Process of Atherosclerosis

            Atherosclerosis is an abnormal inflammatory process inside artery walls as the result of complex interactions among “bad” cholesterol (LDL), platelets, calcium, and inflammatory cells. It is the hardening and narrowing of the arteries caused by the slow buildup of plaque on the inside walls of the arteries. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. It may take decades for atherosclerosis to run its course.

Atherosclerosis may be divided it into five stages:

                        1) Breakdown of the inner layer of the artery’s defense system.

                        2) Invasion of the artery wall by LDL cholesterol.

                        3) A complex local inflammatory reaction.

                        4) Formation of cholesterol plaque.

                        5) Rupture of the plaque causing a heart attack or sometimes death.      

            In stage one, the endothelium, the outer protective layer of the artery, is penetrated. This may be caused by any or all of the following. High levels of LDL (bad) cholesterol; low levels of HDL (good) cholesterol; cigarette smoking – nicotine and other associated toxins lower the HDL cholesterol concentration and play havoc with the endothelium; Uncontrolled diabetes mellitus; High blood pressure; Inherited/generic factors.

Once the endothelium is compromised, the way is open for the LDL cholesterol to burrow in and begin the atherosclerotic process of stage 2, and LDL and other substances start accumulating there. The endothelium is now dysfunctional.

In stage 3 things go from bad to worse. LDL cholesterol continues to invade but now the body itself joins the attack. After letting in the bad cholesterol, the body decreases its production of nitric oxide, which causes the arteries to constrict rather than relax in response to injury. This is really a problem in the later stages of atherosclerosis when the arteries are partially blocked. The dysfunctional endothelium releases free radicals which further damage the artery walls. The artery then releases blood-clotting factors. The results are clotting, and a massive inflammatory response at the site where the endothelium is breached.

In stage 4 clotting and other factors have come together to form a fibrous plaque. The fibrous plaque, or cholesterol plaque, is made up of a core pocket of cholesterol-rich foam cells covered by a fibrous “cap” made from connective tissue. As it continues to grow, it begins to obstruct the artery, limiting blood flow and oxygen to the beating heart muscle.

Up to stage four, it is quite common for the victim to have no symptoms. In stage four with the constriction of the arteries, symptoms may occur such as a tightening in the chest upon exertion.

There are two types of cholesterol plaque: stable and unstable. Stable plaques grow slowly over time and cause symptoms of chest pain, but they are less likely to break free and cause a heart attack. Unstable plaques, however, are the things of nightmares: they are the precursors of chest pain, heart attacks and sudden death. If they break free the victim enters stage 5 of atherosclerosis. Unstable plaques cause blood clots and blockages of the heart artery and death of the associated heart muscle – a heart attack.

Stage 4 is a real danger zone, but you can still stop the disease and reverse the damage before you enter stage 5 - the heart attack or sudden death. With modern medicine today a person is capable of preventing atherosclerosis and avoiding all of these stages. Through eating a proper diet, exercising, not smoking and working with your doctor, you can maintain a healthy heart and live long life free of the worry of a heart attack.