Atherosclerosis

Athersclerosis is the disease process that leads to coronary heart disease and strokes. In athersclerosis fatty deposists can either block an artery directly, or increase its chance of being blocked by a blood clot (thrombosis). The blood supply can be blocked completely. If this happens for long, the affected cells are permantently damaged. In the arteries supplying the brain it results in a stroke. The supply of blood to the brain its restricted or blocked, causing damage or death to cells in the brain. Narrowing of arteries to the legs can result in tissue death and gangrene (decay). An artery can burst where blood builds up behind an artery narrowed as a result of athersclerosis. 

Athersclerosis can be triggered by a number of factors. Whatever the trigger, this is the course of events that follows: The endothelium, a delicate layer of cells that lines the inside of an artery, seperating the blood that flows along the artery from the muscular wall, becomes damaged for some reason. For instance, this endothelial damage can result from high blood pressure, which puts an extra strain on the layer of cells, or it might result from some of the toxins from cigratte smoke in the bloodstrem. Once the inner lining of the artery is breached, there is an inflammatory response. White blood cells leave the blood vessel and move into the artery wall. These cells accumulate chemicals from the blood, particularly cholesterol. A deposit builds up, called an atheroma. 

Calcium salts and fibrous tissues also build up at the site, resulting in a hard swelling called a plaque on the inner wall of the artery. The build-up of fibrous tissue means that the artery wall loses some of its elasticity; in other words, it hardens. Plaques cause the artery to become narrower. This makes it more difficult for the heart to pump blood around the body and can lead to a rise in blood pressure. Now there is a dangerous positive feedback building up. Plaques lead to raised blood pressure and raised blood pressure makes it more likely that further plaques will form. The person is probably unawate of any problem at this stage, but if the arteries become very narrow or completly blocked then they cannot supply enough blood to bring oxygen and nutrients to the tissues. The tissues can no longer function normally and symptoms will start to show. 

When blood vessel walls are damaged or blood flows very slowly, a blood clot is much more likely to form. When platelets, blood cell without a nucleus, comes into contact with the damaged wall they change from flattened discs to spheres with long thin projections. Their cell surfaces change, causing them to stick to the exposed collagen in the wall and to each other to form a temporary platelet plug. They also release substances that activate more platelets. The direct contact of blood with collagen within the damaged wall triggers a complex series of chemical changes in the blood. A cascade of changes results in the soluble plasma protein called prothrombin being converted into thrombin. Thrombin causes the conversion of another soluble plasma protien, fibrinogen, into long insoluble strands of the protein fibrin. These fibrin strands form a tangled mesh that traps blood cells to form a clot. 

The fast flowing blood in arteries is under high pressure so there is a significant chance of damage to the walls. The low pressure in the veins means that there is less risk of damage to the walls. 

Narrowing of the coronary arteries limits the amount of oxygen-rich blood reaching the heary muscle. The result may be a chest pain called angina. It is usually experienced during exertion. Because the heart muscle lacks oxygen, it is forced to respire anaerobically. This results in chemical changes which trigger pain but the detailed mechanism is still not known. If a fatty plaque in the coronary arteries ruptures, chlesterol is released which leads to rapid clot formation. The blood supply to the heart may be blocked completely. The heart muscle supplied by these arteries does not receive any blood, so it is said to be ischaemic (without blood). If the affected muscle cells are starved of oxygen for too long they will be permenently damaged. This is what we call a  mycardial infarction. If the zone of dead cells occupies only a small area of tissue it is less likely to prove fatal. 

If the supply of blood to the brain is only briefly interuppted then a mini-stroke may occur. A mini-stroke has all the symptoms of a full stroke but the effects last for only a short period, and full recovery can happen quite quickly. However, a mini-stroke is a warning of problems with blood supply to the brain that could result in a full stroke in the future.