It is not clear if screening for disease is useful as it has not been properly studied.

Upon suspicion of PAD, the first-line study is the ankle–brachial index (ABI). When the blood pressure readings in the ankles is lower than that in the arms, blockages in the arteries which provide blood from the heart to the ankle are suspected. Normal ABI range of 1.00 to 1.40.The patient is diagnosed with PAD when the ABI is ≤ 0.90 . ABI values of 0.91 to 0.99 are considered "borderline" and values >1.40 indicate noncompressible arteries. PAD is graded as mild to moderate if the ABI is between 0.41 and 0.90, and an ABI less than 0.40 is suggestive of severe PAD. These relative categories have prognostic value.

In people with suspected PAD but normal resting ABIs, exercise testing of ABI can be done. A base line ABI is obtained prior to exercise. The patient is then asked to exercise (usually patients are made to walk on a treadmill at a constant speed) until claudication pain occurs (or a maximum of 5 minutes), following which the ankle pressure is again measured. A decrease in ABI of 15%-20% would be diagnostic of PAD.

It is possible for conditions which stiffen the vessel walls (such as calcifications that occur in the setting of long term diabetes) to produce false negatives usually, but not always, indicated by abnormally high ABIs (> 1.40). Such results and suspicions merit further investigation and higher level studies.

If ABIs are abnormal the next step is generally a lower limb doppler ultrasound examination to look at site and extent of atherosclerosis. Other imaging can be performed by angiography, where a catheter is inserted into the common femoral artery and selectively guided to the artery in question. While injecting a radiodense contrast agent an X-ray is taken. Any flow limiting stenoses found in the x-ray can be identified and treated by atherectomy, angioplasty or stenting. Contrast angiography is the most readily available and widely used imaging technique.

Modern multislice computerized tomography (CT) scanners provide direct imaging of the arterial system as an alternative to angiography.

Magnetic resonance angiography (MRA) is a noninvasive diagnostic procedure that uses a combination of a large magnet, radio frequencies, and a computer to produce detailed images to provide pictures of blood vessels inside the body. The advantages of MRA include its safety and ability to provide high-resolution three-dimensional (3D) imaging of the entire abdomen, pelvis and lower extremities in one sitting.

The gold standard for measuring endothelial function is angiography with acetylcholine injection. Previously, this was not done outside of research because of the invasive and complex nature of the procedure. As mentioned above, the use of acetylcholine injections to test vasodilation is now safely used for procedures where arterial catheterization is employed (this method is less frequently used though, so overall acetylcholine is not used very often in this way).

A noninvasive method to measure endothelial dysfunction is % Flow Mediated Dilation (FMD) as measured by Brachial Artery Ultrasound Imaging (BAUI). Current measurements of endothelial function via FMD vary due to technical and physiological factors. For example, FMD is largely affected by hormones, especially for women. FMD values can differ for the same woman if she is in different phases of her menstrual cycle during the time of measurement. When using this technique on people who suffer from things like heart failure, renal failure, or hypertension, their increased sympathetic tone can often falsify the results. Furthermore, a negative correlation between percent flow mediated dilation and baseline artery size is recognised as a fundamental scaling problem, leading to biased estimates of endothelial function. For research on FMD an ANCOVA approach to adjusting FMD for variation in baseline diameter is more appropriate. Another challenge of FMD is variability across centers and the requirement of highly qualified technicians to perform the procedure.

A non-invasive, FDA-approved device for measuring endothelial function that works by measuring Reactive Hyperemia Index (RHI) is Itamar Medical's EndoPAT™. It has shown an 80% sensitivity and 86% specificity to diagnose coronary artery disease when compared against the gold standard, acetylcholine angiogram. This results suggests that this peripheral test reflects the physiology of the coronary endothelium. Endopat has been tested in several clinical trials at multiple centers (including major cohort studies such as the Framingham Heart Study, the Heart SCORE study, and the Gutenberg Health Study). The results from clinical trials have shown that EndoPAT™ is useful for risk evaluation, stratification and prognosis of getting major cardiovascular events (MACE).

Since NO maintains low tone and high compliance of the small arteries at rest a reduction of age-dependent small artery compliance is a marker for endothelial dysfunction that is associated with both functional and structural changes in the microcirculation that are predictive of subsequent morbid events Small artery compliance or stiffness can be assessed simply and at rest and can be distinguished from large artery stiffness by use of pulsewave analysis with the CV Profilor.

