LDL-cholesterol: the pivotal target for preventing CVD
Lipid metabolism can be disturbed in different ways, leading to changes in plasma lipoprotein function and/or levels6.
Elevated plasma total cholesterol (TC) and in particular LDL-cholesterol is a known cause of coronary atherosclerosis6,7.
Established and compelling evidence based on outcomes from multiple randomized controlled trials (RCTs) has shown that reducing TC and LDL-cholesterol levels can significantly reduce cardiovascular morbidity and mortality7.
In terms of reducing cardiovascular events and CVD mortality, lowering LDL-cholesterol has been shown to be beneficial irrespective of the underlying mechanisms by which this is achieved (reduced absorption or synthesis, or increased clearance of cholesterol)7.
Atherosclerosis, the underlying cause of CVD, is a progressive disease that begins early in life and develops over several decades before becoming clinically manifest. It is a dynamic process however and it can be slowed down and potentially reversed to a certain extent8.
Prolonged exposure to lower LDL-cholesterol beginning early in life is associated with a substantially greater reduction in the risk of CHD compared to treating high LDL-cholesterol levels later in life7,9. Therefore, lowering LDL-cholesterol earlier in the disease process, through changes towards a healthy diet and lifestyle, and eventually resorting to drug therapies, should be encouraged for the prevention of CVD.
Lowering LDL-cholesterol earlier in the disease process, through changes towards a healthy diet and lifestyle, and eventually resorting to drug therapies, should be encouraged for the prevention of CVD.
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- Increasing HDL-cholesterol and lowering triglycerides
- Lowering LDL-cholesterol
- Lowering total cholesterol and HDL cholesterol
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- ...irrespective of the underlying mechanisms by which this is achieved
- ...through reduced cholesterol synthesis in the liver
- ...through reduced absorption of cholesterol from the gut
Cholesterol, fats and cellular waste products accumulate inside the arterial wall. Chemical reactions occurring within the buildup of material cause cholesterol molecules to oxidize. This initiates an inflammatory response in which monocytes from the bloodstream travel to the site. Stimulation from oxidized cholesterol converts the monocytes into macrophages. The macrophages engulf and digest the cholesterol molecules. As a result, the macrophages change into foam cells, which accumulate to form plaque.
As the plaque increases in size, the arterial wall thickens and hardens. At the same time, smooth muscle cells within the arterial wall begin to multiply. Most of the smooth muscle cells move to the surface of the plaque. These cells contribute to the formation of a firm, fibrous cap covering the plaque. Eventually the passageway through the artery narrows, reducing blood flow and the amount of oxygen received by the organs it supplies.