Prognostics factors:

Lower Glasgow coma scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.

Acquired cerebrovascular diseases are those that are obtained throughout a person's life that may be preventable by controlling risk factors. The incidence of cerebrovascular disease increases as an individual ages. Causes of acquired cerebrovascular disease include atherosclerosis, embolism, aneurysms, and arterial dissections. Atherosclerosis leads to narrowing of blood vessels and less perfusion to the brain, and it also increases the risk of thrombosis, or a blockage of an artery, within the brain. Major modifiable risk factors for atherosclerosis include:

Controlling these risk factors can reduce the incidence of atherosclerosis and stroke. Atrial fibrillation is also a major risk factor for strokes. Atrial fibrillation causes blood clots to form within the heart, which may travel to the arteries within the brain and cause an embolism. The embolism prevents blood flow to the brain, which leads to a stroke.

An aneurysm is an abnormal bulging of small sections of arteries, which increases the risk of artery rupture. Intracranial aneurysms are a leading cause of subarachnoid hemorrhage, or bleeding around the brain within the subarachnoid space. There are various hereditary disorders associated with intracranial aneurysms, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, and familial hyperaldosteronism type I. However, individuals without these disorders may also obtain aneurysms. The American Heart Association and American Stroke Association recommend controlling modifiable risk factors including smoking and hypertension.

Arterial dissections are tears of the internal lining of arteries, often associated with trauma. Dissections within the carotid arteries or vertebral arteries may compromise blood flow to the brain due to thrombosis, and dissections increase the risk of vessel rupture.

Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.

The morbidity and of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good blood pressure control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.

The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increases. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

Several studies have concluded that African Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease than non-Hispanic whites. It appears that hypertensive crisis is also more common in African Americans compared with other races.

Although severe hypertension is more common in the elderly, it may occur in children (though very rarely). Also, women have slightly increased risks of developing hypertension crises than do men. The lifetime risk for developing hypertension is 86-90% in females and 81-83% in males.

Although an estimated 50 million or more adult Americans suffer from hypertension, the relative incidence of hypertensive crisis is relatively low (less than 1% annually). Nevertheless, this condition does affect upward of 500,000 Americans each year, and is therefore a significant cause of serious morbidity in the US. About 14% of adults seen in hospital emergency departments in United States have a systolic blood pressure ≥180 mmHg.

As a result of the use of antihypertensives, the rates of hypertensive emergencies has declined from 7% to 1% of people with high blood pressure. The 1–year survival rate has also increased. Before 1950, this survival rate was 20%, but it is now more than 90% with proper medical treatment.

Estimates indicate that approximately 1% to 2% of people with hypertension develop hypertensive crisis at some point in their lifetime. Men are more commonly affected by hypertensive crises than women.

The rates of hypertensive crises has increased and hospital admissions tripled between 1983 and 1990, from 23,000 to 73,000 per year in the United States. The incidence of postoperative hypertensive crisis varies and such variation depends on the population examined. Most studies report and incidence of between 4% to 35%.

Treatment varies with the type of vascular disease; in the case of renal artery disease, information from a meta-analysis indicated that balloon angioplasty results in improvement of diastolic blood pressure and a reduction in antihypertensive drug requirements. In the case of peripheral artery disease, preventing complications is important; without treatment, sores or gangrene (tissue death) may occur. Among the treatments are:

- Quitting smoking

- Lowering cholesterol

- Lower blood pressure

- Lower blood glucose

- Physical activity

Carotid stenosis is a narrowing or constriction of the inner surface (lumen) of the carotid artery, usually caused by atherosclerosis.

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

The largest clinical trial performed, CREST, randomized patients at risk for a stroke from carotid artery blockage to either open surgery (carotid endarterectomy) or carotid stent placement with embolic protection. This trial followed patients for 4 years and found no overall difference in the primary end point of both treatment arms (myocardial infarctions, any perioperative strokes or ipsilateral strokes within 4 years, or death during procedure). Patients assigned to the surgical arm experienced more perioperative myocardial infarctions compared to the stenting group; however, the difference was not statistically significant (6.8% vs or 7.2% HR for stenting is 1.1 CI 0.81-1.51 P value 0.51) whereas patients assigned to the carotid stent arm experienced more periprocedural strokes compared to endarteretomy (6.4% vs 4.7% HR for stenting 1.5 P-0.03). There was no mortality difference and no difference for major (disabling) strokes between surgery and stenting. It was noted that there did seem to exist an age cutoff where below 75 years old endarterectomy provided more positive outcomes and over 75 stenting offered a better risk profile. However, it should be noted that the CREST trial was not designed for subgroup analysis and thus not powered enough to draw any statistically significant conclusions. A later study published in 2013 evaluated how these perioperative complications affect long-term survival. This study showed that experiencing a stroke within the first year conferred a two-fold lower survival rate (Hazard Ratio(HR) 6.6 [CI 3.7-12]) than those who experienced a perioperative myocardial infarction at two years post intervention (HR 3.6 [CI 2-6.8]). This difference in mortality, however, converges and becomes negligible at 5 years (HR 2.7 [CI 1.7-4.3] vs HR 2.8 [CI 1.8-4.3]). A 2010 study found benefits (reduced strokes) from carotid endarterectomy in those without symptoms who are under 75.

