Physicians have theorized that the syndrome is caused by tiny debris and air bubbles (microemboli) that enter the brain via cardiopulmonary bypass. Surgeons attempt to minimize time spent on bypass to decrease postoperative deficits; studies have shown increased bypass time is associated with increased incidence and severity of postperfusion syndrome and mortality. It is unclear how increases in bypass time would result in such increases if pre-existing cardiovascular and cerebrovascular conditions are the principal causative mechanisms of postperfusion syndrome.

Corticosteroids, typically high-dose prednisone (1 mg/kg/day), must be started as soon as the diagnosis is suspected (even before the diagnosis is confirmed by biopsy) to prevent irreversible blindness secondary to ophthalmic artery occlusion. Steroids do not prevent the diagnosis from later being confirmed by biopsy, although certain changes in the histology may be observed towards the end of the first week of treatment and are more difficult to identify after a couple of months. The dose of prednisone is lowered after 2–4 weeks, and slowly tapered over 9–12 months. Tapering may require two or more years. Oral steroids are at least as effective as intravenous steroids, except in the treatment of acute visual loss where intravenous steroids appear to offer significant benefit over oral steroids. It is unclear if adding a small amount of aspirin is beneficial or not as it has not been studied.

A study by McKhann et al. compared the neurocognitive outcome of people with coronary artery disease (CAD) to heart-healthy controls (people with no cardiac risk factors). People with CAD were subdivided into treatment with CABG, OPCAB and non-surgical medical management. The three groups with CAD all performed significantly lower at baseline than the heart-healthy controls. All groups improved by 3 months, and there were minimal intrasubject changes from 3 to 12 months. No consistent difference between the CABG and off-pump patients was observed. The authors concluded patients with long-standing coronary artery disease have some degree of cognitive dysfunction secondary to cerebrovascular disease before surgery; there is no evidence the cognitive test performance of bypass surgery patients differed from similar control groups with coronary artery disease over a 12-month follow-up period. A related study by Selnes et al. concluded patients with coronary artery bypass grafting did not differ from a comparable nonsurgical control group with coronary artery disease 1 or 3 years after baseline examination. This finding suggests that late cognitive decline after coronary artery bypass grafting previously reported by Newman et al. may not be specific to the use of cardiopulmonary bypass, but may also occur in patients with very similar risk factors for cardiovascular and cerebrovascular disease.

The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown.

Giant-cell arteritis (GCA), also called temporal arteritis, is an inflammatory disease of blood vessels. Symptoms may include headache, pain over the temples, flu-like symptoms, double vision, and difficulty opening the mouth. Complication can include blockage of the artery to the eye with resulting blindness, aortic dissection, and aortic aneurysm. GCA is frequently associated with polymyalgia rheumatica.

The cause is unknown. The underlying mechanism involves inflammation of the small blood vessels that occur within the walls of larger arteries. This mainly affects arteries around the head and neck, though some in the chest may also be affected. Diagnosis is suspected based on symptoms, blood tests, and medical imaging, and confirmed by biopsy of the temporal artery. However, in about 10% of people the temporal artery is normal.

Treatment is typically with high doses of steroids, such as prednisone. Once symptoms have resolved the dose is then decreased by about 15% per month. Once a low dose is reached, the taper is slowed further over the subsequent year. Other medications that may be recommended include bisphosphonates to prevent bone loss and a proton pump inhibitor to prevent stomach problems.

It affects about 1 in 15,000 people over the age of 50 a year. The condition typically only occurs in those over the age of 50 being most common among those in their 70s. Females are more often affected than males. Those of northern European descent are more commonly affected. Life expectancy is typically normal. The first description of the condition occurred in 1890.

Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in patients with unstable angina. It is characterized by symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads. A less common variant is biphasic T wave inversions in the same leads.

