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.

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.

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

Risk factors contributing to PAD are the same as those for atherosclerosis:

- Smoking – tobacco use in any form is the single most important modifiable cause of PAD internationally. Smokers have up to a tenfold increase in relative risk for PAD in a dose-response relationship. Exposure to second-hand smoke from environmental exposure has also been shown to promote changes in blood vessel lining (endothelium) which is a precursor to atherosclerosis. Smokers are 2 to 3 times more likely to have lower extremity peripheral arterial disease than coronary artery disease. More than 80%-90% of patients with lower extremity peripheral arterial disease are current or former smokers. The risk of PAD increases with the number of cigarettes smoked per day and the number of years smoked.

- Diabetes mellitus – causes between two and four times increased risk of PAD by causing endothelial and smooth muscle cell dysfunction in peripheral arteries. The risk of developing lower extremity peripheral arterial disease is proportional to the severity and duration of diabetes.

- Dyslipidemia – a high level of low-density lipoprotein (LDL cholesterol) and a low level of high-density lipoprotein (HDL cholesterol) in the blood) - elevation of total cholesterol, LDL cholesterol, and triglyceride levels each have been correlated with accelerated PAD. Correction of dyslipidemia by diet and/or medication is associated with a major improvement in rates of heart attack and stroke.

- Hypertension – elevated blood pressure is correlated with an increase in the risk of developing PAD, as well as in associated coronary and cerebrovascular events (heart attack and stroke). Hypertension increased the risk of intermittent claudication 2.5- to 4-fold in men and women, respectively.

- Risk of PAD also increases in individuals who are over the age of 50, male, obese, heart attack, or stroke or with a family history of vascular disease.

- Other risk factors which are being studied include levels of various inflammatory mediators such as C-reactive protein, fibrinogen, hyperviscosity, hypercoagulable state.

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

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.

Peripheral arterial disease is more common in the following populations of people:

- All people who have leg symptoms with exertion (suggestive of claudication) or ischemic rest pain.

- All people aged 65 years and over regardless of risk factor status.

- All people between the age of 50 to 69 and who have a cardiovascular risk factor (particularly diabetes or smoking).

- Age less than 50 years, with diabetes and one other atherosclerosis risk factor (smoking, dyslipidemia, hypertension, or hyperhomocysteinemia).

- Individuals with an abnormal lower extremity pulse examination.

- Those with known atherosclerotic coronary, carotid, or renal artery disease.

- All people with a Framingham risk score 10%-20%

- All people who have previously experienced chest pain

Coronary thrombosis is the formation of a blood clot inside a blood vessel of the heart. This blood clot restricts blood flow within the heart. It is associated with narrowing of blood vessels subsequent to clotting. The condition is considered as a type of ischaemic heart disease, also known as a heart attack or myocardial infarction.

Thrombosis in the heart can lead to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes used as synonyms, although this is technically inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart contains many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms. Coronary thrombosis is caused by atherosclerosis.This is when there is build up of cholesterol and fats in the artery walls. So the blood will clot because there isn't enough room for it to flow. The main causes of coronary thrombosis are stress, smoking, high blood pressure, and lack of exercise. Symptoms are sharp pains around the chest area, breathing difficulties, dizziness, and fainting. This is treated by taking Aspirin, Nitrates, or Beta Blockers.

Coronary thrombosis can be a complication associated with drug-eluting stents.

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

Currently laboratory testing is not as reliable as observation when it comes to defining the parameters of Thrombotic Storm. Careful evaluation of possible thrombosis in other organ systems is pertinent in expediting treatment to prevent fatality.Preliminary diagnosis consists of evidence documented with proper imaging studies such as CT scan, MRI, or echocardiography, which demonstrate a thromboembolic occlusion in the veins and/or arteries. Vascular occlusions mentioned must include at least two of the clinic events:

- Deep venous thrombosis affecting one (or more) limbs and/or pulmonary embolism.

- Cerebral vein thrombosis.

- Portal vein thrombosis, hepatic vein, or other intra-abdominal thrombotic events.

- Jugular vein thrombosis in the absence of ipsilateral arm vein thrombosis and in the absence of ipsilateral central venous access.