In cardiology, stunned myocardium is a state when some section of the myocardium (corresponding to area of a major coronary occlusion) shows a form of contractile abnormality. This is a segmental dysfunction which persists for a variable period of time, about two weeks, even after ischemia has been relieved (by for instance angioplasty or coronary artery bypass surgery). In this situation, while myocardial blood flow (MBF) returns to normal, function is still depressed for a variable period of time.

Myocardial stunning is the reversible reduction of function of heart contraction after reperfusion not accounted for by tissue damage or reduced blood flow.

After total ischemia occurs, the myocardium switches immediately from aerobic glycolysis to anaerobic glycolysis resulting in the reduced ability to produce high energy phosphates such as ATP and Creatinine Phosphate. At this point, the lack of the energy and lactate accumulation results in cessation of contraction within 60 seconds of ischemia (i.e. Vessel Occlusion). Subsequent to this is a period of "myocardial stunning," in which reversible ischemic damage is taking place. At approximately 30 minutes after the onset of total ischemia the damage becomes irreversible, thereby ending the phase of myocardial stunning.

Clinical situations of stunned myocardium are:

- acute myocardial infarction (AMI)

- after percutaneous transluminal coronary angioplasty (PTCA)

- after cardiac surgery

- 'neurogenic' stunned myocardium following an acute cerebrovascular event such as a subarachnoid hemorrhage

Macrovascular disease is a disease of any large ("macro") blood vessels in the body. It is a disease of the large blood vessels, including the coronary arteries, the aorta, and the sizable arteries in the brain and in the limbs.

This sometimes occurs when a person has had diabetes for an extended period of time. Fat and blood clots build up in the large blood vessels and stick to the vessel walls.

Three common macrovascular diseases are coronary disease (in the heart), cerebrovascular disease (in the brain), and peripheral vascular disease (in the limbs)

Macrovascular disease (macroangiopathy) refers to atherosclerosis. Atherosclerosis is a form of arteriosclerosis (thickening and hardening of arterial walls), characterized by plaque deposits of lipids, fibrous connective tissue, calcium, and other blood substances. Atherosclerosis, by definition, affects only medium and large arteries (excluding arterioles).

Macrovascular disease is associated with the development of coronary artery disease, peripheral vascular disease, brain attack (stroke), and increased risk of infection. Type 2 diabetes is more closely associated with macrovascular diseases than type 1 diabetes. Peripheral vascular disease and increased risk of infection have important implications in the care of the acutely ill patient.

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

There are several types of vascular disease, (which is a subgroup of cardiovascular disease), the signs and symptoms depend on which type, among them are:

- Erythromelalgia - a rare peripheral vascular disease where syndromes includes burning pain, increased temperature, erythema and swelling, of mainly the hands and feet are affected.

- Peripheral artery disease – happens when atheromatous plaques build up in the arteries that supply blood to the arms and legs, plaque causes the arteries to narrow or become blocked.

- Renal artery stenosis - is the narrowing of renal arteries that carry blood to the kidneys from the aorta.

- Buerger's disease – is due to small blood vessels that inflame and swell, vessels then narrow or are blocked by blood clots.

- Raynaud's disease – a rare peripheral vascular disorder of constriction of the peripheral blood vessels, in the fingers and toes when the person is cold.

- Disseminated intravascular coagulation – a widespread activation of clotting in the smaller blood vessels.

- Cerebrovascular disease–a group of vascular diseases that affect brain function.

The goal of treating systolic hypertension is to delay and reduce the extent of damage to the heart, the cerebrovascular system, and the kidneys. Lifestyle interventions are a crucial element of successful treatment, including a diet low in sodium (salt) and rich in whole grains, fruits, and vegetables. Clinical trials have also documented the beneficial effects of weight loss, increased physical activity, and limiting alcohol consumption.

In addition to lifestyle changes, medication can also be used to reduce systolic hypertension to safe levels, although medications frequently have side effects, often serious.

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.

