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

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.

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.

Incidence rates of cranial aneurysms are estimated at between 0.4% and 3.6%. Those without risk factors have expected prevalence of 2–3%. In adults, females are more likely to have aneurysms. They are most prevalent in people ages 35 – 60, but can occur in children as well. Aneurysms are rare in children with a reported prevalence of .5% to 4.6%. The most common incidence are among 50-year-olds, and there are typically no warning signs. Most aneurysms develop after the age of 40.

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".

Incidence rates are two to three times higher in males, while there are more large and giant aneurysms and fewer multiple aneurysms. Intracranial hemorrhages are 1.6 times more likely to be due to aneurysms than cerebral arteriovenous malformations in whites, but four times less in certain Asian populations.

Most patients, particularly infants, present with subarachnoid hemorrhage and corresponding headaches or neurological deficits. The mortality rate for pediatric aneurysms is lower than in adults.

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

Establishing the incidence of aortic dissection has been difficult because many cases are only diagnosed after death (which may have been attributed to another cause), and is often initially misdiagnosed. Aortic dissection affects an estimated 2.0–3.5 people per every 100,000 every year. Studies from Sweden suggest that the incidence of aortic dissection may be rising. Men are more commonly affected than women: 65% of all people with aortic dissection are male. The mean age at diagnosis is 63 years. In females before the age of 40, half of all aortic dissections occur during pregnancy (typically in the third trimester or early postpartum period).

Mortality from aortic rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.

In medical pathology, a dissection is a tear within the wall of a blood vessel, which allows blood to separate the wall layers. By separating a portion of the wall of the artery (a layer of the tunica intima or tunica media), a dissection creates two lumens or passages within the vessel, the native or true lumen, and the "false lumen" created by the new space within the wall of the artery.

Of all people with aortic dissection, 40% die immediately and do not reach a hospital in time. Of the remainder, 1% die every hour, making prompt diagnosis and treatment a priority. Even after diagnosis, 5–20% die during surgery or in the immediate postoperative period. In ascending aortic dissection, if surgery is decided to be not appropriate, 75% die within 2 weeks. With aggressive treatment, 30-day survival for thoracic dissections may be as high as 90%.

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).

There is evidence to suggest that a major cause of spontaneous coronary artery dissection (SCAD) is related to female hormone levels, as most cases appear to arise in pre-menopausal women, although there is evidence that the condition can have various triggers. Other underlying conditions such as hypertension, recent delivery of a baby, fibromuscular dysplasia and connective-tissue disorders (e.g., Marfan syndrome and Ehlers-Danlos syndrome) may occasionally result in SCAD. There is also a possibility that vigorous exercise can be a trigger. However, many cases have no obvious cause.

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 prevalence of intracranial aneurysm is about 1-5% (10 million to 12 million persons in the United States) and the incidence is 1 per 10,000 persons per year in the United States (approximately 27,000), with 30- to 60-year-olds being the age group most affected. Intracranial aneurysms occur more in women, by a ratio of 3 to 2, and are rarely seen in pediatric populations.

Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Lifestyle diseases including hypertension, smoking, excessive alcoholism, and obesity are associated with the development of brain aneurysms. Cocaine use has also been associated with the development of intracranial aneurysms.

Other acquired associations with intracranial aneurysms include head trauma and infections.

Coronary artery dissection results from a tear in the inner layer of the artery, the tunica intima. This allows blood to penetrate and cause an intramural hematoma in the central layer, the tunica media, and a restriction in the size of the lumen, resulting in reduced blood flow which in turn causes myocardial infarction and can later cause sudden cardiac death.

The most common cause of aortic rupture is a ruptured aortic aneurysm. Other causes include trauma and iatrogenic (procedure-related) causes.

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.

The relation between dietary fat and atherosclerosis is controversial. Writing in "Science", Gary Taubes detailed that political considerations played into the recommendations of government bodies. The USDA, in its food pyramid, promotes a diet of about 64% carbohydrates from total calories. The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations. In contrast, Prof Walter Willett (Harvard School of Public Health, PI of the second Nurses' Health Study) recommends much higher levels of fat, especially of monounsaturated and polyunsaturated fat. These differing views reach a consensus, though, against consumption of trans fats.

The role of dietary oxidized fats/lipid peroxidation (rancid fats) in humans is not clear.

