries.

Sometimes, to prevent further occlusion of blood vessels, patients are started on an antiplatelet agent (aspirin, clopidogrel, or aspirin/dipyridamole) or sometimes an anticoagulant (warfarin) once hemorrhage has been excluded with imaging.

For treatment of vertebrobasilar stenosis due to atherosclerosis, researchers from Stanford University found that intracranial angioplasty can be performed with an annual stroke rate in the territory of treatment of 3.2% and 4.4% for all strokes, including periprocedural events. Randomized control trials need to be performed.

Risk factors for thromboembolism, the major cause of arterial embolism, include disturbed blood flow (such as in atrial fibrillation and mitral stenosis), injury or damage to an artery wall, and hypercoagulability (such as increased platelet count). Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke. Endocarditis increases the risk for thromboembolism, by a mixture of the factors above.

Atherosclerosis in the aorta and other large blood vessels is a common risk factor, both for thromboembolism and cholesterol embolism. The legs and feet are major impact sites for these types. Thus, risk factors for atherosclerosis are risk factors for arterial embolisation as well:

- advanced age

- cigarette smoking

- hypertension (high blood pressure)

- obesity

- hyperlipidemia, e.g. hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein (a) or apolipoprotein B, or decreased levels of HDL cholesterol)

- diabetes mellitus

- Sedentary lifestyle

- stress

Other important risk factors for arterial embolism include:

- recent surgery (both for thromboembolism and air embolism)

- previous stroke or cardiovascular disease

- a history of long-term intravenous therapy (for air embolism)

- Bone fracture (for fat embolism)

A septal defect of the heart makes it possible for paradoxical embolization, which happens when a clot in a vein enters the right side of the heart and passes through a hole into the left side. The clot can then move to an artery and cause arterial embolisation.

Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognised cause of stroke that preferentially affects the middle-aged.

The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.

Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have a history of stroke in their family and/or hereditary connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I. IgG4-related disease involving the carotid artery has also been observed as a cause.

However, although an association with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders. Also, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections are highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.

Internal carotid artery dissection can also be associated with an elongated styloid process (known as Eagle syndrome when the elongated styloid process causes symptoms).

Traumatic injury to an extremity may produce partial or total occlusion of a vessel from compression, shearing or laceration. Acute arterial occlusion may develop as a result of arterial dissection in the carotid artery or aorta or as a result of iatrogenic arterial injury (e.g., after angiography).

The thrombi may dislodge and may travel anywhere in the circulatory system, where they may lead to pulmonary embolus, an acute arterial occlusion causing the oxygen and blood supply distal to the embolus to decrease suddenly. The degree and extent of symptoms depend on the size and location of the obstruction, the occurrence of clot fragmentation with embolism to smaller vessels, and the degree of peripheral arterial disease (PAD).

- Thromboembolism (blood clots)

- Embolism (foreign bodies in the circulation, e.g. amniotic fluid embolism)

Non-occlusive disease has a poor prognosis with survival rate between 40-50%.

Carotid stenosis is a narrowing or constriction of the inner surface (lumen) of the carotid artery, usually caused by atherosclerosis.

The largest clinical trial performed, CREST, randomized patients at risk for a stroke from carotid artery blockage to either open surgery (carotid endarterectomy) or carotid stent placement with embolic protection. This trial followed patients for 4 years and found no overall difference in the primary end point of both treatment arms (myocardial infarctions, any perioperative strokes or ipsilateral strokes within 4 years, or death during procedure). Patients assigned to the surgical arm experienced more perioperative myocardial infarctions compared to the stenting group; however, the difference was not statistically significant (6.8% vs or 7.2% HR for stenting is 1.1 CI 0.81-1.51 P value 0.51) whereas patients assigned to the carotid stent arm experienced more periprocedural strokes compared to endarteretomy (6.4% vs 4.7% HR for stenting 1.5 P-0.03). There was no mortality difference and no difference for major (disabling) strokes between surgery and stenting. It was noted that there did seem to exist an age cutoff where below 75 years old endarterectomy provided more positive outcomes and over 75 stenting offered a better risk profile. However, it should be noted that the CREST trial was not designed for subgroup analysis and thus not powered enough to draw any statistically significant conclusions. A later study published in 2013 evaluated how these perioperative complications affect long-term survival. This study showed that experiencing a stroke within the first year conferred a two-fold lower survival rate (Hazard Ratio(HR) 6.6 [CI 3.7-12]) than those who experienced a perioperative myocardial infarction at two years post intervention (HR 3.6 [CI 2-6.8]). This difference in mortality, however, converges and becomes negligible at 5 years (HR 2.7 [CI 1.7-4.3] vs HR 2.8 [CI 1.8-4.3]). A 2010 study found benefits (reduced strokes) from carotid endarterectomy in those without symptoms who are under 75.