- Peripheral arterial occlusions, in the absence of underlying atherosclerotic vascular disease,

- resulting in extremity ischemia and/or infarction.

- Myocardial infarction, in the absence of severe coronary artery disease

- Stroke and/or transient ischemic attack, in the absence of severe atherosclerotic disease and at an age less than 60 years.

- Central retinal vein and/or central retinal arterial thrombosis.

- Small vessel thrombosis affecting one or more organs, systems, or tissue; must be documented by histopathology.

In addition to the previously noted vascular occlusions, development of different thromboembolic manifestations simultaneously or within one or two weeks must occur and the patient must have an underlying inherited or acquired hypercoagulable state (other than Antiphospholipid syndrome)

The annual incidence is about 1.1 per 100,000 annually in population studies from the United States and France. From 1994 to 2003, the incidence increased threefold; this has been attributed to the more widespread use of modern imaging modalities rather than a true increase. Similarly, those living in urban areas are more likely to receive appropriate investigations, accounting for increased rates of diagnosis in those dwelling in cities. It is suspected that a proportion of cases in people with mild symptoms remains undiagnosed.

There is controversy as to whether VAD is more common in men or in women; an aggregate of all studies shows that it is slightly higher incidence in men (56% versus 44%). Men are on average 37–44 years old at diagnosis, and women 34–44. While dissection of the carotid and vertebral arteries accounts for only 2% of strokes (which are usually caused by high blood pressure and other risk factors, and tend to occur in the elderly), they cause 10–25% of strokes in young and middle-aged people.

Dissecting aneurysms of the vertebral artery constitute 4% of all cerebral aneurysms, and are hence a relatively rare but important cause of subarachnoid hemorrhage.

Prognosis of spontaneous cervical arterial dissection involves neurological and arterial results. The overall functional prognosis of individuals with stroke due to cervical artery dissection does not appear to vary from that of young people with stroke due to other causes. The rate of survival with good outcome (a modified Rankin score of 0–2) is generally about 75%, or possibly slightly better (85.7%) if antiplatelet drugs are used. In studies of anticoagulants and aspirin, the combined mortality with either treatment is 1.8–2.1%.

After the initial episode, 2% may experience a further episode within the first month. After this, there is a 1% annual risk of recurrence. Those with high blood pressure and dissections in multiple arteries may have a higher risk of recurrence. Further episodes of cervical artery dissection are more common in those who are younger, have a family history of cervical artery dissection, or have a diagnosis of Ehlers-Danlos syndrome or fibromuscular dysplasia.

Blood clots are a relatively common occurrence in the general population and are seen in approximately 1-2% of the population by age 60. Typically blood clots develop in the deep veins of the lower extremities, deep vein thrombosis (DVT) or as a blood clot in the lung, pulmonary embolism (PE). A very small number of people who develop blood clots have a more serious and often life-threatening condition, known as Thrombotic Storm (TS). TS is characterized by the development of more than one blood clot in a short period of time. These clots often occur in multiple and sometimes unusual locations in the body and are often difficult to treat. TS may be associated with an existing condition or situation that predisposes a person to blood clots such as injury, infection, or pregnancy. In many cases a risk assessment will identify interventions that will prevent the formation of blood clots.

While the mechanism or pathogenesis is not completely understood mostly due to its rarity, the medical community has developed a new interest in learning more about this syndrome. Dr. Craig S. Kitchens first described TS in six case studies. In these cases he described a collection of similar features observed in six patients, suggesting this may be accounted for by a new syndrome.

An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel. The embolus may be a blood clot (thrombus), a fat globule (fat embolism), a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel. Such a blockage (a vascular occlusion) may affect a part of the body distant from where the embolus originated. An embolism in which the embolus is a piece of thrombus is called a thromboembolism. Thrombosis, the process of thrombus formation, often leads to thromboembolism.

An embolism is usually a pathological event, i.e., accompanying illness or injury. Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.

Arterial embolism can cause occlusion in any part of the body. It is a major cause of infarction, tissue death due to the blockage of blood supply.

