Up to 50% of people with PAD may have no symptoms. Symptoms of PAD in the legs and feet are generally divided into 2 categories:

1. Intermittent claudication—pain in muscles when walking or using the affected muscles that is relieved by resting those muscles. This is due to the unmet oxygen demand in muscles with use in the setting of inadequate blood flow.

2. Critical limb ischemia, consisting of:

Medical signs of PAD in the legs, due to inadequate perfusion, include:

- Noticeable change in color – blueness, or in temperature (coolness) when compared to the other limb.

- Buerger's test can check for pallor on elevation of limb and redness (rubor) on a change to a sitting position, in an assessment of arterial sufficiency.

- Diminished hair and nail growth on affected limb and digits

PAD in other parts of the body depends on the organ affected. Renal artery stenosis can cause renovascular hypertension.

Carotid artery disease can cause strokes and transient ischemic attacks.

Coronary artery ectasia is a rare disease that occurs in only 0.3-4.9% of people in North America. Coronary artery ectasia is characterized by the enlargement of a coronary artery to 1.5 times or more than its normal diameter. The disease is commonly asymptomatic and is normally discovered when performing tests for other conditions such as coronary artery disease, stable angina and other acute coronary syndromes. Coronary artery ectasia occurs 4 times more frequently in males than in females and in people who have risk factors for heart disease such as smokers. While the disease is commonly found in patients with atherosclerosis and coronary artery disease, it can occur by itself and in both cases it can cause health problems. The disease can cause the heart tissue to be deprived of blood and die due to decreased blood flow, and blockages due to blood clots or spasms of the blood vessel. This blood flow disruption can cause permanent damage to the muscle if the deprivation is prolonged. Coronary artery ectasia also increases the chance of developing large weak spots in the affected coronary arteries, or aneurysms that can rupture and result in death. The damage can result in angina which is pain in the chest and is a common complaint in these patients.

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

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.

Peripheral artery disease (PAD) is a narrowing of the arteries other than those that supply the heart or the brain. When narrowing occurs in the heart, it is called coronary artery disease, while, in the brain, it is called cerebrovascular disease. Peripheral artery disease most commonly affects the legs, but other arteries may also be involved. The classic symptom is leg pain when walking which resolves with rest, known as intermittent claudication. Other symptoms including skin ulcers, bluish skin, cold skin, or poor nail and hair growth may occur in the affected leg. Complications may include an infection or tissue death which may require amputation; coronary artery disease, or stroke. Up to 50% of cases of PAD are without symptoms.

The main risk factor is cigarette smoking. Other risk factors include diabetes, high blood pressure, and high blood cholesterol. The underlying mechanism is usually atherosclerosis. Other causes include artery spasm. PAD is typically diagnosed by finding an ankle-brachial index (ABI) less than 0.90, which is the systolic blood pressure at the ankle divided by the systolic blood pressure of the arm. Duplex ultrasonography and angiography may also be used. Angiography is more accurate and allows for treatment at the same time; however, it is associated with greater risks.

It is unclear if screening for disease is useful as it has not been properly studied. In those with intermittent claudication from PAD, stopping smoking and supervised exercise therapy improves outcomes. Medications, including statins, ACE inhibitors, and cilostazol also may help. Aspirin does not appear to help those with mild disease but is usually recommended in those with more significant disease. Anticoagulants such as warfarin are not typically of benefit. Procedures used to treat the disease include bypass grafting, angioplasty, and atherectomy.

In 2015 about 155 million people had PAD worldwide. In the developed world it affects about 5.3% of 45 to 50 years olds and 18.6% of 85- to 90-year-olds. In the developing world it affects 4.6% of people between the ages of 45 to 50 and 15% of people between the ages of 85 to 90. In the developed world PAD is equally common among men and women while in the developing world women are more commonly affected. In 2015 PAD resulted in about 52,500 deaths up from 16,000 deaths in 1990.

Atherosclerosis is asymptomatic for decades because the arteries enlarge at all plaque locations, thus there is no effect on blood flow. Even most plaque ruptures do not produce symptoms until enough narrowing or closure of an artery, due to clots, occurs. Signs and symptoms only occur after severe narrowing or closure impedes blood flow to different organs enough to induce symptoms. Most of the time, patients realize that they have the disease only when they experience other cardiovascular disorders such as stroke or heart attack. These symptoms, however, still vary depending on which artery or organ is affected.

