James Hamilton, M. D.
O.K., now for a little cholesterol discussion:
We are all aware that cholesterol elevation is a major contributor to atherosclerotic cardiovascular disease including heart attacks and strokes. LDL-C, the "bad" cholesterol, gets deposited into "plaques" which are underneath the internal lining ("intima") of arteries. That decreases the area of the artery through which blood flows (the "lumen"). If coronary arteries become too occluded the heart may not get enough oxygen (carried on red blood cells) to supply a part of the heart muscle when under stress (exercise, etc.) and angina pain can result. If the "cap" covering the plaque breaks (ruptures) then that lipid laden plaque is exposed to the circulation and the body will try to attack it with platelets and clotting factors which results in a thrombus that totally occludes that artery causing a heart attack (myocardial infarction, MI). Thrombolytic drugs ("clot busters", TPA) and/or stents can treat this.
How does LDL-C gain access to permeate the intima in the first palce? Ahhh... the million dollar question! It is believed that "pores" in the intima exist and, if opened, allow that access. What opens pores? Probably some genetic factors but also other risk factors such as inflammation (even distant from the coronaries), diabetes, smoking, hypertension, etc may contribute. Bottom line - we don't yet know all that goes on there.
Various medical groups - American Heart Association/American College of Cardiology, Framingham Group, Kaiser-Pemanente, and others - have developed "risk assessment tools" (KPARE is Kaiser's) which can help predict a patient's risk of having a cardiovascular "event" in the next 10 years. Based on that risk some doctors will discuss with patients how best to modify that risk with interventions such as lifestyle, diet, drugs, etc.
If drugs, usually statins, are prescribed the LDL-C value and the risk percentage come into play regarding the dosage ("intensity") of statin therapy: low, medium or high intensity. Many of us, including myself, are on statin therapy. Oatmeal can help lower LDL-C by about 5-8%, low intensity statins ~15-28%, medium ~30-50%, and high ~50-60%.
So, what are the goals of LDL-C levels? This is a question to which the answer changes almost yearly. It also depends on other co-morbidities of the patient (i.e. other risk factors).
In answer to you, Mark, your doctor knows your individual case and needs better than I or anyone else. It sounds like she has your best interest at heart (pun intended) and a "shared decision" between you and her should result in a good approach to risk reduction.
Mike, some people believe the lower the LDL-C the better and there is no lower level that exists. This may not be the case. Cholesterol plays a beneficial role in the body as it is part of the synthesis of certain hormones. Also, it is a component of cell walls. If our cells had no walls we would end up being blobs of protoplasm!
Dave, I assume the drug you mentioned was probably "simvastatin" which is the one I take. As for sleep apnea it has become a hot topic in the last decade or two and is now well established on the list of risk factors for cardiovascular disease.
Hope this helps,
Jim
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