First described by Hein J. J. Wellens and colleagues in 1982 in a subgroup of patients with unstable angina, it does not seem to be rare, appearing in 18% of patients in his original study. A subsequent prospective study identified this syndrome in 14% of patients at presentation and 60% of patients within the first 24 hours.

The presence of Wellens' syndrome carries significant diagnostic and prognostic value. All patients in the De Zwann's study with characteristic findings had more than 50% stenosis of the left anterior descending artery (mean = 85% stenosis) with complete or near-complete occlusion in 59%. In the original Wellens' study group, 75% of those with the typical syndrome manifestations had an anterior myocardial infarction. Sensitivity and specificity for significant (more or equal to 70%) stenosis of the LAD artery was found to be 69% and 89%, respectively, with a positive predictive value of 86%.

Wellens' sign has also been seen as a rare presentation of Takotsubo cardiomyopathy or stress cardiomyopathy.

The mainstay of treatment for CCF is endovascular therapy. This may be transarterial (mostly in the case of direct CCF) or transvenous (most commonly in indirect CCF). Occasionally, more direct approaches, such as direct transorbital puncture of the cavernous sinus or cannulation of the draining superior orbital vein are used when conventional approaches are not possible. Spontaneous resolution of indirect fistulae has been reported but is uncommon. Staged manual compression of the ipsilateral carotid has been reported to assist with spontaneous closure in selected cases.

Direct CCF may be treated by occlusion of the affected cavernous sinus (coils, balloon, liquid agents), or by reconstruction of the damaged internal carotid artery (stent, coils or liquid agents).

Indirect CCF may be treated by occlusion of the affected cavernous sinus with coils, liquid agents or a combination of both.

Endothelial function can be improved significantly by exercise, smoke cessation, weight loss in overweight or obese persons, and improved diet. Treatment of hypertension and hypercholesterolemia are also critical; the major pharmacological interventions to improve endothelial function in those set of patients are statins(HMGCoA-reductase inhibitor), and renin angiotensin system inhibitors, (such as ACE inhibitors and angiotensin II receptor antagonists).

Some studies have found the consumption of flavonoid-rich fruit and vegetables, potassium

and arginine supplementation to restore impaired endothelial function. A positive relationship exists between the consumption of trans fat (commonly found in hydrogenated products such as margarine) and the development of endothelial dysfunction.

New third-generation β-blockers and 5-phosphodiesterase inhibitors may affect endothelial function. New non-invasive strategies that measure endothelial function will prove critical to assess which set of patients are improving their endothelial function. Statins have major pleiotropic anti-inflammatory and anti-hypertensive effects besides the cholesterol reduction effect. This immunomodulatory effects of statins may explain why some patients improve their endothelial function with those drugs. Another anti-inflammatory drug that has shown to be effective for treating endothelial dysfunction in patients who also have coronary artery disease is the ipeptidyl peptidase 4 (DPP4) inhibitor.

Horner's syndrome is acquired as a result of disease, but may also be congenital (inborn, associated with heterochromatic iris) or iatrogenic (caused by medical treatment). Although most causes are relatively benign, Horner syndrome may reflect serious disease in the neck or chest (such as a Pancoast tumor (tumor in the apex of the lung) or thyrocervical venous dilatation).

Causes can be divided according to the presence and location of anhidrosis:

- Central (anhidrosis of face, arm and trunk)

- Syringomyelia

- Multiple sclerosis

- Encephalitis

- Brain tumors

- Lateral medullary syndrome

- Preganglionic (anhidrosis of face)

- Cervical rib traction on stellate ganglion

- Thyroid carcinoma

- Thyroidectomy

- Goiter

- Bronchogenic carcinoma of the superior fissure (Pancoast tumor) on apex of lung

- Klumpke paralysis

- Trauma - base of neck, usually blunt trauma, sometimes surgery.

