LDLs are the most common fat-and-protein particles in your body. Like their parents, the VLDLs and their cousins the IDLs, LDLs are soft enough to squeeze between the cells of your blood vessel walls, dragging cholesterol into your coronary arteries (the blood vessels leading away from your heart).
Once inside an artery, cholesterol particles may get caught on the infinite number of chinks in the artery wall. Stuck in place, the cholesterol now snags other particles floating by, eventually creating deposits called plaque. In time, the plaque on the artery wall may grow thick enough to block the flow of blood through the blood vessel, or a piece of plaque may break off, triggering the formation of a blood clot that can also block the artery. Either way, the sequence is called a heart attack.
As a general rule, heart docs assume that the more cholesterol you have floating through your bloodstream — especially the “bad” LDL cholesterol — the higher your risk for plaque build-up in your arteries and the higher your risk of a heart attack. In other words, to lower your risk of heart attack, you must lower your cholesterol, particularly those “bad” LDLs.
But this simple equation may not be the solution for every human body. In December 2007, the results from a clinical trial of the new drug ezetimibe (Zetia) showed that taking the medicine, either alone or in combination with the statin drug simvastatin (Zocor), definitely lowered “bad” cholesterol, but also hastened the buildup of arterial plaque for some of the people in the trial.
In other words, simply lowering their LDLs did not protect these people from a heart attack. Something else, such as an individual tendency to pile up arterial plaque, also seemed to be at work. (Conversely, people with high cholesterol but clear arteries may have the opposite attribute — an inherent ability to resist plaque — that explains the puzzle of why some people with high cholesterol do not have heart attacks.)