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.

An atheroma is a reversible accumulation of degenerative material in the inner layer of an artery wall. The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue. The accumulated material forms a swelling in the artery wall, which may intrude into the channel of the artery, narrowing it and restricting blood flow. Atheroma occurs in atherosclerosis, which is one of the three subtypes of arteriosclerosis (which are atherosclerosis, Monckeberg's arteriosclerosis and arteriolosclerosis).

In the context of heart or artery matters, atheromata are commonly referred to as atheromatous plaques. It is an unhealthy condition found in most humans.

Veins do not develop atheromata, because they are not subjected to the same hemodynamic pressure that arteries are, unless surgically moved to function as an artery, as in bypass surgery. The accumulation (swelling) is always in the tunica intima, between the endothelium lining and the smooth muscle middle layer of the artery wall. While the early stages, based on gross appearance, have traditionally been termed fatty streaks by pathologists, they are not composed of fat cells but of accumulations of white blood cells, especially macrophages, that have taken up oxidized low-density lipoprotein (LDL). After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called foam cells. When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the center to inner surface of each atherosclerotic plaque. Conversely, the outer, older portions of the plaque become more calcified, less metabolically active and more physically stiff over time.

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

Typically, Mönckeberg's arteriosclerosis is not associated with symptoms unless complicated by atherosclerosis, calciphylaxis, or accompanied by some other disease. However presence of Mönckeberg's arteriosclerosis is associated with poorer prognosis. This is probably due to vascular calcification causing increased arterial stiffness, increased pulse pressure and resulting in exaggerated damage to the heart and kidneys.

Mönckeberg's arteriosclerosis, or Mönckeberg's sclerosis, also called medial calcific sclerosis or Mönckeberg medial sclerosis, is a form of arteriosclerosis or vessel hardening, where calcium deposits are found in the muscular middle layer of the walls of arteries (the tunica media). It is an example of dystrophic calcification. This condition occurs as an age-related degenerative process. However, it can occur in pseudoxanthoma elasticum and idiopathic arterial calcification of infancy as a pathological condition, as well. Its clinical significance and cause are not well understood and its relationship to atherosclerosis and other forms of vascular calcification are the subject of disagreement.

Mönckeberg's arteriosclerosis is named after Johann Georg Mönckeberg, who first described it in 1903.

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.

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.

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 first skin changes in calciphylaxis lesions are mottling of the skin and induration in a livedo reticularis pattern. As tissue thrombosis and infarction occurs, a black, leathery eschar in an ulcer with adherent black slough are found. Surrounding the ulcers is usually a plate-like area of indurated skin. These lesions are always extremely painful and most often occur on the lower extremities, abdomen, buttocks, and penis. Because the tissue has infarcted, wound healing seldom occurs, and ulcers are more likely to become secondarily infected. Many cases of calciphylaxis end with systemic bacterial infection and death.

Calciphylaxis is characterized by the following histologic findings:

1. systemic medial calcification of the arteries, i.e. calcification of tunica media. Unlike other forms of vascular calcifications (e.g., intimal, medial, valvular), calciphylaxis is characterized also by

2. small vessel mural calcification with or without endovascular fibrosis, extravascular calcification and vascular thrombosis, leading to tissue ischemia (including skin ischemia and, hence, skin necrosis).

Calciphylaxis, or calcific uremic arteriolopathy (CUA), is a syndrome of calcification of the blood vessels, blood clots, and skin necrosis. It is seen mostly in patients with stage 5 chronic kidney disease, but can occur in the absence of kidney failure. It results in chronic non-healing wounds and is usually fatal. Calciphylaxis is a rare but serious disease, believed to affect 1-4% of all dialysis patients.

Calciphylaxis is one type of extraskeletal calcification. Similar extraskeletal calcifications are observed in some patients with hypercalcemic states, including patients with milk-alkali syndrome, sarcoidosis, primary hyperparathyroidism, and hypervitaminosis D.

Dystrophic calcification (DC) is the calcification occurring in degenerated or necrotic tissue, as in hyalinized scars, degenerated foci in leiomyomas, and caseous nodules. This occurs as a reaction to tissue damage, including as a consequence of medical device implantation. Dystrophic calcification can occur even if the amount of calcium in the blood is not elevated. (A systemic mineral imbalance would elevate calcium levels in the blood and all tissues and cause metastatic calcification.) Basophilic calcium salt deposits aggregate, first in the mitochondria, and progressively throughout the cell. These calcifications are an indication of previous microscopic cell injury. It occurs in areas of cell necrosis in which activated phosphatases bind calcium ions to phospholipids in the membrane.

Calcification can occur in dead or degenerated tissue.

Arteriosclerosis obliterans is an occlusive arterial disease most prominently affecting the abdominal aorta and the small- and medium-sized arteries of the lower extremities, which may lead to absent dorsalis pedis, posterior tibial, and/or popliteal artery pulses.

