Coronary artery disease is a gradual process: Rancid cholesterol-particles incorporate into the vessel wall. The cholesterol-particles trigger an inflammation. Over time 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. The artery opening gradually narrows and the vessel wall hardens – a process called arteriosclerosis.
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.
And even worse: There is an extremely high risk of heart attack, when the calcified cap of the plaque ruptures leading to exposure of the fatty substances to the bloodstream. The exposed fatty compounds trigger the blood to clump together, similar to the way blood clots at the site of a wound to stem bleeding. The blood clot can block blood flow to the heart. Deprived of oxygen, heart tissue fed by the blocked artery will quickly die. This can lead to heart attack.