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

Non-occlusive disease has a poor prognosis with survival rate between 40-50%.

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).

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.

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.

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.

CT angiography would be helpful in differentiating occlusive from non-occlusive causes of mesenteric ischaemia.

Causes include:

- Thrombosis (approximately 40% of cases)

- Arterial embolism (approximately 40%)

- arteriosclerosis obliterans

Another cause of limb infarction is "skeletal muscle infarction" as a rare complication of long standing, poorly controlled diabetes mellitus.

Several factors may increase the tendency for clot formation, such as specific infections (such as infectious mononucleosis, cytomegalovirus infection, malaria, or babesiosis), inherited clotting disorders (thrombophilia, such as Factor V Leiden, antiphospholipid syndrome), malignancy (such as pancreatic cancer) or metastasis, or a combination of these factors.

In some conditions, blood clots form in one part of the circulatory system and then dislodge and travel to another part of the body, which could include the spleen. These emboligenic disorders include atrial fibrillation, patent foramen ovale, endocarditis or cholesterol embolism.

Splenic infarction is also more common in hematological disorders with associated splenomegaly, such as the myeloproliferative disorders. Other causes of splenomegaly (for example, Gaucher disease or hemoglobinopathies) can also predispose to infarction. Splenic infarction can also result from a sickle cell crisis in patients with sickle cell anemia. Both splenomegaly and a tendency towards clot formation feature in this condition. In sickle cell disease, repeated splenic infarctions lead to a non-functional spleen (autosplenectomy).

Any factor that directly compromises the splenic artery can cause infarction. Examples include abdominal traumas, aortic dissection, torsion of the splenic artery (for example, in wandering spleen) or external compression on the artery by a tumor. It can also be a complication of vascular procedures.

Splenic infarction can be due to vasculitis or disseminated intravascular coagulation. Various other conditions have been associated with splenic infarction in case reporters, for example granulomatosis with polyangiitis or treatment with medications that predispose to vasospasm or blood clot formation, such as vasoconstrictors used to treat esophageal varices, sumatriptan or bevacizumab.

Splenic infarction can be induced for the treatment of such conditions as portal hypertension or splenic injury. It can also be used prior to splenectomy for the prevention of blood loss.

The major tissues affected are nerves and muscles, where irreversible damage starts to occur after 4–6 hours of cessation of blood supply.Skeletal muscle, the major tissue affected, is still relatively resistant to infarction compared to the heart and brain because its ability to rely on anaerobic metabolism by glycogen stored in the cells may supply the muscle tissue long enough for any clot to dissolve, either by intervention or the body's own system for thrombus breakdown. In contrast, brain tissue (in cerebral infarction) does not store glycogen, and the heart (in myocardial infarction) is so specialized on aerobic metabolism that not enough energy can be liberated by lactate production to sustain its needs.

Bone is more susceptible to ischemia, with hematopoietic cells usually dying within 2 hours, and other bone cells (osteocytes, osteoclasts, osteoblasts etc.) within 12–20 hours. On the other hand, it has better regenerative capacity once blood supply is reestablished, as the remaining dead inorganic osseous tissue forms a framework upon which immigrating cells can reestablish functional bone tissue in optimal conditions.

Whether a cerebral infarction is thrombotic or embolic based, its pathophysiology, or the observed conditions and underlying mechanisms of the disease. In thrombotic ischemic stroke, a thrombus forms and blocks blood flow. A thrombus forms when the endothelium is activated by a variety of signals to result in platelet aggregation in the artery. This clump of platelets interacts with fibrin to form a platelet plug. This platelet plug grows into a thrombus, resulting in a stenotic artery. Thrombotic ischemia can occur in large or small blood vessels. In large vessels, the most common causes of thrombi are atherosclerosis and vasoconstriction. In small vessels, the most common cause is lipohyalinosis. Lipohyalinosis is when high blood pressure and aging causes a build-up of fatty hyaline matter in blood vessels. Atheroma formation can also cause small vessel thrombotic ischemic stroke.

An embolic stroke refers to the blockage of an artery by an embolus, a traveling particle or debris in the arterial bloodstream originating elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). The embolus may be of cardiac origin due to Atrial fibrillation, Patent foramen ovale or from atherosclerotic plaque of another (or the same) large artery. Cerebral artery gas embolism (e.g. during ascent from a SCUBA dive) is also a possible cause of infarction (Levvett & Millar, 2008)

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.

After return of heart function, there has been a moderately higher risk of death in the hospital when compared to MI patients without PVF. Whether this still holds true with the recent changes in treatment strategies of earlier hospital admission and immediate angioplasty with thrombus removal is unknown. PVF does not affect the long-term prognosis.

One of the most important features differentiating ischemic cardiomyopathy from the other forms of cardiomyopathy is the shortened, or worsened all-cause mortality in patients with ischemic cardiomyopathy. According to several studies, coronary artery bypass graft surgery has a survival advantage over medical therapy (for ischemic cardiomyopathy) across varied follow-ups.

Coronary artery disease has a number of well determined risk factors. These include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, family history, and excessive alcohol. About half of cases are linked to genetics. Smoking and obesity are associated with about 36% and 20% of cases, respectively. Lack of exercise has been linked to 7–12% of cases. Exposure to the herbicide Agent orange may increase risk. Both rheumatoid arthritis and systemic lupus erythematosus are independent risk factors as well.

Job stress appears to play a minor role accounting for about 3% of cases.

In one study, women who were free of stress from work life saw an increase in the diameter of their blood vessels, leading to decreased progression of atherosclerosis. In contrast, women who had high levels of work-related stress experienced a decrease in the diameter of their blood vessels and significantly increased disease progression. Having a type A behavior pattern, a group of personality characteristics including time urgency, competitiveness, hostility, and impatience is linked to an increased risk of coronary disease.

The prevalence of LVT with AMI is 5-15%. The rates of AMI associated with LVT is declining due to the use of better therapies and percutaneous coronary intervention used to treat myocardial infarction. LVT formation has been found to be higher in anterior wall AMI than other types of AMI.

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.

Nitroglycerin can be used immediately to widen the coronary arteries and help increase blood flow to the heart. In addition, nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload. These reductions allow for decreased stress on the heart and therefore lower the oxygen demand of the heart's muscle cells.

Antiplatelet drugs such as aspirin and clopidogrel can help reduce the progression of atherosclerotic plaque formation, as well as combining these with an anticoagulant such as a low molecular weight heparin.

The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial infarction. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction. On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered. The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.

The pathophysiology of unstable angina is controversial. Until recently, unstable angina was assumed to be angina pectoris caused by disruption of an atherosclerotic plaque with partial thrombosis and possibly embolization or vasospasm leading to myocardial ischemia. However, sensitive troponin assays reveal rise of cardiac troponin in the bloodstream with episodes of even mild myocardial ischemia. Since unstable angina is assumed to occur in the setting of acute myocardial ischemia without troponin release, the concept of unstable angina is being questioned with some calling for retiring the term altogether.

The survival of PVF largely depends on the promptness of defibrillation. The success rate of prompt defibrillation during monitoring is currently higher than 95%. It is estimated that the success rate decreases by 10% for each additional minute of delay.

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.

There is varying evidence about the importance of saturated fat in the development of myocardial infarctions. Eating polyunsaturated fat instead of saturated fats has been shown in studies to be associated with a decreased risk of myocardial infarction, while other studies find little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake affects heart attack risk. Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed. Trans fats do appear to increase risk. Acute and prolonged intake of high quantities of alcoholic drinks (3–4 or more) increases the risk of a heart attack.

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.