It is characterized by fibrosis of the tunica intima and calcification of the tunica media.

Metastatic calcification involves a systemic calcium excess imbalance, which can be caused by hypercalcemia, kidney failure, milk-alkali syndrome, lack or excess of other minerals, or other causes.

The most common type of calcinosis is dystrophic calcification. This type of calcification can occur as a response to any soft tissue damage, including that involved in implantation of medical devices.

Ectopic ossification of the heart valves is an indicator of future heart problems, hyperparathyroidism, and necrosis of tissues.

Absorption of calcium salts normally occurs in bony tissues and is facilitated by parathyroid hormone and vitamin D. However, increased amounts of parathyroid hormone in the blood result in the deposit of calcium in soft tissues. This can be an indication of hyperparathyroidism, arteriosclerosis, or trauma to tissues.

Calcification of muscle can occur after traumatic injury and is known as myositis ossificans. It can be recognized by muscle tenderness and loss of stretch in the affected area. To reduce the risk of calcification after an injury, initiate what is commonly known as "RICE" (rest, ice, compression, and elevation).

Calcinosis cutis (or cutaneous calcification) is a type of calcinosis wherein calcium deposits form in the skin. A variety of factors can result in this condition. The most common source is dystrophic calcification, which occurs in soft tissue as a response to injury. In addition, calcinosis is seen in Limited Cutaneous Systemic Sclerosis, also known as CREST syndrome (the "C" in CREST). In dogs, calcinosis cutis is found in young, large breed dogs and is thought to occur after a traumatic injury.

Pseudohypertension, also known as pseudohypertension in the elderly, noncompressibility artery syndrome, and Osler's sign of pseudohypertension is a falsely elevated blood pressure reading obtained through sphygmomanometry due to calcification of blood vessels which cannot be compressed. There is normal blood pressure when it is measured from within the artery. This condition however is associated with significant cardiovascular disease risk.

Because the stiffened arterial walls of arteriosclerosis do not compress with pressure normally, the blood pressure reading is theoretically higher than the true intra-arterial measurement.

To perform the test, one first inflates the blood pressure cuff above systolic pressure to obliterate the radial pulse. One then attempts to palpate the radial artery, a positive test is if it remains palpable as a firm "tube".

It occurs frequently in the elderly irrespective of them being hypertensive, and has moderate to modest intraobserver and interobserver agreement. It is also known as "Osler's maneuver".

The sign is named for William Osler.

Calcinosis cutis may be divided into the following types:

- Dystrophic calcinosis cutis

- Metastatic calcinosis cutis

- Iatrogenic calcinosis cutis

- Traumatic calcinosis cutis

- Idiopathic calcinosis cutis

- Idiopathic scrotal calcinosis

- Subepidermal calcified nodule

- Tumoral calcinosis

- Osteoma cutis

Metastatic calcification is deposition of calcium salts in otherwise normal tissue, because of elevated serum levels of calcium, which can occur because of deranged metabolism as well as increased absorption or decreased excretion of calcium and related minerals, as seen in hyperparathyroidism.

In contrast, dystrophic calcification is caused by abnormalities or degeneration of tissues resulting in mineral deposition, though blood levels of calcium remain normal. These differences in pathology also mean that metastatic calcification is often found in many tissues throughout a person or animal, whereas dystrophic calcification is localized.

Metastatic calcification can occur widely throughout the body but principally affects the interstitial tissues of the vasculature, kidneys, lungs, and gastric mucosa. For the latter three, acid secretions or rapid changes in pH levels contribute to the formation of salts.

The cause is not well defined. Originally considered idiopathic condition. Now accepted that majority of cases develop from dystrophic calcification of cyst contents.

Normophosphatemic familial tumoral calcinosis is a cutaneous disorder characterized by cutaneous calcification or ossification.

Arteritis may be primary or secondary to some other disease process. The primary types are:

An example of a secondary arteritis is arteritis caused by infection with the fungal pathogen "Candida albicans".

Idiopathic scrotal calcinosis (also known as idiopathic calcified nodules of the scrotum) is a cutaneous condition characterized by calcification of the skin resulting from the deposition of calcium and phosphorus occurring on the scrotum. However, the levels of calcium and phosphate in the blood are normal. Idiopathic scrotal calcinosis typically affects young males, with an onset between adolescence and early adulthood. The scrotal calcinosis appears, without any symptoms, as yellowish nodules that range in size from 1 mm to several centimeters.

Arteritis is the inflammation of the walls of arteries, usually as a result of infection or autoimmune response. Arteritis, a complex disorder, is still not entirely understood. Arteritis may be distinguished by its different types, based on the organ systems affected by the disease. A complication of arteritis is thrombosis, which can be fatal. Arteritis and phlebitis are forms of vasculitis.