Typically, atherosclerosis begins in childhood, as a thin layer of white-yellowish streaks with the inner layers of the artery walls (an accumulation of white blood cells, mostly monocytes/macrophages) and progresses from there.

Clinically, given enlargement of the arteries for decades, symptomatic atherosclerosis is typically associated with men in their 40s and women in their 50s to 60s. Sub-clinically, the disease begins to appear in childhood, and rarely is already present at birth. Noticeable signs can begin developing at puberty. Though symptoms are rarely exhibited in children, early screening of children for cardiovascular diseases could be beneficial to both the child and his/her relatives. While coronary artery disease is more prevalent in men than women, atherosclerosis of the cerebral arteries and strokes equally affect both sexes.

Marked narrowing in the coronary arteries, which are responsible for bringing oxygenated blood to the heart, can produce symptoms such as the chest pain of angina and shortness of breath, sweating, nausea, dizziness or light-headedness, breathlessness or palpitations. Abnormal heart rhythms called arrhythmias (the heart is either beating too slow or too fast) are another consequence of ischemia.

Carotid arteries supply blood to the brain and neck. Marked narrowing of the carotid arteries can present with symptoms such as a feeling of weakness, not being able to think straight, difficulty speaking, becoming dizzy and difficulty in walking or standing up straight, blurred vision, numbness of the face, arms, and legs, severe headache and losing consciousness. These symptoms are also related to stroke (death of brain cells). Stroke is caused by marked narrowing or closure of arteries going to the brain; lack of adequate blood supply leads to the death of the cells of the affected tissue.

Peripheral arteries, which supply blood to the legs, arms, and pelvis, also experience marked narrowing due to plaque rupture and clots. Symptoms for the marked narrowing are numbness within the arms or legs, as well as pain. Another significant location for the plaque formation is the renal arteries, which supply blood to the kidneys. Plaque occurrence and accumulation leads to decreased kidney blood flow and chronic kidney disease, which, like all other areas, are typically asymptomatic until late stages.

According to United States data for 2004, in about 66% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is a heart attack or sudden cardiac death (death within one hour of onset of the symptom).

Cardiac stress testing, traditionally the most commonly performed non-invasive testing method for blood flow limitations, in general, detects only lumen narrowing of ≈75% or greater, although some physicians claim that nuclear stress methods can detect as little as 50%.

Case studies have included autopsies of U.S. soldiers killed in World War II and the Korean War. A much-cited report involved autopsies of 300 U.S. soldiers killed in Korea. Although the average age of the men was 22.1 years, 77.3 percent had "gross evidence of coronary arteriosclerosis". Other studies done of soldiers in the Vietnam War showed similar results, although often worse than the ones from the earlier wars. Theories include high rates of tobacco use and (in the case of the Vietnam soldiers) the advent of processed foods after World War II.

The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis, and atherosclerosis. "Arteriosclerosis" is a general term describing any hardening (and loss of elasticity) of medium or large arteries (); "arteriolosclerosis" is any hardening (and loss of elasticity) of arterioles (small arteries); "atherosclerosis" is a hardening of an artery specifically due to an atheromatous plaque. The term "atherogenic" is used for substances or processes that cause atherosclerosis.

To discover the extent and severity of coronary artery ectasia there are a variety of diagnostic tools used. The most common method for discovering the disease is through angiography. Angiography is the procedure where a contrast dye is entered into the vessels and an x-ray is taken, which will allow the vessels to be seen on the x-ray. Using angiography clinicians are able to display the size, location and number of vessels affected by the disease. Is can also be analyzed through other methods such as intravascular ultrasound, and magnetic resonance imaging. Using these diagnostic methods, it has been discovered that the disease normally occurs most often in the right coronary artery, followed by the left anterior descending artery, and finally the left anterior circumflex artery. Using these methods Coronary artery ectasia can be divided into four different types: Type 1¬→diffuse ectasia in 2-3 different vessels, Type 2¬→ diffuse disease in 1 vessel and local disease in another, Type 3¬→ diffuse disease in one vessel and Type 4¬→ localized or segmental ectasia.

