In peripheral procedures, rates are still high. A 2003 study of selective and systematic stenting for limb-threatening ischemia reported restenosis rates at 1 year follow-up in 32.3% of selective stenting patients and 34.7% of systematic stenting patients.

The 2006 SIROCCO trial compared the sirolimus drug-eluting stent with a bare nitinol stent for atherosclerotic lesions of the superficial femoral artery, reporting restenosis at 2 year follow-up was 22.9% and 21.1%, respectively.

A 2009 study compared bare nitinol stents with percutaneous transluminal angioplasty (PTA) in superficial femoral artery disease. At 1 year follow-up, restenosis was reported in 34.4% of stented patients versus 61.1% of PTA patients.

Examples include:

- Aortic dissection (aorta)

- Coronary artery dissection (coronary artery)

- Carotid artery dissection (carotid artery)

- Vertebral artery dissection (vertebral artery)

Carotid and vertebral artery dissection are grouped together as "cervical artery dissection".

In cardiac procedures, balloon angioplasty has been associated with a high incidence of restenosis, with rates ranging from 25% to 50%, and the majority of these patients need further angioplasty within 6 months.

A 2010 study in India comparing coronary drug-eluting stents (DES) with coronary bare-metal stents (BMS) reported that restenosis developed in 23.1% of DES patients vs 48.8% in BMS patients, and female sex was found to be a statistically significant risk factor for developing restenosis.

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.

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.

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

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.

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

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.

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.

In Heyde's syndrome, aortic stenosis is associated with gastrointestinal bleeding due to angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve.

If untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a 3-year survival rate of less than 30%. Prognosis after aortic valve replacement for people who are younger than 65 is about five years less than that of the general population; for people older than 65 it is about the same.

A stenosis is an abnormal narrowing in a blood vessel or other tubular organ or structure. It is also sometimes called a stricture (as in urethral stricture).

Stricture as a term is usually used when narrowing is caused by contraction of smooth muscle (e.g., achalasia, prinzmetal angina); stenosis is usually used when narrowing is caused by lesion that reduces the space of lumen (e.g., atherosclerosis). The term coarctation is another synonym, but is commonly used only in the context of aortic coarctation.

Restenosis is the recurrence of stenosis after a procedure. The term is from Ancient Greek στενός, "narrow".

Aberrant subclavian artery, or aberrant subclavian artery syndrome, is a rare anatomical variant of the origin of the right or left subclavian artery. This abnormality is the most common congenital vascular anomaly of the aortic arch, occurring in approximately 1% of individuals.

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 resulting syndrome depends on the structure affected.

Examples of vascular stenotic lesions include:

- Intermittent claudication (peripheral artery stenosis)

- Angina (coronary artery stenosis)

- Carotid artery stenosis which predispose to (strokes and transient ischaemic episodes)

- Renal artery stenosis

The types of stenoses in heart valves are:

- Pulmonary valve stenosis, which is the thickening of the pulmonary valve, therefore causing narrowing

- Mitral valve stenosis, which is the thickening of the mitral valve (of the left heart), therefore causing narrowing

- Tricuspid valve stenosis, which is the thickening of the tricuspid valve (of the right heart), therefore causing narrowing

- Aortic valve stenosis, which is the thickening of the aortic valve, therefore causing narrowing

Stenoses/strictures of other bodily structures/organs include:

- Pyloric stenosis (gastric outflow obstruction)

- Lumbar, cervical or thoracic spinal stenosis

- Subglottic stenosis (SGS)

- Tracheal stenosis

- Obstructive jaundice (biliary tract stenosis)

- Bowel obstruction

- Phimosis

- Non-communicating hydrocephalus

- Stenosing tenosynovitis

- Atherosclerosis

- Esophageal stricture

- Achalasia

- Prinzmetal angina

- Vaginal stenosis

Stenosis of the pulmonary artery is a condition where the pulmonary artery is subject to an abnormal constriction (or stenosis). Peripheral pulmonary artery stenosis may occur as an isolated event or in association with Alagille syndrome, Berardinelli-Seip congenital lipodystrophy type 1, Costello syndrome, Keutel syndrome, nasodigitoacoustic syndrome (Keipert syndrome), Noonan syndrome or Williams syndrome.

It should not be confused with a pulmonary valve stenosis, which is in the heart, but can have similar hemodynamic effects. Both stenosis of the pulmonary artery and pulmonary valve stenosis are causes of pulmonic stenosis.

In some cases it is treated with surgery.

