The causes of internal carotid artery dissection can be broadly categorised into two classes: spontaneous or traumatic.

The signs and symptoms of carotid artery dissection may be divided into ischemic and non-ischemic categories:

"Non-ischemic signs and symptoms"

- Localised headache, particularly around one of the eyes.

- Neck pain

- Decreased pupil size with drooping of the upper eyelid (Horner syndrome)

- Pulsatile tinnitus

"Ischemic signs and symptoms"

- Temporary vision loss

- Ischemic stroke

Non-occlusive mesenteric ischemia occurs due to severe vasoconstriction of mesenteric vessels supplying the intestine. Acute abdominal pain is the only early acute symptom in those patients, which makes early diagnosis difficult.

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

The symptoms are often very similar to those of myocardial infarction (heart attack), with the most common being persistent chest pain.

Symptoms of cerebral infarction are determined by the parts of the brain affected. If the infarct is located in primary motor cortex, contralateral hemiparesis is said to occur. With brainstem localization, brainstem syndromes are typical: Wallenberg's syndrome, Weber's syndrome, Millard-Gubler syndrome, Benedikt syndrome or others.

Infarctions will result in weakness and loss of sensation on the opposite side of the body. Physical examination of the head area will reveal abnormal pupil dilation, light reaction and lack of eye movement on opposite side. If the infarction occurs on the left side brain, speech will be slurred. Reflexes may be aggravated as well.

Early symptoms of an arterial embolism in the arms or legs appear as soon as there is ischemia of the tissue, even before any frank infarction has begun. Such symptoms may include:

A major presentation of diabetic "skeletal muscle infarction" is painful thigh or leg swelling.

There are various classification systems for a cerebral infarction.

- The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms. Based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.

- The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).

A spontaneous coronary artery dissection (SCAD) (occasionally coronary artery dissection) is a rare, sometimes fatal traumatic condition, with eighty percent of cases affecting women. One of the coronary arteries develops a tear, causing blood to flow between the layers which forces them apart. Studies of the disease place the mortality rate at around 70%.

SCAD is a primary cause of myocardial infarction (MI) in young, fit, healthy women (and some men) with no obvious risk factors. These can often occur during late pregnancy, postpartum and peri-menopausal periods.

A limb infarction is an area of tissue death of an arm or leg. It may cause "skeletal muscle infarction", avascular necrosis of bones, or necrosis of a part of or an entire limb.

Splenic infarction is a condition in which oxygen supply to the spleen is interrupted, leading to partial or complete infarction (tissue death due to oxygen shortage) in the organ.

Splenic infarction occurs when the splenic artery or one of its branches are occluded, for example by a blood clot. Although it can occur asymptomatically, the typical symptom is severe pain in the left upper quadrant of the abdomen, sometimes radiating to the left shoulder. Fever and chills develop in some cases. It has to be differentiated from other causes of acute abdomen.

An abdominal CT scan is the most commonly used modality to confirm the diagnosis, although abdominal ultrasound can also contribute.

There is no specific treatment, except treating the underlying disorder and providing adequate pain relief. Surgical removal of the spleen (splenectomy) is only required if complications ensue; surgical removal predisposes to overwhelming post-splenectomy infections.

In one series of 59 patients, mortality amounted to 5%. Complications include a ruptured spleen, bleeding, an abscess of the spleen (for example, if the underlying cause is infective endocarditis) or pseudocyst formation. Splenectomy may be warranted for persistent pseudocysts due to the high risk of subsequent rupture.

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.

Arterial emboli often occur in the legs and feet. Some may occur in the brain, causing a stroke, or in the heart, causing a heart attack. Less common sites include the kidneys, intestines, and eyes.

Symptoms may begin quickly or slowly depending on the size of the embolus and how much it blocks the blood flow. Symptoms of embolisation in an organ vary with the organ involved but commonly include:

- Pain in the involved body part

- Temporarily decreased organ function

Later symptoms are closely related to infarction of the affected tissue. This may cause permanently decreased organ function.

For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations.

Symptoms of limb infarction include coldness, decreased or no pulse beyond the site of blockage, pain, muscle spasm, numbness and tingling, pallor and muscle weakness, possibly to the grade of paralysis in the affected limb.

Unstable angina (UA) is a type of angina pectoris that is irregular. It is also classified as a type of acute coronary syndrome (ACS).

It can be difficult to distinguish unstable angina from non-ST elevation (non-Q wave) myocardial infarction (NSTEMI). They differ primarily in whether the ischemia is severe enough to cause sufficient damage to the heart's muscular cells to release detectable quantities of a marker of injury (typically troponin T or troponin I). Unstable angina is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia (e.g., ST segment depression or transient elevation or new T wave inversion). Since an elevation in troponin may not be detectable for up to 12 hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation.

Patients will present with a sudden onset of cramps/abdominal pain or a 'stitch'. The pain localises in the area of the umbilicus and can radiate to the lumbar and surrounding regions.

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.

Omental infarction, or omental torsion, is an acute vascular disorder which compromises tissue of the greater omentum—the largest peritoneal fold in the abdomen.

Symptoms of myocardial rupture are recurrent or persistent chest pain, syncope, and distension of jugular vein. Sudden death caused by a myocardial rupture is sometimes preceded by no symptoms.

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.

Signs and symptoms of ischemic cardiomyopathy include sudden fatigue, shortness of breath, dizziness and palpitations.

For most people, the first symptoms result from atheroma progression within the heart arteries, most commonly resulting in a heart attack and ensuing debility. However, the heart arteries, because (a) they are small (from about 5 mm down to microscopic), (b) they are hidden deep within the chest and (c) they never stop moving, have been a difficult target organ to track, especially clinically in individuals who are still asymptomatic. Additionally, all mass-applied clinical strategies focus on both (a) minimal cost and (b) the overall safety of the procedure. Therefore, existing diagnostic strategies for detecting atheroma and tracking response to treatment have been extremely limited. The methods most commonly relied upon, patient symptoms and cardiac stress testing, do not detect any symptoms of the problem until atheromatous disease is very advanced because arteries enlarge, not constrict in response to increasing atheroma. It is plaque ruptures, producing debris and clots which obstruct blood flow downstream, sometimes also locally (as seen on angiograms), which reduce/stop blood flow. Yet these events occur suddenly and are not revealed in advance by either stress testing, stress tests or angiograms.

The risk of PVF during acute myocardial infarction is related to the amount of ST elevation, the presence of hypokalemia, the absence of pre-infarction angina, the size of the infarction, and the presence of a blocked left coronary artery. Other risk factors could include younger age, male gender, and history of sudden cardiac death in first degree relatives.

Cavernous sinus thrombosis is a specialised form of cerebral venous sinus thrombosis, where there is thrombosis of the cavernous sinus of the basal skull dura, due to the retrograde spread of infection and endothelial damage from the danger triangle of the face. The facial veins in this area anastomose with the superior and inferior ophthalmic veins of the orbit, which drain directly posteriorly into the cavernous sinus through the superior orbital fissure. Staphyloccoal or Streptococcal infections of the face, for example nasal or upper lip pustules may thus spread directly into the cavernous sinus, causing stroke-like symptoms of double vision, squint, as well as spread of infection to cause meningitis.

Myocardial rupture is a laceration or t

e ventricles or atria of the heart, of the interatrial or interventricular septum, or of the papillary muscles. It is most commonly seen as a serious sequela of an acute myocardial infarction (heart attack).

It can also be caused by trauma.