Binary restenosis is traditionally defined as a reduction in the percent diameter stenosis of 50% or more (≥50%). It is also known as just "binary stenosis". The term "binary" means that patients are placed in 2 groups, those who have ≥50% stenosis and those who have <50% stenosis. Binary restenosis is an epidemiological method of analyzing percent diameter stenosis for observing not only an individual patient, but also performing statistical techniques on group of patients to determine averages (descriptive measures of central tendency) or as a predictive variable.

Restenosis is the recurrence of stenosis, a narrowing of a blood vessel, leading to restricted blood flow. Restenosis usually pertains to an artery or other large blood vessel that has become narrowed, received treatment to clear the blockage and subsequently become renarrowed. This is usually restenosis of an artery, or other blood vessel, or possibly a vessel within an organ.

Restenosis is a common adverse event of endovascular procedures. Procedures frequently used to treat the vascular damage from atherosclerosis and related narrowing and renarrowing (restenosis) of blood vessels include vascular surgery, cardiac surgery, and angioplasty.

When a stent is used and restenosis occurs, this is called in-stent restenosis or ISR. If it occurs following balloon angioplasty, this is called post-angioplasty restenosis or PARS. The diagnostic threshold for restenosis in both ISR or PARS is ≥50% stenosis.

If restenosis occurs after a procedure, follow-up imaging is not the only way to initially detect compromised blood flow. Symptoms may also suggest or signal restenosis, but this should be confirmed by imaging. For instance, a coronary stent patient who develops restenosis may experience recurrent chest pain (angina) or suffer from a minor or major heart attack (myocardial infarction), though they may not report it. This is why it is important that a patient comply with follow-up screenings and the clinician follows through with a thorough clinical assessment. But it is also important to note that not all cases of restenosis lead to clinical symptoms, nor are they asymptomatic.

Stenoses of the vascular type are often associated with unusual blood sounds resulting from turbulent flow over the narrowed blood vessel. This sound can be made audible by a stethoscope, but diagnosis is generally made or confirmed with some form of medical imaging.

A stenosis is an abnormal narrowing in a blood vessel or other tubular organ or structure. It is also sometimes called a stricture (as in urethral stricture).

Stricture as a term is usually used when narrowing is caused by contraction of smooth muscle (e.g., achalasia, prinzmetal angina); stenosis is usually used when narrowing is caused by lesion that reduces the space of lumen (e.g., atherosclerosis). The term coarctation is another synonym, but is commonly used only in the context of aortic coarctation.

Restenosis is the recurrence of stenosis after a procedure. The term is from Ancient Greek στενός, "narrow".

Patients with mesenteric, or intestinal FMD, may experience abdominal pain after eating or weight loss. FMD within the extremities may cause claudication or may be detectable by bruits. If the lower limb arteries are affected, the patient may present with cold legs or evidence of distal embolic disease. FMD present in the subclavian artery may cause arm weakness, parenthesis, claudication, and subclavial steal syndrome.

The carotid and vertebral arteries are most commonly affected. Middle and distal regions of the internal carotid arteries are frequently involved. Patients with FMD in the carotid arteries typically present around 50 years of age. Symptoms of craniocervical involvement include headaches (mostly migraine), pulsatile tinnitus, dizziness, and neck pain, although patients are often asymptomatic. On physical examination, one may detect neurological symptoms secondary to a stroke or transient ischemic attack (TIA), a bruit over an affected artery, and diminished distal pulses. Complications of cerebrovascular FMD include TIA, ischemic stroke, Horner syndrome, or subarachnoid hemorrhage.

Signs and symptoms of mitral stenosis include the following:

- Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)

- Palpitations

- Chest pain

- Hemoptysis

- Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation.

- Ascites and edema and hepatomegaly (if right-side heart failure develops)

Fatigue and weakness increase with exercise and pregnancy.

Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart.

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.

A cerebral infarction is an area of necrotic tissue in the brain resulting from a blockage or narrowing in the arteries supplying blood and oxygen to the brain. The restricted oxygen due to the restricted blood supply causes an ischemic stroke that can result in an infarction if the blood flow is not restored within a relatively short period of time. The blockage can be due to a thrombus, an embolus or an atheromatous stenosis of one or more arteries. Which arteries are problematic will determine which areas of the brain are affected (infarcted). These varying infarcts will produce different symptoms and outcomes. About one third will prove fatal.

In vascular diseases, endothelial dysfunction is a systemic pathological state of the endothelium (the inner lining of blood vessels). Along with acting as a semi-permeable membrane, the endothelium is responsible for maintaining a relaxed vascular tone and low levels of oxidative stress by releasing mediators such as nitric oxide (NO), prostacyclin (PGI2) and endothelin (ET-1), and controlling local angiotensin-II activity. This allows the endothelium, specifically in the vessels of the heart, to ensure proper blood flow to and from the heart. In terms of endothelium dysfunction, nitric oxide (causes the widening of vessels; a vasodilator) is important to consider and focus on.

Endothelial dysfunction can happen as a result of many different things, including diabetes. In diabetic patients, circulating platelets can increase endothelial dysfunction by decreasing the production of nitric oxide. It can also result from increased oxidative stress (one of the causes of oxidative stress being platelets disrupting the carotid artery), hypertension, or obesity.

One of the environmental factors that can also lead to the development of endothelial dysfunction is smoking tobacco products. Endothelial dysfunction is a major pathophysiological mechanism that leads towards coronary artery disease, and other atherosclerotic diseases.

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.

Loss of consciousness, headache, and vomiting usually occur more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and the posterior column–medial lemniscus pathway, symptoms may include:

- hemiplegia and muscle weakness of the face

- numbness

- reduction in sensory or vibratory sensation

- initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies.

In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is "usually" on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.In addition to the above CNS pathways, the "brainstem" gives rise to most of the twelve cranial nerves. A brainstem stroke affecting the brainstem and brain, therefore, can produce symptoms relating to deficits in these cranial nerves:

- altered smell, taste, hearing, or vision (total or partial)

- drooping of eyelid (ptosis) and weakness of ocular muscles

- decreased reflexes: gag, swallow, pupil reactivity to light

- decreased sensation and muscle weakness of the face

- balance problems and nystagmus

- altered breathing and heart rate

- weakness in sternocleidomastoid muscle with inability to turn head to one side

- weakness in tongue (inability to stick out the tongue or move it from side to side)

If the "cerebral cortex" is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

- aphasia (difficulty with verbal expression, auditory comprehension, reading and writing; Broca's or Wernicke's area typically involved)

- dysarthria (motor speech disorder resulting from neurological injury)

- apraxia (altered voluntary movements)

- visual field defect

- memory deficits (involvement of temporal lobe)

- hemineglect (involvement of parietal lobe)

- disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)

- lack of insight of his or her, usually stroke-related, disability

If the "cerebellum" is involved, ataxia might be present and this includes:

- altered walking gait

- altered movement coordination

- vertigo and or disequilibrium