It can be difficult to make a Vascular disease diagnosis since there are a variety of symptoms that a person can have, also family history and a physical examination are important. The physical exam may be different depending on the type of vascular disease. In the case of a peripheral vascular disease the physical exam consists in checking the blood flow in the legs.

Stent implantation has been correlated with impaired endothelial function in several studies. According to Mischie et al., sirolimus eluting stent implantation induces a higher rate of endothelial dysfunction compared to bare metal stents. This is problematic because stents have been used to treat many diseases related to endothelial dysfunction, including coronary artery disease. Sirolimus eluting stents were previously used because they showed very low rates of in-stent restenosis but further investigation showed that they often impair endothelial dysfunction in humans and worsen conditions. Therefore, now the commonly used drug is iopromide-paclitaxel because it showed low rates of in-stent restenosis and thrombosis and it does not worsen the person's health condition.

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

The prevalence of Mönckeberg's arteriosclerosis increases with age and is more frequent in diabetes mellitus, chronic kidney disease, systemic lupus erythematosus, chronic inflammatory conditions, hypervitaminosis D and rare genetic disorders, such as Keutel syndrome. The prevalence of Monckeberg's arteriosclerosis in the general population has been estimated as 1.5; however the validity of this criterion is questionable.

It is the lack of specific symptoms and its potential to appear anywhere that makes FMD a challenge to detect early on. The most accurate diagnosis comes from combining clinical presentation and angiographic imaging. According to the Michigan Outcomes Research and Reporting Program (MCORRP, 2013) the length of time from a patient’s first signs or symptoms to diagnosis is commonly 5 years.

FMD is currently diagnosed through the use of both invasive and non-invasive tests. Non-invasive testing includes duplex ultrasonography, magnetic resonance angiography (MRA), and computed tomographic angiography (CTA). Invasive testing through angiography is the gold standard. However, due to the higher risk of complications this is typically not done early on. Occasionally, FMD is diagnosed asymptomatically after an unrelated x-ray presents the classic ‘string of beads’ appearance of the arteries, or when a practitioner investigates an unexpected bruit found during an exam. When a diagnosis of FMD is considered for a patient thorough medical history, family history as well as vascular examination should be completed.

A definitive diagnosis of FMD can only be made with imaging studies. Catheter-based angiography (with contrast) has proven to be the most accurate imaging technique: this test involves a catheter is inserted into a large artery and advanced until it reaches the vessel of question. The catheter allows practitioners to view and measure the pressure of the artery aiding in the categorization and severity of the FMD diseased artery. According to Olin, “catheter-based angiography is the only imaging modality that can accurately identify the changes of FMD, aneurysm formation, and dissection in the branch vessels.” Practitioners believe it is important to utilize IVUS imaging because stenosis can sometimes only be detected through the methods of pressure gradient or IVUS imaging. In addition, computed tomography angiography and magnetic resonance angiography are commonly used to evaluate arteries in the brain. Doppler ultrasound may be used in both the diagnosis and follow-up of FMD.

The differentiating presentations are suggestive of FMD being a unique syndrome in respect to the pediatric population. Experienced FMD clinicians warn against relying in the “string of beads” angiography for a diagnosis. In fact, it is suggested that FMD may be both under and over-diagnosed in children with stroke.

Often Mönckeberg's arteriosclerosis is discovered as an incidental finding in an X-ray radiograph, on mammograms, in autopsy, or in association with investigation of some other disease, such as diabetes mellitus or chronic kidney disease. Typically calcification is observed in the arteries of the upper and lower limb although it has been seen in numerous other medium size arteries. In the radial or ulnar arteries it can cause "pipestem" arteries, which present as a bounding pulse at the end of the calcific zone. It may also result in "pulselessness." Epidemiological studies have used the ratio of ankle to brachial blood pressure (ankle brachial pressure index, ABPI or ABI) as an indicator of arterial calcification with ABPI >1.3 to >1.5 being used as a diagnostic criterion depending on the study.

Arteriosclerotic heart disease (ASHD), is a thickening and hardening of the walls of the coronary arteries. Atherosclerosis is a potentially serious condition where arteries become clogged with fatty substances called plaques, or atheroma.

Diagnosis is based on the demonstration of vascular lesions in large and middle-sized vessels on angiography, CT scan, magnetic resonance angiography or FDG PET. FDG PET can help in diagnosis of active inflammation not just in patients with active Takayasu arteritis prior to treatment but also in addition in relapsing patients receiving immunosuppressive agents.

Contrast angiography has been the gold standard. The earliest detectable lesion is a local narrowing or irregularity of the lumen. This may develop into stenosis and occlusion. The characteristic finding is the presence of "skip lesions," where stenosis or aneurysms alternate with normal vessels. Angiography provides information on vessel anatomy and patency but does not provide information on the degree of inflammation in the wall.