- As a complication of tube thoracostomy

- Thoracic aortic aneurysm

- Postganglionic (no anhidrosis)

- Cluster headache - combination termed Horton's headache

- An episode of Horner's syndrome may occur during a migraine attack and be relieved afterwards

- Carotid artery dissection/carotid artery aneurysm

- Cavernous sinus thrombosis

- Middle ear infection

- Sympathectomy

- Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block

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.

Anomalous origin of the right coronary artery originating from the pulmonary trunk (ARCAPA) is a rare but potentially fatal anomaly. The goal of surgical therapy is establishment of a physiologic bi-coronary circulation.

The Registry has been enrolling new patients from participating institutions that are member of the Congenital Heart Surgeons' Society. Hospitals from across North America continue to join the study group and enroll patients. Over 140 patients with AAOCA have been enrolled by June 2011, making it the largest cohort ever assembled of this anomaly.

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.

The goal of treatment is to prevent the development or continuation of neurologic deficits. Treatments include observation, anticoagulation, stent implantation and carotid artery ligation.

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

If restenosis occurs without a stent, it is usually treated with more angioplasty. Once restenosis has occurred and been treated by angioplasty, the chances of restenosis occurring again are increased by a factor of 2. This treatment is also used if restenosis occurs at either the proximal or distal end of the stent.

If restenosis occurs within a stent (also known as in-stent stenosis), it may be treated with repeated angioplasty and insertion of another stent inside the original, sometimes with a drug-eluting stent.

Over the past 5 years, ISR is preferentially treated with a drug eluting balloon, which is a balloon coated with the same anticancer drugs that prevent restenosis. The Balloon avoids the need for a double layer of metal which is used when an in-stent restenosis is treated with another stent within the original stent

Alternative treatments include brachytherapy, or intracoronary radiation. The radiation kills cells and inhibits tissue growth (similar to a patient undergoing cancer therapy).

As a chromosomal condition, there is no cure for Turner syndrome. However, much can be done to minimize the symptoms. For example:

- Growth hormone, either alone or with a low dose of androgen, will increase growth and probably final adult height. Growth hormone is approved by the U.S. Food and Drug Administration for treatment of Turner syndrome and is covered by many insurance plans. There is evidence that this is effective, even in toddlers.

- Estrogen replacement therapy such as the birth control pill, has been used since the condition was described in 1938 to promote development of secondary sexual characteristics. Estrogens are crucial for maintaining good bone integrity, cardiovascular health and tissue health. Women with Turner Syndrome who do not have spontaneous puberty and who are not treated with estrogen are at high risk for osteoporosis and heart conditions.

- Modern reproductive technologies have also been used to help women with Turner syndrome become pregnant if they desire. For example, a donor egg can be used to create an embryo, which is carried by the Turner syndrome woman.

- Uterine maturity is positively associated with years of estrogen use, history of spontaneous menarche, and negatively associated with the lack of current hormone replacement therapy.

It is initially treated with medications, including diuretics, and medications for blood pressure control. When high-grade renal artery stenosis is documented and blood pressure cannot be controlled with medication, or if renal function deteriorates, surgery may be resorted to. The most commonly used procedure is a minimally-invasive angioplasty with or without stenting. It is unclear if this approach yields better results than the use of medications alone. It is a relatively safe procedure. If all else fails and the kidney is thought to be worsening hypertension and revascularization with angioplasty or surgery does not work, then surgical removal of the affected kidney (nephrectomy) may significantly improve high blood pressure.

The treatment of coronary artery ectasia is normally done in conjunction with therapies of other heart disorders such as atherosclerosis and hypertension. To prevent the formation of blood clots and the blockage of the vessels, patients are commonly placed on anticoagulant therapy (e.g. warfarin, and aspirin), as well as anti-spasm therapy of calcium channel blockers. Coronary artery ectasia also responds to statins and ACE inhibitors.

