(greek: skleros = hard, stiff)

Arteriosclerosis is the hardening of the arteries caused by the incorporation of fatty particles, calcium cellular waste products and fibrous elements into the blood vessel wall.

As the body ages the walls of blood vessels become stiffer caused by increasing cross-linkage of the connective tissue compounds and the steady deposition of calcium in the walls of the artery walls. This results in loss of elasticity – the blood vessel become hard and stiff.

However, there is a severe form of arteriosclerosis that involves Cholesterol-containing particles and our immune system.

Arteriosclerosis – an inflammation of blood vessels?

Cholesterol-containing particles constantly shuttle between the blood stream and the inner vessel wall. However, certain lifestyle habits (e.g. smoking, unhealthy diet, etc.) in combination with genetic factors can lead to the generation of highly reactive oxygen compounds that damage and modify the so-called “LDL-cholesterol-particles". The fatty particles in the vessel wall have gone "rancid".

The rancid cholesterol-particles stay in the vessel wall - they can not leave the vessel wall as easily. Instead they trigger the immune system to send out its cleaning company that attempt to eliminate the rancid fat particles by “devouring” them.

These immune cells migrate into the blood vessel wall, take up the rancid cholesterol-particles and form so-called foam cells. With time, the immune cells die and a plaque builds up which is made of fatty compounds, the debris of the dead immune cells, calcium and a blood-clotting material called fibrin. As the plaque builds up, the artery opening gradually narrows. The consequence is that the blood cannot flow unobstructed any longer, and parts of the body are not sufficiently supplied with nutrients and oxygen. The patients experience symptoms such as chest pain and breathlessness – a warning of an increased risk for heart attack.

The plaque is capped by a small layer of cells and fibrous elements. A rupture of this layer has grave consequences since the blood-clotting process is triggered. It starts with specific blood cells, called platelets, accumulating at the rupture point. The platelets and the fatty content of the plaque stick together and form a blood clot that suddenly blocks the artery.

Risk factors

The importance of genetics and environment in arteriosclerosis has been examined in many family and twin studies. The studies showed that arteriosclerosis is caused half by environmental factors and half by genetic factors.

Some of the environmental risk factors for arteriosclerosis are wellknown: cigarette smoke that floods the blood with highly reactive oxygen compound that damage and modify the LDL-cholesterol-particles. Nutritional evildoers, such as fat, are also harmful, as they raise the amount of LDL-cholesterol in the blood, thereby promoting arteriosclerosis.

In addition to unhealthy lifestyle, it is likely that a limited number of genes may be involved in the development of acute coronary syndromes. For example, the generation of rancid cholesterol-particles could be at least partly caused by defects in genes that protect us against higly reactive oxygen compounds. However, many disease genes are yet unknown. When scientist unravel those genes that cause heart disease, it might be possible to develop improved therapies.