The age at onset helps to differentiate Takayasu's arteritis from other types of large vessel vasculitis. For example, Takaysu's arteritis has an age of onset of 60 years.

Takayasu arteritis is not associated with ANCA, rheumatoid factor, ANA, and anticardiolipin antibodies.

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.

Most people with Takayasu’s arteritis respond to steroids such as prednisone. The usual starting dose is approximately 1 milligram per kilogram of body weight per day (for most people, this is approximately 60 milligrams a day). Because of the significant side effects of long-term high-dose prednisone use, the starting dose is tapered over several weeks to a dose which controls symptoms while limiting the side effects of steroids.

Promising results are achieved with mycophenolate and tocilizumab. If treatment is not kept to a high standard, long-term damage or death can occur.

For patients who do not respond to steroids may require revascularization, either via vascular bypass or angioplasty and stenting. Outcomes following revascularization vary depending on the severity of the underlying disease

For most patients, health care providers diagnose high blood pressure when blood pressure readings are consistently 140/90 mmHg or above. A blood pressure test can be done in a health care provider’s office or clinic. To track blood pressure readings over a period of time, the health care provider may ask the patient to come into the office on different days and at different times. The health care provider also may ask the patient to check readings at home or at other locations that have blood pressure equipment and to keep a written log of results. The health care provider usually takes 2–3 readings at several medical appointments to diagnose high blood pressure. Using the results of the blood pressure test, the health care provider will diagnose prehypertension or high blood pressure if:

- For an adult, systolic or diastolic readings are consistently higher than 120/80 mmHg.

- A child’s blood pressure numbers are outside average numbers for children of the same age, gender, and height.

Once the health care provider determines the severity, he or she can order additional tests to determine if the blood pressure is due to other conditions or medicines or if there is primary high blood pressure. Health care providers can use this information to develop a treatment plan.

Regular physical exercise reduces blood pressure. The UK National Health Service advises 150 minutes (2 hours and 30 minutes) of moderate-intensity aerobic activity per week to help prevent hypertension.

For people considered likely to have PAH based on the above tests, the specific associated condition is then determined based on the physical examination, medical/family history and further specific diagnostic tests (for example, serological tests to detect underlying connective tissue disease, HIV infection or hepatitis, ultrasonography to confirm the presence of portal hypertension, echocardiography/cardiac magnetic resonance imaging for congenital heart disease, laboratory tests for schistosomiasis, and high resolution CT for PVOD and pulmonary capillary hemangiomatosis). Routine lung biopsy is discouraged in patients with PAH, because of the risk to the patient and because the findings are unlikely to alter the diagnosis and treatment.

A concrete diagnosis of thromboangiitis obliterans is often difficult as it relies heavily on exclusion of other conditions. The commonly followed diagnostic criteria are outlined below although the criteria tend to differ slightly from author to author. Olin (2000) proposes the following criteria:

1. Typically between 20–40 years old and male, although recently females have been diagnosed.

2. Current (or recent) history of tobacco use.

3. Presence of distal extremity ischemia (indicated by claudication, pain at rest, ischemic ulcers or gangrene) documented by noninvasive vascular testing such as ultrasound.

4. Exclusion of other autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory tests.

5. Exclusion of a proximal source of emboli by echocardiography and arteriography.

6. Consistent arteriographic findings in the clinically involved and noninvolved limbs.

Buerger’s disease can be mimicked by a wide variety of other diseases that cause diminished blood flow to the extremities. These other disorders must be ruled out with an aggressive evaluation, because their treatments differ substantially from that of Buerger’s disease, for which there is no treatment known to be effective.

Diseases with which Buerger’s disease may be confused include atherosclerosis (build-up of cholesterol plaques in the arteries), endocarditis (an infection of the lining of the heart), other types of vasculitis, severe Raynaud's phenomenon associated with connective tissue disorders (e.g., lupus or scleroderma), clotting disorders of the blood, and others.

Angiograms of the upper and lower extremities can be helpful in making the diagnosis of Buerger’s disease. In the proper clinical setting, certain angiographic findings are diagnostic of Buerger’s. These findings include a “corkscrew” appearance of arteries that result from vascular damage, particularly the arteries in the region of the wrists and ankles. Collateral circulation gives "tree root" or "spider leg" appearance. Angiograms may also show occlusions (blockages) or stenosis (narrowings) in multiple areas of both the arms and legs. Distal plethysmography also yields useful information about circulatory status in digits.