In 2008, the US had an estimate of 16 million atherosclerotic heart disease and 5.8 million strokes. Cardiovascular diseases that were caused by arteriosclerosis also caused almost 812,000 deaths in 2008, more than any other cause, including cancer. About 1.2 million Americans are predicted to have a heart attack each year.

CT angiography would be helpful in differentiating occlusive from non-occlusive causes of mesenteric ischaemia.

When the heart contracts it generates a pulse or energy wave that travels through the circulatory system. The speed of travel of this pulse wave (pulse wave velocity (PWV)) is related to the stiffness of the arteries. Other terms that are used to describe the mechanical properties of arteries include elastance, or the reciprocal (inverse) of elastance, compliance. The relationship between arterial stiffness and pulse wave velocity was first predicted by Thomas Young in his Croonian Lecture of 1808 but is generally described by the Moens–Korteweg equation or the Bramwell–Hill equation. Typical values of PWV in the aorta range from approximately 5 m/s to >15 m/s.

Measurement of aortic PWV provides some of the strongest evidence concerning the prognostic significance of large artery stiffening. Increased aortic PWV has been shown to predict cardiovascular, and in some cases all cause, mortality in individuals with end stage renal failure, hypertension, diabetes mellitus and in the general population. However, at present, the role of measurement of PWV as a general clinical tool remains to be established. Devices are on the market that measure arterial stiffness parameters (augmentation index, pulse wave velocity). These include the Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, BP Plus (Pulsecor), PulsePen, BPLab Vasotens, Arteriograph, Vascular Explorer, and SphygmoCor.

An arterial embolism is caused by one or more emboli getting stuck in an artery and blocking blood flow, causing ischemia, possibly resulting in infarction with tissue death (necrosis). Individuals with arterial thrombosis or embolism often develop collateral circulation to compensate for the loss of arterial flow. However, it takes time for sufficient collateral circulation to develop, making affected areas more vulnerable for sudden occlusion by embolisation than for e.g. gradual occlusion as in atherosclerosis.

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.

Arterial stiffness occurs as a consequence of biological aging and arteriosclerosis. Inflammation plays a major role in arteriosclerosis development, and consequently it is a major contributor in large arteries stiffening. Increased arterial stiffness is associated with an increased risk of cardiovascular events such as myocardial infarction and stroke, the two leading causes of death in the developed world. The World Health Organisation predicts that in 2010, cardiovascular disease will also be the leading killer in the developing world and represents a major global health problem.

Several degenerative changes that occur with age in the walls of large elastic arteries are thought to contribute to increased stiffening over time, including the mechanical fraying of lamellar elastin structures within the wall due to repeated cycles of mechanical stress; changes in the kind and increases in content of arterial collagen proteins, partially as a compensatory mechanism against the loss of arterial elastin and partially due to fibrosis; and crosslinking of adjacent collagen fibers by advanced glycation endproducts (AGEs).

Most commonly, intermittent (or vascular or arterial) claudication is due to peripheral arterial disease which implies significant atherosclerotic blockages resulting in arterial insufficiency. It is distinct from neurogenic claudication, which is associated with lumbar spinal stenosis. It is strongly associated with smoking, hypertension, and diabetes.

Classically, SSS is a consequence of a redundancy in the circulation of the brain and the flow of blood.

SSS results when the short low resistance path (along the subclavian artery) becomes a high resistance path (due to narrowing) and blood flows around the narrowing via the arteries that supply the brain (left and right vertebral artery, left and right internal carotid artery). The blood flow from the brain to the upper limb in SSS is considered to be "" as it is blood flow the brain must do without. This is because of collateral vessels.

As in vertebral-subclavian steal, coronary-subclavian steal may occur in patients who have received a coronary artery bypass graft using the internal thoracic artery (ITA), also known as internal mammary artery. As a result of this procedure, the distal end of the ITA is diverted to one of the coronary arteries (typically the LAD), facilitating blood supply to the heart. In the setting of increased resistance in the proximal subclavian artery, blood may flow backward away from the heart along the ITA, causing myocardial ischemia due to coronary steal. Vertebral-subclavian and coronary-subclavian steal can occur concurrently in patients with an ITA CABG.

