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Atherosclerosis and How it Relates to Coronary Artery Disease

The tragedy of Coronary Artery Disease is that it is essentially an “after the fact” diagnosis. This means that a clinical event has to have happened: anginal chest discomfort, acute coronary syndrome, heart attack, placement of a stent, or coronary bypass operation. Once any of these have occurred, a patient is now diagnosed with Coronary Artery Disease.

The actual blockage in the artery, or the limitation of blood flow in the artery is NOT the actual disease. It is a consequence of the disease. The root cause is a disease process called Atherosclerosis. This disease is an insidious culprit, located within the wall of the artery, smoldering over decades until it may unpredictably disrupt through the wall into the Lumen (where the blood flows) and compromise the flow of blood.

An artery is like a hose that delivers oxygenated blood and other substances to the heart muscle. It is circular, and the structure like the plastic of the hose is actually a three- layered muscle. The inner wall where the blood flows, is called the endothelium which is the lining into the artery. Think of the endothelium as the bricks and mortar, though this “mortar” is permeable, meaning that “things” such as cells, proteins, cholesterol, etc. can pass through the lining into the inner arterial structure.

The arteries do not maintain the same diameter, nor the same direction. They vary in caliber size, they change direction, and they have bifurcating branches that twist and turn as well; and the flow of blood is by no means constant! With the contraction of every heartbeat from the left ventricle, there is a sudden, rapid amount of blood ejected through the artery.

Therefore, arteries, particularly coronary arteries, which are smaller size arteries, are subject to great stresses throughout life.

I like to explain the insidious nature of atherosclerosis with the analogy of termites penetrating into the wood structure of your home. Termites penetrate into the wood structure and eat the wood from the inside out – much the same with the atherosclerotic process.

Simply put, it is an infiltration process with cholesterol products, mainly LDL, penetrating through the lining and into the interior of the artery wall. This is associated with the attachment of inflammation cells, called macrophages, which enter the vessel wall and displace and disrupt the integrity of the muscle cells. Associated with this displacement is also a leaking out of “poisonous toxins” that further cause degradation and destruction to the architectural integrity of the arterial wall. This interior disruption eventually breaks through the arterial lining and causes bleeding and further inflammation of the vessel wall, into the lumen where the blood flows. The bleeding of the vessel wall, as well as the inflammation process, causes clotting products to accumulate with the creation of “plaque” which is a combination of clotting products, fibrin and thrombin, and cholesterol products, and inflammatory cells. It is not a “linear process” but accumulates sporadically and unpredictably with shear stress, flow stress, and variable plaque rupture.

This may lead to a gradual growth of plaque that becomes hardened and calcified and may block the interior lumen to 70, 80, 90 percent and interfere with the flow of blood through the artery.

These are the types of plaques and narrowing that we look for in cardiology practices, and these will often be associated with the onset of chest discomfort, often with exertion (angina), or with the presentation of an abnormal exercise stress test, or an abnormal nuclear stress test.

When angiography is done, we will see one or more narrowing in the coronary arteries, and depending on location, number, degree of narrowing, it will usually lead to opening up the vessel (angioplasty) and placement of a stent, or possibly the consideration of coronary artery bypass surgery.

The task at hand with these very significant narrowing that interfere with coronary blood flow, is to utilize medications that improve flow, that stabilize the heart, and slow or stop the process of further plaque accumulation.

The procedures discussed above do NOT AT ALL cure the disease, or control the development of the disease, but restore flow through or around the artery (stent of bypass) to deliver the appropriate amount of blood to the heart muscle and protect it.

Brian Chesnie, M.D., is a cardiologist at Hoag.