Laboratory animals fed rancid fats develop atherosclerosis. Rats fed DHA-containing oils experienced marked disruptions to their antioxidant systems, and accumulated significant amounts of phospholipid hydroperoxide in their blood, livers and kidneys.

Rabbits fed atherogenic diets containing various oils were found to undergo the greatest amount of oxidative susceptibility of LDL via polyunsaturated oils. In another study, rabbits fed heated soybean oil "grossly induced atherosclerosis and marked liver damage were histologically and clinically demonstrated." However, Fred Kummerow claims that it is not dietary cholesterol, but oxysterols, or oxidized cholesterols, from fried foods and smoking, that are the culprit.

Rancid fats and oils taste very bad even in small amounts, so people avoid eating them.

It is very difficult to measure or estimate the actual human consumption of these substances. Highly unsaturated omega-3 rich oils such as fish oil are being sold in pill form so that the taste of oxidized or rancid fat is not apparent. The health food industry's dietary supplements are self regulated and outside of FDA regulations. To properly protect unsaturated fats from oxidation, it is best to keep them cool and in oxygen free environments.

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.

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.

In developed countries, with improved public health, infection control and increasing life spans, atheroma processes have become an increasingly important problem and burden for society.

Atheromata continue to be the primary underlying basis for disability and death, despite a trend for gradual improvement since the early 1960s (adjusted for patient age). Thus, increasing efforts towards better understanding, treating and preventing the problem are continuing to evolve.

According to United States data, 2004, for about 65% of men and 47% of women, the first symptom of cardiovascular disease is myocardial infarction (heart attack) or sudden death (death within one hour of symptom onset).

A significant proportion of artery flow-disrupting events occur at locations with less than 50% lumenal narrowing. Cardiac stress testing, traditionally the most commonly performed noninvasive testing method for blood flow limitations, generally only detects lumen narrowing of ~75% or greater, although some physicians advocate nuclear stress methods that can sometimes detect as little as 50%.

The sudden nature of the complications of pre-existing atheroma, vulnerable plaque (non-occlusive or soft plaque), have led, since the 1950s, to the development of intensive care units and complex medical and surgical interventions. Angiography and later cardiac stress testing was begun to either visualize or indirectly detect stenosis. Next came bypass surgery, to plumb transplanted veins, sometimes arteries, around the stenoses and more recently angioplasty, now including stents, most recently drug coated stents, to stretch the stenoses more open.

Yet despite these medical advances, with success in reducing the symptoms of angina and reduced blood flow, atheroma rupture events remain the major problem and still sometimes result in sudden disability and death despite even the most rapid, massive and skilled medical and surgical intervention available anywhere today. According to some clinical trials, bypass surgery and angioplasty procedures have had at best a minimal effect, if any, on improving overall survival. Typically mortality of bypass operations is between 1 and 4%, of angioplasty between 1 and 1.5%.

Additionally, these vascular interventions are often done only after an individual is symptomatic, often already partially disabled, as a result of the disease. It is also clear that both angioplasty and bypass interventions do not prevent future heart attack.

The older methods for understanding atheroma, dating to before World War II, relied on autopsy data. Autopsy data has long shown initiation of fatty streaks in later childhood with slow asymptomatic progression over decades.

One way to see atheroma is the very invasive and costly IVUS ultrasound technology; it gives us the precise volume of the inside intima plus the central media layers of about of artery length. Unfortunately, it gives no information about the structural strength of the artery. Angiography does not visualize atheroma; it only makes the blood flow within blood vessels visible. Alternative methods that are non or less physically invasive and less expensive per individual test have been used and are continuing to be developed, such as those using computed tomography (CT; led by the electron beam tomography form, given its greater speed) and magnetic resonance imaging (MRI). The most promising since the early 1990s has been EBT, detecting calcification within the atheroma before most individuals start having clinically recognized symptoms and debility. Interestingly, statin therapy (to lower cholesterol) does not slow the speed of calcification as determined by CT scan. MRI coronary vessel wall imaging, although currently limited to research studies, has demonstrated the ability to detect vessel wall thickening in asymptomatic high risk individuals. As a non-invasive, ionising radiation free technique, MRI based techniques could have future uses in monitoring disease progression and regression. Most visualization techniques are used in research, they are not widely available to most patients, have significant technical limitations, have not been widely accepted and generally are not covered by medical insurance carriers.

