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“My cholesterol is normal.
How did I get cholesterol build-up in my coronaries?”
Although people with hypercholesterolemia have a much higher incidence of coronary artery disease, hypercholesterolemia is not a must for atherosclerotic build-up in the coronary system. The term “cholesterol build-up” is an oversimplified version of the real fact. In fact, only 50% of hypercholesterolemic patients have symptomatic CAD, and in 50% of hypercholesterolemic patients there is no evidence of symptomatic CAD.
The inner lining of the coronary arteries (the endothelial cells) can become dysfunctional from many reasons including high blood pressure, high cholesterol, diabetes, cigarette smoking, family history of coronary artery disease, infections, etc. Via such dysfunctional endothelial cells, molecules of low-density lipoproteins (LDL) will gain access into the intima of the artery. Those intracellular LDL molecules are soon oxidized. The oxidized lipids are engulfed by monocytes in large quantities and transform them into foam cells. This initial reaction is followed by a cascade of interrelated reactions, resulting in vasoconstriction, migration and proliferation of smooth muscle cells. There will be further accumulation of lipids, monocytes, and macrophages, resulting in the formation of a plaque. This plaque is the common denominator in all forms of atherosclerotic vascular diseases irrespective of the site (coronaries or elsewhere). Sometimes these plaques are heavily impregnated with lipids, making it quite susceptible to rupture and hemorrhage. Such lipid-rich unstable plaques can cause any level of coronary instability including unstable angina, nontransmural myocardial infarction, transmural myocardial infarction, or sudden death. High cholesterol plays a very important role in the formation of cholesterol plaques in arteries, but hypercholesterolemia is not a must for atherosclerosis.
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