An embolus lodging in the brain from either the heart or a carotid artery will most likely be the cause of a stroke due to ischemia.

An arterial embolus might originate in the heart (from a thrombus in the left atrium, following atrial fibrillation or be a septic embolus resulting from endocarditis). Emboli of cardiac origin are frequently encountered in clinical practice. Thrombus formation within the atrium occurs mainly in patients with mitral valve disease, and especially in those with mitral valve stenosis (narrowing), with atrial fibrillation (AF). In the absence of AF, pure mitral regurgitation has a low incidence of thromboembolism.

The risk of emboli forming in AF depends on other risk factors such as age, hypertension, diabetes, recent heart failure, or previous stroke.

Thrombus formation can also take place within the ventricles, and it occurs in approximately 30% of anterior-wall myocardial infarctions, compared with only 5% of inferior ones. Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming.

Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the position (mitral or aortic); and the presence of other factors such as AF, left-ventricular dysfunction, and previous emboli.

Emboli often have more serious consequences when they occur in the so-called "end circulation": areas of the body that have no redundant blood supply, such as the brain and heart.

The best course of treatment varies from case to case. The physician must take into account the details in the case before deciding on the appropriate treatment. No treatment is effective for every patient.

Treatment depends on many factors, including:

- Location of lesions

- Anatomy of lesions

- Patient risk factors

- Procedural risk

- Clinical presentation of symptoms

- Duration of symptoms

- etc.

Major risk factors for cerebral infarction are generally the same as for atherosclerosis: high blood pressure, Diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke. The AHA/ASA guidelines also provide information on how to prevent stroke if someone has more specific concerns, such as Sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study.

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

Although there is a lack of robust studies demonstrating the efficacy of lifestyle changes in preventing TIA, many medical professionals recommend them. These include:

- Avoiding smoking

- Cutting down on fats to help reduce the amount of plaque build up

- Eating a healthy diet including plenty of fruits and vegetables

- Limiting sodium in the diet, thereby reducing blood pressure

- Exercising regularly

- Moderating intake of alcohol, stimulants, sympathomimetics, etc.

- Maintaining a healthy weight

In addition, it is important to control any underlying medical conditions that may increase the risk of stroke or TIA, including:

- Hypertension

- High cholesterol

- Diabetes mellitus

- Atrial fibrillation

By definition, TIAs are transient, self-resolving, and do not cause permanent impairment. However, they are associated with an increased risk of subsequent ischemic strokes, which can be permanently disabling. Therefore, management centers around the prevention of future ischemic strokes and addressing any modifiable risk factors. The optimal regimen depends on the underlying cause of the TIA.

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.

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).

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)

Acquired cerebrovascular diseases are those that are obtained throughout a person's life that may be preventable by controlling risk factors. The incidence of cerebrovascular disease increases as an individual ages. Causes of acquired cerebrovascular disease include atherosclerosis, embolism, aneurysms, and arterial dissections. Atherosclerosis leads to narrowing of blood vessels and less perfusion to the brain, and it also increases the risk of thrombosis, or a blockage of an artery, within the brain. Major modifiable risk factors for atherosclerosis include:

Controlling these risk factors can reduce the incidence of atherosclerosis and stroke. Atrial fibrillation is also a major risk factor for strokes. Atrial fibrillation causes blood clots to form within the heart, which may travel to the arteries within the brain and cause an embolism. The embolism prevents blood flow to the brain, which leads to a stroke.

An aneurysm is an abnormal bulging of small sections of arteries, which increases the risk of artery rupture. Intracranial aneurysms are a leading cause of subarachnoid hemorrhage, or bleeding around the brain within the subarachnoid space. There are various hereditary disorders associated with intracranial aneurysms, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, and familial hyperaldosteronism type I. However, individuals without these disorders may also obtain aneurysms. The American Heart Association and American Stroke Association recommend controlling modifiable risk factors including smoking and hypertension.

Arterial dissections are tears of the internal lining of arteries, often associated with trauma. Dissections within the carotid arteries or vertebral arteries may compromise blood flow to the brain due to thrombosis, and dissections increase the risk of vessel rupture.

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).