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.

TIF is a rare condition with a .7% frequency, and an mortality rate approaching 100% without surgical intervention. Immediate diagnosis and intervention of an TIF is critical for the surgical intervention success. 25-30% of TIF patients who reach the operating room survive. Recently, the incidence of TIF may have declined due to advances in tracheostomy tube technology and the introduction of the bedside percutaneous dilatational tracheostomy (PDT).

In the first stage of restenosis, administering anti-platelet drugs (called IIb/IIIa inhibitors) immediately after surgery greatly reduces the chance of a thrombosis occurring.

Drug-eluting stents are now being trialled in Europe, Canada and the USA, as well as in Asia-Pacific. These stents are coated with pharmaceuticals that inhibit tissue growth and thus reduce the risk of restenosis from scar-tissue and cell proliferation.

There has been some success with these new stents in reducing the occurrence of restenosis, with clinical studies showing an incidence rate of 5% or lower.

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.

Vascular occlusion is a blockage of a blood vessel, usually with a clot. It differs from thrombosis in that it can be used to describe any form of blockage, not just one formed by a clot. When it occurs in a major vein, it can, in some cases, cause deep vein thrombosis. The condition is also relatively common in the retina, and can cause partial or total loss of vision. An occlusion can often be diagnosed using Doppler sonography (a form of ultrasound).

Some medical procedures, such as embolisation, involve occluding a blood vessel to treat a particular condition. This can be to reduce pressure on aneurysms (weakened blood vessels) or to restrict a haemorrhage. It can also be used to reduce blood supply to tumours or growths in the body, and therefore restrict their development. Occlusion can be carried out using a ligature; by implanting small coils which stimulate the formation of clots; or, particularly in the case of cerebral aneurysms, by clipping.

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.

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 innominate artery usually crosses the trachea at the ninth cartilage ring, however this can vary from the sixth to the thirteenth cartilage ring in patients. A TIF runs between the trachea and the innominate artery. Through this connection blood from within the artery may pass into the trachea or alternatively air from within the trachea may cross into the artery.

TIF is a late complication of a tracheotomy and is associated with prolonged endotracheal intubation, as a result of cuff over inflation or a poorly positioned tracheostomy tube. Over inflation of the cuff causes the tracheostomy tube to erode into the posterior aspect of the innominate artery leading to the formation of a fistula. The pathogenesis of an TIF by the aforementioned method is pressure necrosis by tracheostomy tube on the tracheal wall. An TIF can also occur due to innominate artery injury as a result of an bronchoscopy.

Patients whose tracheotomies are placed beneath the third tracheal ring cartilage and patients with innominate arteries crossing higher on the trachea have an increased risk of developing an TIF. Other factors contributing to the development of TIF include steroids, which weaken the endotracheal mucosa, episodes of hypotension in which the pressure in the tracheostomy tube exceeds that of the endotracheal mucosa, and radiation therapy.

An endotracheal tumor can mimic a TIF and present with massive bleeding during a rigid bronchoscopy.

Complete vascular rings represent about 0.5-1% of all congenital cardiovascular malformations. The majority of these are double aortic arches.

There is no known gender preference, i.e. males and females are about equally affected. There is also no known ethnic or geographic disposition.

Associated cardiovascular anomalies are found in 10-15% of patients. These include:

- Atrial septal defect (ASD)

- Ventricular septal defect (VSD)

- Patent ductus arteriosus (PDA)

- Tetralogy of Fallot (ToF)

- Transposition of the great arteries (D-TGA)

Various classifications have been proposed for CCF. They may be divided into low-flow or high-flow, traumatic or spontaneous and direct or indirect. The traumatic CCF typically occurs after a basal skull fracture. The spontaneous dural cavernous fistula which is more common usually results from a degenerative process in older patients with systemic hypertension

and atherosclerosis. Direct fistulas occur when the Internal Carotid artery (ICA) itself fistulizes into the Cavernous sinus whereas indirect is when a branch of the ICA or External Carotid artery (ECA) communicates with the cavernous sinus.

A popular classification divides CCF into four varieties depending on the type of arterial supply.

Carotid cavernous fistulae may form following closed or penetrating head trauma, surgical damage, rupture of an intracavernous aneurysm, or in association with connective tissue disorders, vascular diseases and dural fistulas.

