The animation below displays the progression of atherosclerosis or "hardening of the arteries" in a coronary artery, starting with early signs of disease to total blockage of the artery and a heart attacke. The additional tabs above provide explanations for each stage of the disease process.

Normal coronary arteryThe image symbolizes cuts of a normal coronary artery. The one on the left is a cross-section showing the inner hollow channel or lumen of the artery while the one on the right is a longitudinal section. The walls of the coronary artery is made up of three layers.

  1. The inner most layer of the artery is known as the intima or tunica intima. I is made up of flat endothelial cells and comes in contact with the flow of blood. Normally, the lining is smooth and shiny.
  2. The middle layer or the artery is known as the media or tunica media. It is made up of smooth muscle cells and elastic tissue that allows the normal coronary artery to dilate and constrict. This increases and decreases blood flow and  regulates blood supply to different portions of the heart muscle.
  3. The outermost layer of the artery is the tunica externa and is made of connective tissue.
Fatty streaks on inner lining of coronary arteryAn atheroma or plaque in the wall of a coronary artery is due to a a build up of substances that contain lipids (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue. In the first stage of atherosclerosis, fatty streaks appear on the inner lining or intima of the coronary artery. This can occur as early as one year of age and is caused by the following:
  1. The inner lining of the coronary artery becomes vulnerable to damage because of several known risk factors for the disease (high cholesterol levels, high blood pressure, family history of the disease, diabetes and smoking). "Bad cholesterol or low-density lipoproteins (LDLs) enter into the intima layer of the vessel wall.
  2. The LDLs are taken up by macrophages. Macrophages (Greek for big eaters) are white blood cells that acts in defence of the body). As more lipid accumalates it collects outside the macrophages and a visible fatty streak.
Plaque buildup
  1. Macrophages that are filled with debris and fatty tissue are called foam cells.
  2. When foam cells die, their contents are released and attracts more macrophages.
  3. This creates a fatty or lipid core between the center to inner surface of each atherosclerotic plaque.
  4. With progression of the disease, the outer, older portions of the plaque become more calcific, less metabolically active and more stiff.
Further progression of atherosclerosis
  1. The progression and build up of plaque is called "hardeing of the arteries" or atherosclerosis.
  2. The increased size and thickness of the plaque pushes into the media or the middle lining of the artery, causing it to stretch out. This is called remodeling and is usually just enough to maintain the caliber of the artery open channel (lumen).
  3. Th remodelling usually maintains an acceptable lumen until over 50% of the cross sectional area of the artery wall is made up of plaque tissue. Beyond that, remodeling fails and the plaque pushes into the lumen, causing it to become progressively narrower.

Plaque rupture with partal obstructions

  1. If a plaque grows rapidly it  becomes "vulnerable" as it has a thinner cap or cover separating the large and soft fatty content pool from the bloodstream. Tearing of the cover is called plaque rupture.
  2. The constant stress of pulsating expansion and recoil of the artery with each heart beat creates mechanical stress on the vulnerable plaque, causing it to rupture. The rupture of the thin covering membrane spills material into the blood stream and promotes the formation of clot.
  3. Most plaque rupture, clotting and healing events do not produce symptoms or a heart attack. However, it can result in progressive muscle damage and eventual heart failure due to ischemic heart disease.
    Also, repeated plaque rupture, clot formation, healing and contraction, over time, can cause the plaques to become bigger. This creates progressively increasing stenosis or blockages of the artery.
  4. The stenosis or narrowing result in cardiac symptoms such as chest discomfort. It is identified after the fact by cardiac cath and angiography and may be treated with coronary bypass surgery or balloon angioplasty, with or without stents.
Plaque rupture with total obstructions
  1. During plaque rupture, a sticky substance on the inner lining of the artery (called cytokine) captures blood cells (mainly platelets) that accumulate at the site of injury. When these cells clump together, they form a clot, sometimes large enough to block the artery.
  2. If large enough, the clot can abruptly and completely block the flow of blood to the heart muscle that is supplied by the artery. This is the most common cause of a heart attack.

 

 
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