Based on these studies, treating to a systolic blood pressure of 140, as long as the diastolic blood pressure is 68 or more, seems safe. Corroborating this, a reanalysis of the SHEP data suggests allowing the diastolic to go below 70 may increase adverse effects.

A meta-analysis of individual patient data from randomized controlled trials found the lowest diastolic blood pressure for which cardiovascular outcomes improve is 85 mm Hg for untreated hypertensives and 80 mm Hg for treated hypertensives. The authors concluded "poor health conditions leading to low blood pressure and an increased risk for death probably explain the J-shaped curve". Interpreting the meta-analysis is difficult, but avoiding a diastolic blood pressure below 68–70 mm Hg seems reasonable because:

- The low value of 85 mm Hg for treated hypertensives in the meta-analysis is higher than the value of 68–70 mm Hg that is suggested by the two major randomized controlled trials of isolated systolic hypertension

- The two largest trials in the meta-analysis, Hypertension Detection and Follow-up Program (HDFP) and Medical Research Council trial in mild hypertension (MRC1) were predominantly middle-aged subjects, all of whom had diastolic hypertension before treatment.

- The independent contributions of diseases and factors other than hypertension versus effects of treatment are not clear in the meta-analysis.

A more contemporary meta-analysis by the Cochrane Hypertension group found no benefits in terms of reduced mortality or morbidity from treating patients to lower diastolic targets than 90–100 mmHg.

"Maternal floor infarcts" are "not" considered to be true placental infarcts, as they result from deposition of fibrin around the chorionic villi, i.e. perivillous fibrin deposition.

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.

A placental infarction results from the interruption of blood supply to a part of the placenta, causing its cells to die.

Small placental infarcts, especially at the edge of the placental disc, are considered to be normal at term. Large placental infarcts are associated with vascular abnormalities, e.g. hypertrophic decidual vasculopathy, as seen in hypertension. Very large infarcts lead to placental insufficiency and may result in fetal death.

A paradoxical embolism, also called a crossed embolism, refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa. It is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin, which travels to the arterial side through a lateral opening in the heart, such as a patent foramen ovale, or arteriovenous shunts in the lungs.

The opening is typically an atrial septal defect, but can also be a ventricular septal defect.

Paradoxical embolisms represent two percent of arterial emboli.

Passage of a clot (thrombus) from a systemic vein to a systemic artery. When clots in systemic veins break off (embolize), they travel first to the right side of the heart and, normally, then to the lungs where they lodge, causing pulmonary embolism. On the other hand, when there is a hole at the septum, either upper chambers of the heart (an atrial septal defect) or lower chambers of the heart (ventricular septal defects), a clot can cross from the right to the left side of the heart, then pass into the systemic arteries as a paradoxical embolism. Once in the arterial circulation, a clot can travel to the brain, block a vessel there, and cause a stroke (cerebrovascular accident).

Placental insufficiency or utero-placental insufficiency is the failure of the placenta to deliver sufficient nutrients to the fetus during pregnancy, and is often a result of insufficient blood flow to the placenta. The term is also sometimes used to designate late decelerations of fetal heart rate as measured by electronic monitoring, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.

In treating pulmonary insufficiency, it should be determined if pulmonary hypertension is causing the problem to therefore begin the most appropriate therapy as soon as possible (primary pulmonary hypertension or secondary pulmonary hypertension due to thromboembolism). Furthermore, pulmonary insufficiency is generally treated by addressing the underlying condition, in certain cases, the pulmonary valve may be surgically replaced.

Placental insufficiency can affect the fetus, causing Fetal distress. Placental insufficiency may cause oligohydramnios, preeclampsia, miscarriage or stillbirth. Placental insufficiency is most frequent cause of asymmetric IUGR.

Vascular dementia is the second-most-common form of dementia after Alzheimer's disease (AD) in older adults. The prevalence of the illness is 1.5% in Western countries and approximately 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe and 15% in Latin America. The incidence of dementia is nine times higher in patients who have had a stroke than in controls. 25% of stroke patients develop new-onset dementia within 1 year of their stroke. The relative risk of incident dementia is 5.5% within four years of suffering a stroke.

One study found that in the United States specifically, the prevalence of vascular dementia in all individuals over the age of 71 is 2.43%, and another found that the prevalence of the dementias doubles with every 5.1 years of age.

The incidence peaks between the fourth and the seventh decades of life and 80% of patients have a history of hypertension.

Hahner et al. investigated the frequency, causes and risk factors for adrenal crisis in patients with chronic adrenal insufficiency. Annane et al.'s landmark 2002 study found a very high rate of relative adrenal insufficiency among the enrolled patients with septic shock.