From human clinical trials, it has become increasingly evident that a more effective focus of treatment is slowing, stopping and even partially reversing the atheroma growth process. There are several prospective epidemiologic studies including the Atherosclerosis Risk in Communities (ARIC) Study and the Cardiovascular Health Study (CHS), which have supported a direct correlation of Carotid Intima-media thickness (CIMT) with myocardial infarction and stroke risk in patients without cardiovascular disease history. The ARIC Study was conducted in 15,792 individuals between 5 and 65 years of age in four different regions of the US between 1987 and 1989. The baseline CIMT was measured and measurements were repeated at 4- to 7-year intervals by carotid B mode ultrasonography in this study. An increase in CIMT was correlated with an increased risk for CAD. The CHS was initiated in 1988, and the relationship of CIMT with risk of myocardial infarction and stroke was investigated in 4,476 subjects ≤65 years of age. At the end of approximately six years of follow-up, CIMT measurements were correlated with cardiovascular events.

Paroi artérielle et Risque Cardiovasculaire in Asia Africa/Middle East and Latin America (PARC-AALA) is another important large-scale study, in which 79 centers from countries in Asia, Africa, the Middle East, and Latin America participated, and the distribution of CIMT according to different ethnic groups and its association with the Framingham cardiovascular score was investigated. Multi-linear regression analysis revealed that an increased Framingham cardiovascular score was associated with CIMT, and carotid plaque independent of geographic differences.

Cahn et al. prospectively followed-up 152 patients with coronary artery disease for 6–11 months by carotid artery ultrasonography and noted 22 vascular events (myocardial infarction, transient ischemic attack, stroke, and coronary angioplasty) within this time period. They concluded that carotid atherosclerosis measured by this non-interventional method has prognostic significance in coronary artery patients.

In the Rotterdam Study, Bots et al. followed 7,983 patients >55 years of age for a mean period of 4.6 years, and reported 194 incident myocardial infarctions within this period. CIMT was significantly higher in the myocardial infarction group compared to the other group. Demircan et al. found that the CIMT of patients with acute coronary syndrome were significantly increased compared to patients with stable angina pectoris.

It has been reported in another study that a maximal CIMT value of 0.956 mm had 85.7% sensitivity and 85.1% specificity to predict angiographic CAD. The study group consisted of patients admitted to the cardiology outpatient clinic with symptoms of stable angina pectoris. The study showed CIMT was higher in patients with significant CAD than in patients with non-critical coronary lesions. Regression analysis revealed that thickening of the mean intima-media complex more than 1.0 was predictive of significant CAD our patients. There was incremental significant increase in CIMT with the number coronary vessel involved. In accordance with the literature, it was found that CIMT was significantly higher in the presence of CAD. Furthermore, CIMT was increased as the number of involved vessels increased and the highest CIMT values were noted in patients with left main coronary involvement. However, human clinical trials have been slow to provide clinical & medical evidence, partly because the asymptomatic nature of atheromata make them especially difficult to study. Promising results are found using carotid intima-media thickness scanning (CIMT can be measured by B-mode ultrasonography), B-vitamins that reduce a protein corrosive, homocysteine and that reduce neck carotid artery plaque volume and thickness, and stroke, even in late-stage disease.

Additionally, understanding what drives atheroma development is complex with multiple factors involved, only some of which, such as lipoproteins, more importantly lipoprotein subclass analysis, blood sugar levels and hypertension are best known and researched. More recently, some of the complex immune system patterns that promote, or inhibit, the inherent inflammatory macrophage triggering processes involved in atheroma progression are slowly being better elucidated in animal models of atherosclerosis.

In 2011, coronary atherosclerosis was one of the top ten most expensive conditions seen during inpatient hospitalizations in the U.S., with aggregate inpatient hospital costs of $10.4 billion.

Many approaches have been promoted as methods to reduce or reverse atheroma progression:

- eating a diet of raw fruits, vegetables, nuts, beans, berries, and grains;

- consuming foods containing omega-3 fatty acids such as fish, fish-derived supplements, as well as flax seed oil, borage oil, and other non-animal-based oils;

- abdominal fat reduction;

- aerobic exercise;

- inhibitors of cholesterol synthesis (known as statins);

- low normal blood glucose levels (glycosylated hemoglobin, also called HbA1c);

- micronutrient (vitamins, potassium, and magnesium) consumption;

- maintaining normal, or healthy, blood pressure levels;

- aspirin supplement

- cyclodextrin can solubilize cholesterol, removing it from plaques

Put simply, take steps to live a healthy, sustainable lifestyle.