Currently, there is controversy over whether or not inheritance truly plays a role in FAD, and if so which gene it acts upon. FAD does not come from strictly one predisposing factor, such as hypertension. It is suggested that the combination of environmental factors along with genetics may contribute to causing FAD. Before newer and more effective cures and therapies can be developed, first the specific gene mutation must be identified. Until such a gene is determined, scientists say patient education, and physician awareness is vital. Currently scientists have found animal models to be beneficial in understanding the pathology behind FAD. In the future there is hope to develop drugs that will better support and strengthen the aortic wall. Endovascular methods of treatment are becoming increasingly popular, and scientists hope to use this technique in both acute and chronic cases.

Quick determination of the cause may lead to urgent measures to save the eye and life of the patient. High clinical suspicion should be kept for painless vision loss in patients with atherosclerosis, deep venous thrombosis, atrial fibrillation, pulmonary thromboembolism or other previous embolic episodes. Those caused by a carotid artery embolism or occlusion have the potential for further stroke by detachment of embolus and migration to an end-artery of the brain. Hence, proper steps to prevent such an eventuality need to be taken.

Retinal arterial occlusion is an ophthalmic emergency, and prompt treatment is essential. Completely anoxic retina in animal models causes irreversible damage in about 90 minutes. Nonspecific methods to increase blood flow and dislodge emboli include digital massage, 500 mg IV acetazolamide and 100 mg IV methylprednisolone (for possible arteritis). Additional measures include paracentesis of aqueous humor to decrease IOP acutely. An ESR should be drawn to detect possible giant cell arteritis. Improvement can be determined by visual acuity, visual field testing, and by ophthalmoscopic examination.

At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.

The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.

In 2009, the Undersea and Hyperbaric Medical Society added "central retinal artery occlusion" to their list of approved indications for hyperbaric oxygen (HBO). When used as an adjunctive therapy, the edema reducing properties of HBO, along with down regulation of inflammatory cytokines may contribute to the improvement in vision. Prevention of vision loss requires that certain conditions be met: the treatment be started before irreversible damage has occurred (over 24 hours), the occlusion must not also occur at the ophthalmic artery, and treatment must continue until the inner layers of the retina are again oxygenated by the retinal arteries.

Inflammatory involvement of tertiary syphilis begins at the adventitia of the aortic arch which progressively causes obliterative endarteritis of the vasa vasorum. This leads to narrowing of the lumen of the vasa vasorum, causing ischemic injury of the medial aortic arch and then finally loss of elastic support and dilation of the vessel. Dissection of the aortic arch is rare due to medial scarring. As a result of this advanced disease process, standard methods of angiography/angioplasty may be impossible for those with suspected coronary heart disease. However, these patients may be candidates for diagnostic CT as a less invasive modality. This disorder is also known eponymously as Heller-Döhle syndrome.

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.

In those who have developed critically poor blood flow to the legs, it is unclear if autotransplantation of autologous mononuclear cells is useful or not.

Only one randomized controlled trial has been conducted comparing vascular bypass to angioplasty for the treatment of severe PAD. The trial found no difference in amputation-free survival between vascular bypass and angioplasty at the planned clinical endpoint, however the trial has been criticized as being underpowered, limiting endovascular options, and comparing inappropriate endpoints. As of 2017, two randomized clinical trials are being conducted to better understand the optimal revascularization technique for severe PAD and critical limb ischemia (CLI), the BEST-CLI (Best Endovascular Versus Best Surgical Therapy for Patients With Critical Limb Ischemia) Trial, and the BASIL-2 (Bypass Versus Angio plasty in Severe Ischaemia of the Leg – 2 )Trial.

In 2011, pCMV-vegf165 was registered in Russia as the first-in-class gene therapy drug for treatment of peripheral artery disease, including the advanced stage of critical limb ischemia.

Familial thoracic aortic aneurysm is an autosomal dominant disorder of large arteries.

There is an association between familial thoracic aortic aneurysm, Marfan syndrome and massive baclofen overdose as well as other hereditary connective tissue disorders.