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

The vascular subtype of Ehlers-Danlos Syndrome (type IV) has been associated with multi-focal FMD. This syndrome should be suspected in patients with multiple aneurysms and/or tears (dissections) in arteries in addition to the typical angiographic findings of FMD. There have been isolated reports of FMD associated with other disorders, including Alport syndrome, pheochromocytoma, Marfan syndrome, Moyamoya disease, and Takayasu's arteritis.

Blood, like electric current, flows along the path of least resistance. Resistance is affected by the length and width of a vessel (i.e. a long, narrow vessel has the greatest resistance and a short, wide one the least), but crucially in the human body width is generally more limiting than length because of Poiseuille's Law. Thus, if blood is presented with two paths, a short one that is narrow (with a high overall resistance) and a long one that is wide (with a low overall resistance), it will take the long and wide path (the one with the lower resistance).

Treatment involves revascularization typically using either angioplasty or a type of vascular bypass

- Kissing balloon angioplasty +/- stent, so named because the two common iliac stents touch each other in the distal aorta.

- Aorto-iliac bypass graft

- Axillary-bi-femoral and femoral-femoral bypass (sometimes abbreviated "ax-fem fem-fem")

Risk factors include:

- Hypertension

- Elevated lipid levels

- cigarette smoking

- Diabetes

Penile Revascularization is a specialized vascular-surgical treatment option for Erectile Dysfunction. The 2009 International Consultation on Sexual Dysfunctions recommended that revascularization be limited to nonsmoker, nondiabetic men younger than 55 years of age with isolated stenosis of the internal pudendal artery with absence of venous leak.

Patients with persistent erectile dysfunction after revascularization may benefit from repeat penile duplex ultrasound and pelvic angiography to evalauate the status of the bypass graft and to exclude the presence of a PASS as the cause. The prevalence of an aberrant obturator artery arising from the inferior epigastric artery is approximately 10.5%. If an aberrant obturator artery is visualized arising from the inferior epigastric artery prior to surgical penile revascularization, consideration should be given toward using an alternative source artery or to embolization to avoid the creation of a Penile Artery Shunt Syndrome encountered in this described case.

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.

Little is known regarding the exact causes of aortic arch anomalies. However, the association with chromosome 22q11 deletion (CATCH 22) implies that a genetic component is likely in certain cases. Esophageal atresia also occurs in some patients with double aortic arch.

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 mean age of affected patients is 60 years. The right eye is affected more commonly than the left eye which probably reflects the greater possibility of cardiac or aortic emboli traveling to the right carotid artery.

Most of the cases are due to emboli to the retinal circulation. Three main types of retinal emboli have been identified: Cholesterol, calcific, and fibrin-platelet.

Thrombotic Storm has been seen in individuals of all ages and races. The initial symptoms of TS present in a similar fashion to the symptoms experienced in deep vein thrombosis. Symptoms of a DVT may include pain, swelling and discoloration of the skin in the affected area. As with DVTs patients with TS may subsequently develop pulmonary emboli. Although the presentation of TS and DVTs are similar, TS typically progresses rapidly, with numerous clots occurring within a short period of time. After the formation of the initial clot a patient with TS typically begins a “clotting storm” with the development of multiple clots throughout the body. Rapid progression within a short period of time is often seen, affecting multiple organs systems. The location of the clot is often unusual or found in a spot in the body that is uncommon such as the dural sinus. Patients tend to respond very well to anticoagulation such as coumadin or low molecular weight heparin but may become symptomatic when treatment is withheld.

While the key clinical characteristics of thrombotic storm are still being investigated, it is believed that the clinical course is triggered by a preexisting condition, known as a hypercoagulable state. These can include such things as pregnancy, trauma or surgery. Hypercoagulable states can be an inherited or acquired risk factor that then serves as a trigger to initiate clot formation. However, in a subset of patient with TS a trigger cannot be identified. Typically people with TS will have no personal or family history of coagulations disorders.

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.

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.

The epidemiology of endothelial dysfunction is unknown, as %FMD varies with baseline artery diameter. This can make cross-sectional comparisons of %FMD difficult. Endothelial dysfunction was found in approximately half of women with chest pain, in the absence of overt blockages in large coronary arteries. This endothelial dysfunction cannot be predicted by typical risk factors for atherosclerosis (e.g., obesity, cholesterol, smoking) and hormones.