Intermittent claudication (Latin: "claudicatio intermittens") is a symptom that describes muscle pain on mild exertion (ache, cramp, numbness or sense of fatigue), classically in the calf muscle, which occurs during exercise, such as walking, and is relieved by a short period of rest. It is classically associated with early-stage peripheral artery disease, and can progress to critical limb ischemia unless treated or risk factors are modified.

Claudication derives from the Latin verb "claudicare", "to limp".

Treatment is often in the form of preventative measures of prophylaxis. Drug therapy for underlying conditions, such as drugs for the treatment of high cholesterol, drugs to treat high blood pressure (ACE inhibitors), and anti-coagulant drugs, are often prescribed to help prevent arteriosclerosis. Lifestyle changes such as increasing exercise, stopping smoking, and moderating alcohol intake are also advised. Experimental treatments include senolytic drugs, or drugs that selectively eliminate senescent cells, which enhance vascular reactivity and reduce vascular calcification in a mouse model of atherosclerosis, as well as improving cardiovascular function in old mice.

There are a variety of types of surgery:

- Angioplasty and stent placement: A catheter is first inserted into the blocked/narrowed part of your artery, followed by a second one with a deflated balloon which is passed through the catheter into the narrowed area. The balloon is then inflated, pushing the deposits back against the arterial walls, and then a mesh tube is usually left behind to prevent the artery from retightening.

- Coronary artery bypass surgery: This surgery creates a new pathway for blood to flow to the heart. Taking a healthy piece of vein, the surgeon attaches it to the coronary artery, just above and below the blockage to allow bypass.

- Endarterectomy: This is the general procedure for the surgical removal of plaque from the artery that has become narrowed, or blocked.

- Thrombolytic therapy: is a treatment used to break up masses of plaque inside the arteries via intravenous clot-dissolving medicine.

There are many causes of TOS. The most frequent cause is trauma, either sudden (as in a clavicle fracture caused by a car accident), or repetitive (as in a legal secretary who works with his/her hands, wrists, and arms at a fast paced desk station with non-ergonomic posture for many years). TOS is also found in certain occupations involving lots of lifting of the arms and repetitive use of the wrists and arms.

One cause of arterial compression is trauma, and a recent case involving fracture of the clavicle has been reported.

The two groups of people most likely to develop TOS are those suffering from neck injuries due to traffic accidents and those who use computers in non-ergonomic postures for extended periods of time. TOS is frequently a repetitive stress injury (RSI) caused by certain types of work environments. Other groups which may develop TOS are athletes who frequently raise their arms above the head (such as swimmers, volleyball players, dancers, badminton players, baseball pitchers, and weightlifters), rock climbers, electricians who work long hours with their hands above their heads, and some musicians.

Although an estimated 50 million or more adult Americans suffer from hypertension, the relative incidence of hypertensive crisis is relatively low (less than 1% annually). Nevertheless, this condition does affect upward of 500,000 Americans each year, and is therefore a significant cause of serious morbidity in the US. About 14% of adults seen in hospital emergency departments in United States have a systolic blood pressure ≥180 mmHg.

As a result of the use of antihypertensives, the rates of hypertensive emergencies has declined from 7% to 1% of people with high blood pressure. The 1–year survival rate has also increased. Before 1950, this survival rate was 20%, but it is now more than 90% with proper medical treatment.

Estimates indicate that approximately 1% to 2% of people with hypertension develop hypertensive crisis at some point in their lifetime. Men are more commonly affected by hypertensive crises than women.

The rates of hypertensive crises has increased and hospital admissions tripled between 1983 and 1990, from 23,000 to 73,000 per year in the United States. The incidence of postoperative hypertensive crisis varies and such variation depends on the population examined. Most studies report and incidence of between 4% to 35%.

Although the cause of Takayasu arteritis is unknown, the condition is characterized by segmental and patchy granulomatous inflammation of the aorta and its major derivative branches. This inflammation leads to arterial stenosis, thrombosis, and aneurysms. There is irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis (fibrosis of the inner section of the blood vessels). Prominent narrowing due to inflammation, granuloma, and fibrosis is often seen in arterial studies such as magnetic resonance angiography (MRA), computed tomography angiography (CTA), or arterial angiography (DSA).

Many factors and causes are contributory in hypertensive crises. One main cause is the discontinuation of antihypertensive medications. Other common causes of hypertensive crises are autonomic hyperactivity, collagen-vascular diseases, drug use (particularly stimulants, especially cocaine and amphetamines and their substituted analogues), glomerulonephritis, head trauma, neoplasias, preeclampsia and eclampsia, and renovascular hypertension.

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.