Nearly half of all deaths in the United States are due to the arterial disease atheroscierosis, in which soft masses of fatty materials, particularly cholesterol, accumulate on the inside of the arterial walls. Such deposits, called plaque, protrude into the lumens of the vessels and interfere with blood flow. Furthermore, plaque often forms a surface that can initiate formation of a blood clot, increasing the risk of developing thrombi or emboli that cause blood deficiency (ischemia) or tissue death (necrosis) downstream from the obstructions.

The walls of affected arteries also tend to degenerate, losing their elasticity and becoming hardened or sclerotic. This stage of the disease, called arteriosclerosis, introduces the danger that a sclerotic vessel will rupture under the force of blood pressure.

Atheroscierosis is often associated with a fatty diet, elevated blood pressure, cigarette smoking, obesity, and lack of physical exercise. Emotional and genetic factors may also increase susceptibility to atherosclerosis.

If atheroscierosis so weakens the wall of an artery that blood pressure dilates a region of it, a pulsating sac called an aneurysm may form. Aneurysms tend to grow. If the resulting sac develops by a longitudinal splitting of the middle layer of the arterial wall, it is called a dissecting aneurysm. An aneurysm may cause symptoms by pressing on nearby organs, or it may rupture and produce a great loss of blood.

Aneurysms may also result from trauma, high blood pressure, infections, inherited disorders such as Marfan syndrome, or congenital defects in blood vessels. Common sites of aneurysms include the thoracic and abdominal aorta, and an arterial circle at the base of the brain (circle of Willis).

Phlebitis, or inflammation of a vein, is relatively common. It may occur in association with an injury or infection or after surgery, or it may develop for no apparent reason.

If inflammation is restricted to a superficial vein, such as the greater of lesser saphenous veins, blood flow may be rechanneled through other vessels. But if it occurs in a deep vein, such as the tibial, peroneal, popliteal, or femoral veins, the consequences can be quite serious, particularly if the blood within the affected vessel clots and blocks normal circulation. This condition is called thrombophlebitis. There is now a risk that a blood clot within a vein will detach, move with the venous blood, pass through the heart, and lodge in the pulmonary arterial system within a lung. Such an obstruction is called a pulmonary embolism.

Varicose veins are abnormal and irregular dilations in superficial veins, particularly in the legs. This condition is usually associated with prolonged, increased back pressure within the affected vessels due to gravity, as occurs when a person stands. Crossing the legs or sitting in a chair so that its edge presses against the area behind the knee can obstruct venous blood flow and aggravate varicose veins.

Increased venous back pressure stretches the veins and increases their diameters. Because the valves within these vessels do not change size, they soon lose their abilities to block the backward flow of blood, and blood tends to accumulate in the enlarged regions.

Increased venous pressure is also accompanied by rising pressure within the venules and capillaries that supply the veins. Consequently, tissues in affected regions typically become edematous and painful.

Heredity, pregnancy, obesity, and standing for long periods raise the risk of developing varicose veins. Elevating the legs above the level of the heart or putting on support hosiery before arising in the morning can relieve discomfort. Intravenous injection of a substance that destroys veins (a sclerosing agent) or surgical removal of the affected veins may be necessary.