The healthy epicardial coronary artery consists of three layers, the intima, media, and adventitia. Atheroma and changes in the artery wall usually result in small aneurysms (enlargements) just large enough to compensate for the extra wall thickness with no change in the lumen diameter. However, eventually, typically as a result of rupture of vulnerable plaques and clots within the lumen over the plaque, stenosis (narrowing) of the vessel develops in some areas. Less frequently, the artery enlarges so much that a gross aneurysmal enlargement of the artery results. All three results are often observed, at different locations, within the same individual.

Acquired causes include atherosclerosis, Kawasaki disease and coronary catheterization.

It can also be congenital.

Among the signs/symptoms of arteriosclerosis are: sudden weakness, facial or lower limbs numbness, confusion, difficulty understanding speech and problems seeing.

A vulnerable plaque is a kind of atheromatous plaque – a collection of white blood cells (primarily macrophages) and lipids (including cholesterol) in the wall of an artery – that is particularly unstable and prone to produce sudden major problems such as a heart attack or stroke.

The defining characteristics of a vulnerable plaque include but are not limited to: a thin fibrous cap, large lipid-rich necrotic core, increased plaque inflammation, positive vascular remodeling, increased vasa-vasorum neovascularization, and intra-plaque hemorrhage. These characteristics together with the usual hemodynamic pulsating expansion during systole and elastic recoil contraction during diastole contribute to a high mechanical stress zone on the fibrous cap of the atheroma, making it prone to rupture. Increased hemodynamic stress, e.g. increased blood pressure, especially pulse pressure (systolic blood pressure vs. diastolic blood pressure difference), correlates with increased rates of major cardiovascular events associated with exercise, especially exercise beyond levels the individual does routinely. This video , examining autopsy specimens from an actual heart attack resulting in sudden death, shows the sequence. These videos, and , illustrate the sequence of events and why, though the underlying process develops over decades, the symptoms are usually of sudden onset.

Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen. Tearing of the cover is called "plaque rupture".

Repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, that creates artery stenosis.

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.

Coronary artery aneurysm is an abnormal dilatation of part of the coronary artery.

Arteriosclerosis is the thickening, hardening and loss of elasticity of the walls of arteries. This process gradually restricts the blood flow to one's organs and tissues and can lead to severe health risks brought on by atherosclerosis, which is a specific form of arteriosclerosis caused by the buildup of fatty plaques, cholesterol, and some other substances in and on the artery walls.

Chest pain that occurs regularly with activity, after eating, or at other predictable times is termed stable angina and is associated with narrowings of the arteries of the heart.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction. In adults who go to the emergency department with an unclear cause of pain, about 30% have pain due to coronary artery disease.

Chest pain is a major indication of coronary ischemia. If chest pain occurs while exercising, or during sex, but it doesn't persist after rest, it may be coronary ischemia, or what is called, "angina". Some people characterize the pain they feel as though an elephant is sitting on their chest.

Other typical symptoms include diaphoresis which is sweaty palms, and clammy skin, nausea or vomiting, or shortness of breath. Chest pain radiating down the left arm is also a symptom of coronary ischemia and the pain can also be radiating directly to the back in some instances.

Coronary vasospasm is a sudden, intense vasoconstriction of an epicardial coronary artery that causes occlusion (stoppage) or near-occlusion of the vessel.

It can cause Prinzmetal's angina.

It can occur in multiple vessels.

Atropine has been used to treat the condition.

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.

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

Most atypical symptoms are seen in women, diabetics, and the elderly more than anyone else.

These type of symptoms include stomach pain, and simply fatigue. It can also include heartburn and anxiety.

If no symptoms are present it is called silent ischemia.

Coronary artery disease (CAD), also known as ischemic heart disease (IHD), refers to a group of diseases which includes stable angina, unstable angina, myocardial infarction, and sudden cardiac death. It is within the group of cardiovascular diseases of which it is the most common type. A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no symptoms are present. Occasionally, the first sign is a heart attack. Other complications include heart failure or an abnormal heartbeat.

Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, and excessive alcohol. The underlying mechanism involves reduction of blood flow and oxygen to the heart muscle due to atherosclerosis of the arteries of the heart. A number of tests may help with diagnoses including: electrocardiogram, cardiac stress testing, coronary computed tomographic angiography, and coronary angiogram, among others.

