LDL cholesterol is a carrier of cholesterol. The liver does not produce LDL cholesterol. The liver makes and secretes VLDL cholesterol into the blood stream. VLDL cholesterol is a carrier for triglycerides which it delivers to the muscles. The release of triglycerides cause the VLDL to shrink in size, transforming it to LDL cholesterol. Under normal condition, LDL cholesterol returns to the liver and where it is recycled.
There are many branches of the coronary tree. Under certain conditions, LDL cholesterol penetrates into the wall of the artery.
The endothelium is a very thin layer of cells the separates the blood compartment and the rest of the arterial wall. LDL penetrates the endothelium and becomes oxidized. Oxidized LDL cholesterol triggers an inflammatory response mediated by the macrophages. The amount of LDL cholesterol the gets into the wall is influenced by several factors - high LDL cholesterol, high blood pressure, diabetes and smoking. All of these increase the number of LDL particles the passes through the endothelium.
Cholesterol plaque formation starts early in life and occurs in different arteries and in multiple segments of the same artery. It is a diffuse process and progresses quietly. Rupture of this plaque is the cause of most cardiovascular events.
The time when a plaque will rupture can not be predicted ahead to time. It usually occurs unexpectedly.
Plague development takes years. Once rupture occurs, there is only a few minutes until sudden death or acute heart attack ensues.
Very advanced plaques cause blockages shown by cardiac cath above. But most heart attacks and sudden cardiac deaths are caused by rupture of less advanced but unstable plaques which are prone to rupture.
The part of the plaque that protrudes into the lumen is only the tip of the iceberg. A large plaque above is not detectable by cardiac cath. The rupture of this plaque may be the first and the only sign of significant heart disease.