To rule out other forms of vasculitis (by excluding involvement of vascular regions atypical for Buerger’s), it is sometimes necessary to perform angiograms of other body regions (e.g., a mesenteric angiogram).

Skin biopsies of affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well.

If heart disease and lung disease have been excluded, a ventilation/perfusion scan is performed to rule out CTEPH. If unmatched perfusion defects are found, further evaluation by CT pulmonary angiography, right heart catheterization, and selective pulmonary angiography is performed.

Currently laboratory testing is not as reliable as observation when it comes to defining the parameters of Thrombotic Storm. Careful evaluation of possible thrombosis in other organ systems is pertinent in expediting treatment to prevent fatality.Preliminary diagnosis consists of evidence documented with proper imaging studies such as CT scan, MRI, or echocardiography, which demonstrate a thromboembolic occlusion in the veins and/or arteries. Vascular occlusions mentioned must include at least two of the clinic events:

- Deep venous thrombosis affecting one (or more) limbs and/or pulmonary embolism.

- Cerebral vein thrombosis.

- Portal vein thrombosis, hepatic vein, or other intra-abdominal thrombotic events.

- Jugular vein thrombosis in the absence of ipsilateral arm vein thrombosis and in the absence of ipsilateral central venous access.

- Peripheral arterial occlusions, in the absence of underlying atherosclerotic vascular disease,

- resulting in extremity ischemia and/or infarction.

- Myocardial infarction, in the absence of severe coronary artery disease

- Stroke and/or transient ischemic attack, in the absence of severe atherosclerotic disease and at an age less than 60 years.

- Central retinal vein and/or central retinal arterial thrombosis.

- Small vessel thrombosis affecting one or more organs, systems, or tissue; must be documented by histopathology.

In addition to the previously noted vascular occlusions, development of different thromboembolic manifestations simultaneously or within one or two weeks must occur and the patient must have an underlying inherited or acquired hypercoagulable state (other than Antiphospholipid syndrome)

The diagnosis of pulmonary heart disease is not easy as both lung and heart disease can produce similar symptoms. Therefore, the differential diagnosis should assess:

Among the investigations available to determine cor pulmonale are:

- Chest x-ray – right ventricular hypertrophy, right atrial dilatation, prominent pulmonary artery

- ECG – right ventricular hypertrophy, dysrhythmia, P pulmonale (characteristic peaked P wave)

- Thrombophilia screen- to detect chronic venous thromboembolism (proteins C and S, antithrombin III, homocysteine levels)

Several classes of antihypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the usual blood pressure of the person before the hypertensive crisis. In most cases, the administration of intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect, is suitable (but in many cases not readily available). Besides, nitroprusside runs a risk of cyanide poisoning. Other intravenous agents like nitroglycerine, nicardipine, labetalol, fenoldopam or phentolamine can also be used, but all have a delayed onset of action (by several minutes) compared to sodium nitroprusside.

In addition, non-pharmacological treatment could be considered in cases of resistant malignant hypertension due to end stage kidney failure, such as surgical nephrectomy, laparoscopic nephrectomy, and renal artery embolization in cases of anesthesia risk.

It is also important that the blood pressure is lowered smoothly, not too abruptly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% (within minutes to 1 or 2 hours), and then toward a level of 160/100 mm Hg within a total of 2–6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.

The diagnosis of a hypertensive emergency is not based solely on an absolute level of blood pressure, but also on the typical blood pressure level of the patient before the hypertensive crisis occurs. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.

Vitamins B6, B9, or B12 supplements, while they lower homocysteine level do not change the risk of heart disease, stroke, or death. This also applies to people with kidney disease on dialysis.

Hypotheses have been offered to address the failure of homocysteine-lowering therapies to reduce cardiovascular events. When folic acid is given as a supplement, it may increase the build-up of arterial plaque. A second hypothesis involves the methylation of genes in vascular cells by folic acid and vitamin B12, which may also accelerate plaque growth. Finally, altered methylation may catalyse l-arginine to asymmetric dimethylarginine, which is known to increase the risk of vascular disease.

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.

Intermittent claudication is a symptom and is by definition diagnosed by a patient reporting a history of leg pain with walking relieved by rest. However, as other conditions such as sciatica can mimic intermittent claudication, testing is often performed to confirm the diagnosis of peripheral artery disease.

Magnetic resonance angiography and duplex ultrasonography appear to be slightly more cost-effective in diagnosing peripheral artery disease among people with intermittent claudication than projectional angiography.