Ways to reduce CAD risk include eating a healthy diet, regularly exercising, maintaining a healthy weight, and not smoking. Medications for diabetes, high cholesterol, or high blood pressure are sometimes used. There is limited evidence for screening people who are at low risk and do not have symptoms. Treatment involves the same measures as prevention. Additional medications such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be recommended. Procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG) may be used in severe disease. In those with stable CAD it is unclear if PCI or CABG in addition to the other treatments improves life expectancy or decreases heart attack risk.

In 2015 CAD affected 110 million people and resulted in 8.9 million deaths. It makes up 15.9% of all deaths making it the most common cause of death globally. The risk of death from CAD for a given age has decreased between 1980 and 2010, especially in developed countries. The number of cases of CAD for a given age has also decreased between 1990 and 2010. In the United States in 2010 about 20% of those over 65 had CAD, while it was present in 7% of those 45 to 64, and 1.3% of those 18 to 45. Rates are higher among men than women of a given age.

Subclavian steal syndrome (SSS), also called subclavian steal phenomenon or subclavian steal steno-occlusive disease, is a constellation of signs and symptoms that arise from retrograde (reversed) blood flow in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. The arm may be supplied by blood flowing in a retrograde direction down the vertebral artery at the expense of the vertebrobasilar circulation. This is called the "subclavian steal". It is more severe than typical vertebrobasilar insufficiency.

In contrast to patient with unstable angina secondary to coronary atherosclerosis, patients with variant angina are generally younger and have fewer coronary risk factors (except smoking). Episode of chest pain usually does not progress from a period of chronic stable angina. Cardiac examination is usually normal in the absence of ischemia.

Symptoms typically occur at rest, rather than on exertion (thus attacks usually occur in early morning hours). Two-thirds of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms.

Prinzmetal's should be suspected by a cardiologist when the pain occurs at rest and/or in clusters, and in the absence of a positive treadmill stress test, as Prinzmetal's is exercise tolerant and can generally only be diagnosed after other forms of cardiac disease have been ruled out.

It is associated with specific ECG changes (elevation rather than depression of the ST segment) together with small elevation of cardiac enzymes (especially with long attacks). However, in order to be diagnosed, these ECG changes can only be tracked when the electrocardiogram occurs while the patient is experiencing an attack. Therefore, many experts recommend provocative testing during electrocardiogram testing to attempt to induce an attack when Prinzmetal's is suspected.

While a single ruptured plaque can be identified during autopsy as the cause of a coronary event, there is currently no way to identify a culprit lesion before it ruptures.

Because artery walls typically enlarge in response to enlarging plaques, these plaques do not usually produce much stenosis of the artery lumen. Therefore, they are not detected by cardiac stress tests or angiography, the tests most commonly performed clinically with the goal of predicting susceptibility to future heart attack. In contrast to conventional angiography, cardiac CT angiography does enable visualization of the vessel wall as well as plaque composition. Some of the CT derived plaque characteristics can help predict for acute coronary syndrome. In addition, because these lesions do not produce significant stenoses, they are typically not considered "critical" and/or interventionable by interventional cardiologists, even though research indicates that they are the more important lesions for producing heart attacks.

The tests most commonly performed clinically with the goal of testing susceptibility to future heart attack include several medical research efforts, starting in the early to mid-1990s, using intravascular ultrasound (IVUS), thermography, near-infrared spectroscopy, careful clinical follow-up, and other methods, to predict these lesions and the individuals most prone to future heart attacks. These efforts remain largely research with no useful clinical methods to date (2006). Furthermore, the usefulness of detecting individual vulnerable plaques by invasive methods has been questioned because many "vulnerable" plaques rupture without any associated symptoms and it remains unclear if the risk of invasive detection methods is outweighed by clinical benefit.

Another approach to detecting and understanding plaque behavior, used in research and by a few clinicians, is to use ultrasound to non-invasively measure wall thickness (usually abbreviated IMT) in portions of larger arteries closest to the skin, such as the carotid or femoral arteries. While stability vs. vulnerability cannot be readily distinguished in this way, quantitative baseline measurements of the thickest portions of the arterial wall (locations with the most plaque accumulation). Documenting the IMT, location of each measurement and plaque size, a basis for tracking and partially verifying the effects of medical treatments on the progression, stability, or potential regression of plaque, within a given individual over time, may be achieved.