While the cause of FMD remains unclear, current theory suggest that there may be a genetic predisposition as case reports have identified clusters of the disease and prevalence among twins. In fact, according to the Cleveland Clinic approximately 10% of cases appear to be inherited and often coexists with other genetic abnormalities that affect the blood vessels. Approximately 10% of patients with FMD have an affected family member. A study conducted from the patient registry at Michigan Cardiovascular Outcomes Research and Reporting Program (MCORRP) at the University of Michigan Health System reported a high prevalence of a family history of stroke (53.5%), aneurysm (23.5%), and sudden death (19.8%). Even though FMD is a non-atherosclerotic disease family histories of hypertension and hyperlipidemia were also common among those diagnosed with FMD. It is believed that the cause of FMD is not a single identifier such as genetics but has multiple underlying factors. Theories of hormonal influence, mechanical stress from trauma and stress to the artery walls, and also the effect of loss of oxygen supply to the blood vessel wall caused by fibrous lesions. It has been suggested that environmental factors, such as smoking and estrogen, may play role in addition to genetic factors.

The exact prevalence of the syndrome is unknown, because both aortic stenosis and angiodysplasia are common diseases in the elderly. A retrospective chart review of 3.8 million people in Northern Ireland found that the incidence of gastrointestinal bleeding in people with any diagnosis of aortic stenosis (they did not subgroup people by severity) was just 0.9%. They also found that the reverse correlation—the incidence of aortic stenosis in people with gastrointestinal bleeding—was 1.5%. However, in 2003 a study of 50 people with aortic stenosis severe enough to warrant immediate valve replacement found GI bleeding in 21% of people, and another study done in the USA looking at angiodysplasia rather than GI bleeding found that the prevalence of aortic stenosis was 31% compared to 14% in the control group.

This condition is usually asymptomatic. The aberrant artery usually arises just distal to the left subclavian artery and crosses in the posterior part of the mediastinum on its way to the right upper extremity. In 80% of individuals it crosses behind the esophagus. Such course of this aberrant vessel may cause a vascular ring around the trachea and esophagus.

Dysphagia due to an aberrant right subclavian artery is termed dysphagia lusoria, although this is a rare complication. In addition to dysphagia, aberrant right subclavian artery may cause stridor, dyspnoea, chest pain, or fever. An aberrant right subclavian artery may compress the recurrent laryngeal nerve causing a palsy of that nerve, which is termed Ortner's syndrome.

The aberrant right subclavian artery frequently arises from a dilated segment of the proximal descending aorta, the so-called Diverticulum of Kommerell (which was named for the German Radiologist, Burkhard Friedrich Kommerell (1901–1990), who discovered it in 1936). It is alternatively known as a lusorian artery.

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 epidemiology of pulmonary valve stenosis can be summed up by the congenital aspect which is the majority of cases, in broad terms PVS is rare in the general population.

About 10% of cases of moyamoya disease are familial, and some cases result from specific genetic mutations. Susceptibility to moyamoya disease-2 (MYMY2; 607151) is caused by variation in the RNF213 gene (613768) on chromosome 17q25. Moyamoya disease-5 (MYMY5; 614042) is caused by mutation in the ACTA2 gene (102620) on chromosome 10q23.3; and moyamoya disease-6 with achalasia (MYMY6; 615750) is caused by mutation in the GUCY1A3 gene (139396) on chromosome 4q32. Loci for the disorder have been mapped to chromosome 3p (MYMY1) and chromosome 8q23 (MYMY3; 608796). See also MYMY4 (300845), an X-linked recessive syndromic disorder characterized by moyamoya disease, short stature, hypergonadotropic hypogonadism, and facial dysmorphism. and linked to q25.3, on chromosome 17". (Online Mendelian Inheritance in Man, omim.org/entry/252350).

In Japan the overall incidence is higher (0.35 per 100,000). In North America, women in the third or fourth decade of life are most often affected, but the condition may also occur during infancy or childhood. These women frequently experience transient ischaemic attacks (TIA), cerebral hemorrhage, or may not experience any symptoms at all. They have a higher risk of recurrent stroke and may be experiencing a distinct underlying pathophysiology compared to patients from Japan.

Moyamoya disease can be either congenital or acquired. Patients with Down syndrome, sickle cell anemia, neurofibromatosis type 1, congenital heart disease, fibromuscular dysplasia, activated protein C resistance, or head trauma can develop moyamoya malformations. It is more common in women than in men, although about a third of those affected are male.

It may occur as the result of carotid artery stenosis (though some disagree); however, most carotid bruits, particularly those found in younger or asymptomatic patients, are not related to any disease and are termed "innocent carotid bruits". A carotid bruit is unlikely to be heard if the stenosis occludes less than 40% of the diameter of the artery. Likewise, a stenosis of greater than 90% may not be heard, as the flow may be too low.

Many carotid bruits are discovered incidentally in an otherwise asymptomatic patient. The presence of a carotid bruit alone does not necessarily indicate the presence of stenosis, and the physical examination cannot be used to estimate the degree of stenosis, if present; therefore, any bruit must be evaluated by ultrasound or imaging.