Friday, January 20, 2006

Understanding coronary artery disease: Atherosclerosis

This is part three in our series on the Heart of the Matter. The second part is here. Read our disclaimer if you haven't already done so.

Cholesterol accumulation in the inner lining of arteries, is called atherosclerosis (athero – of the artery, sclerosis – hardening). This process can occur in any of the arteries of the body, although some arteries are more prone then others.

How does this life threatening process come about?

We do not know as yet know what cause atherosclerosis. It is very likely that atherosclerosis is not cause by a single etiology (cause or origin). We however understand that many factors contribute to the development of atherosclerosis. These are commonly called cardiac risk factors. These cardiac risk factors include age, sex, hypertension, cigarette smoking, diabetes mellitus and blood fat abnormalities, especially total blood cholesterol (the good and bad cholesterol levels).

Atherosclerosis (hardening of arteries), in most instances, begin when we are young and is slowly progressive, taking maybe fifteen or possibly twenty years to become medically relevant. Of course, some do have accelerated forms of atherosclerosis, but these are the exceptions. By and large, atherosclerosis is slowly progressive.

It begins as a fat lining in the artery. These fat linings consist of blood cells loaded with bad cholesterol. They tend to accumulate in the beginning portions of arteries, and also junction of arteries. Over years of unhealthy living, these fat laden blood cells pile up from one cell layer thick to multi-layers and a plaque (cholesterol accumulation in blood vessel wall) is formed.

Blood vessels are essentially conduits to channel blood (laden with vital oxygen and nutrients) to vital structures like heart muscle. When the plaque becomes thick enough, they encroach into the blood channel, thereby impeding the smooth flow of the vital, life sustaining blood. We say that the heart muscle becomes "ischemic".

If the plaque builds-up slowly, the heart muscle gets starved of oxygen and nutrients slowly and they have time to adapt to it. This narrowing of the heart artery, with progressive restriction to blood flow, ischemia, may result in chest pain for the subject whenever he or she exerts (angina pectoris). It also allows for the heart muscle to adapt to a lesser blood oxygen and nutrient level, ischemic pre-conditioning. Life goes on albeit at a slower pace. Hearts that are ischemic pre-conditioned, can withstand temporary lack of oxygen episodes better. They also tend to stimulate the growth of new blood vessels, collaterals, to provide alternative channels of blood flow to blood flow deprived regions of the heart.

A heart attack results, when the slowly progressive plaque, cracks, often due to stress with a sudden rise in blood pressure. This cracking of the plaque is called plaque rupture. What triggers the crack in the surface of the plaque is currently the subject of much medical research. We know that certain plaques are very vulnerable to rupture, and others are more resistant to rupture. We also know that certain types of subjects, tend to have plaque that tend to rupture while other subjects, are not the cardiac vulnerable type.

One of the ways to identify the vulnerable patient is to risk assess the individual with the Framingham cardiac risk score. The higher the score, the higher the risk and the more vulnerable the patient. Doctors and the public can use the two linked calculators to do a quick risk assesment. The calculators are the same except for the words used.

When plaque cracks (or ruptures), the inside of the plaque is exposed to the blood flowing pass. The inside of the plaque contains cells and proteins which attract the blood flowing pass to clot instantly. This blood clot, forming instantly in the lumen of the artery will occlude (block) the lumen of the artery, thereby preventing all blood from flowing through. This would mean an instant cessation of blow flow to the area of heart muscle supplied, and over the next 20 minutes or so, the beginning of heart muscle cell death. If the total blockage continues, the heart muscle cell death proceeds from a dying but reversible stage to an irreversible stage.

The suddenness of the blockage of the blood vessel does not allow enough time for collaterals to develop, or for ischemic pre-conditioning to occur.

The next part of the series can be found here.

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