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.

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.

Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.

The morbidity and of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good blood pressure control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.

The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increases. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

Several studies have concluded that African Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease than non-Hispanic whites. It appears that hypertensive crisis is also more common in African Americans compared with other races.

Although severe hypertension is more common in the elderly, it may occur in children (though very rarely). Also, women have slightly increased risks of developing hypertension crises than do men. The lifetime risk for developing hypertension is 86-90% in females and 81-83% in males.

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%.

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

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.

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.

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)

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 prognosis of pulmonary arterial hypertension (WHO Group I) has an "untreated" median survival of 2–3 years from time of diagnosis, with the cause of death usually being right ventricular failure (cor pulmonale). A recent outcome study of those patients who had started treatment with bosentan (Tracleer) showed that 89% patients were alive at 2 years. With new therapies, survival rates are increasing. For 2,635 patients enrolled in The Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management (REVEAL Registry) from March 2006 to December 2009, 1-, 3-, 5-, and 7-year survival rates were 85%, 68%, 57%, and 49%, respectively. For patients with idiopathic/familial PAH, survival rates were 91%, 74%, 65%, and 59%. Levels of mortality are very high in pregnant women with severe pulmonary arterial hypertension (WHO Group I). Pregnancy is sometimes described as contraindicated in these women.

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.

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

The epidemiology of IPAH is about 125–150 deaths per year in the U.S., and worldwide the incidence is similar to the U.S. at 4 cases per million. However, in parts of Europe (France) indications are 6 cases per million of IPAH. Females have a higher incidence rate than males (2–9:1).

Other forms of PH are far more common. In systemic scleroderma, the incidence has been estimated to be 8 to 12% of all patients; in rheumatoid arthritis it is rare. However, in systemic lupus erythematosus it is 4 to 14%, and in sickle cell disease, it ranges from 20 to 40%. Up to 4% of people who suffer a pulmonary embolism go on to develop chronic thromboembolic disease including pulmonary hypertension. A small percentage of patients with COPD develop pulmonary hypertension with no other disease to explain the high pressure. On the other hand, obesity-hypoventilation syndrome is very commonly associated with right heart failure due to pulmonary hypertension.

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

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.

Hahner et al. investigated the frequency, causes and risk factors for adrenal crisis in patients with chronic adrenal insufficiency. Annane et al.'s landmark 2002 study found a very high rate of relative adrenal insufficiency among the enrolled patients with septic shock.

A paradoxical embolism, also called a crossed embolism, refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa. It is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin, which travels to the arterial side through a lateral opening in the heart, such as a patent foramen ovale, or arteriovenous shunts in the lungs.

The opening is typically an atrial septal defect, but can also be a ventricular septal defect.

Paradoxical embolisms represent two percent of arterial emboli.

Passage of a clot (thrombus) from a systemic vein to a systemic artery. When clots in systemic veins break off (embolize), they travel first to the right side of the heart and, normally, then to the lungs where they lodge, causing pulmonary embolism. On the other hand, when there is a hole at the septum, either upper chambers of the heart (an atrial septal defect) or lower chambers of the heart (ventricular septal defects), a clot can cross from the right to the left side of the heart, then pass into the systemic arteries as a paradoxical embolism. Once in the arterial circulation, a clot can travel to the brain, block a vessel there, and cause a stroke (cerebrovascular accident).

The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.

Adrenal crisis is triggered by physiological stress (such as trauma). Activities that have an elevated risk of trauma are best avoided. Treatment must be given within two hours of trauma and consequently it is advisable to carry injectable hydrocortisone in remote areas.

In treating pulmonary insufficiency, it should be determined if pulmonary hypertension is causing the problem to therefore begin the most appropriate therapy as soon as possible (primary pulmonary hypertension or secondary pulmonary hypertension due to thromboembolism). Furthermore, pulmonary insufficiency is generally treated by addressing the underlying condition, in certain cases, the pulmonary valve may be surgically replaced.

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).

Options include:

- Medications alone (an antiplatelet drug (or drugs) and control of risk factors for atherosclerosis).

- Medical management plus carotid endarterectomy or carotid stenting, which is preferred in patients at high surgical risk and in younger patients.

- Control of smoking, high blood pressure, and high levels of lipids in the blood.

The goal of treatment is to reduce the risk of stroke (cerebrovascular accident). Intervention (carotid endarterectomy or carotid stenting) can cause stroke; however, where the risk of stroke from medical management alone is high, intervention may be beneficial. In selected trial participants with asymptomatic severe carotid artery stenosis, carotid endarterectomy reduces the risk of stroke in the next 5 years by 50%, though this represents a reduction in absolute incidence of all strokes or perioperative death of approximately 6%. In most centres, carotid endarterectomy is associated with a 30-day stroke or mortality rate of < 3%; some areas have higher rates.

Clinical guidelines (such as those of National Institute for Clinical Excellence (NICE) ) recommend that all patients with carotid stenosis be given medication, usually blood pressure lowering medications, anti-clotting medications, anti-platelet medications (such as aspirin or clopidogrel), and especially statins (which were originally prescribed for their cholesterol-lowering effects but were also found to reduce inflammation and stabilize plaque).

NICE and other guidelines also recommend that patients with "symptomatic" carotid stenosis be given carotid endarterectomy urgently, since the greatest risk of stroke is within days. Carotid endarterectomy reduces the risk of stroke or death from carotid emboli by about half.

For people with stenosis but no symptoms, the interventional recommendations are less clear. Such patients have a historical risk of stroke of about 1-2% per year. Carotid endarterectomy has a surgical risk of stroke or death of about 2-4% in most institutions. In the large Asymptomatic Carotid Surgery Trial (ACST) endarterectomy reduced major stroke and death by about half, even after surgical death and stroke was taken into account. According to the Cochrane Collaboration the absolute benefit of surgery is small. For intervention using stents, there is insufficient evidence to support stenting rather than open surgery, and several trials, including the ACST-2, are comparing these 2 procedures.

The prognosis of tricuspid insufficiency is less favorable for males than females. Furthermore, increased tricuspid insufficiency (regurgitation) severity is an indication of a poorer prognosis according to Nath, et al. It is also important to note that since tricuspid insufficiency most often arises from left heart failure or pulmonary hypertension, the person's prognosis is usually dictated by the prognosis of the latter conditions and not by the tricuspid insufficiency "per se".

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow.