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  1. Identify appropriate standards for the diagnosis of dyslipidemia and determine risk and prognosis for developing cardiovascular disease.

  2. Use available parameters to measure and monitor target lipid goals for patients under treatment for dyslipidemia.

  3. Conduct a comprehensive follow-up visit for a patient with dyslipidemia using appropriate history-taking techniques, physical examination, and laboratory tests. The visit includes assessment of disease control, plus assessment and support of compliance with lifestyle modifications and medication regimens.

  4. Evaluate patients for complications from dyslipidemia and the medication regimen.


In 2011, Centers for Disease Control estimated that 29% of all deaths in the U.S. will be caused by heart and cerebrovascular disease, the vast majority of which are caused by atherosclerotic cardiovascular disease (ASCVD), also known as coronary heart disease (CHD). Atherosclerosis is a process that causes oxidative endothelial damage and inflammation that eventually leads to the formation of cholesterol-laden atheromas or plaque lining the arterial intima. The inflammation ultimately causes the plaque to rupture, which leads to platelet adhesion and aggregation resulting in arterial occlusion. If vessels in the heart and brain are occluded they cause a myocardial infarction or cerebrovascular accidents (strokes or CVA). Since dyslipidemia is a major factor in the atheroscerlotic process, the advent of highly effective cholesterol-lowering medication has become a major tool in preventing atherosclerosis and subsequent heart attacks and strokes. Pharmacists play a key role in monitoring and managing the therapeutic regimens of patients with dyslipidemia.


There are three major types of cholesterol found in the bloodstream. They are carried in the blood by lipoproteins, which combine with cholesterol and other fats. LDL cholesterol (low-density lipoprotein or LDL-C) is the cholesterol intimately involved in the formation of arterial plaque and high levels are associated with a greater risk of heart attack and stroke. Since lowering LDL-C blood concentration has been shown to prevent heart attacks and strokes, it is the focus of current lipid-lowering therapy. LDL-C is made by the liver from VLDL cholesterol (very-low-density lipoprotein or VLDL-C), which has the highest concentration of triglycerides. HDL cholesterol (high-density lipoprotein or HDL-C) serves as a scavenger, transporting LDL-C back to the liver for recycling, and maintaining the integrity of the endothelium of the arteries. High levels of HDL-C markedly reduce the incidence of heart attacks and strokes, so increased HDL-C blood levels reduce the risk of cardiovascular disease. Some authors refer to LDL as the “bad” cholesterol and the HDL as the “good” cholesterol. These terms can be very useful in helping patients understand their illness and the importance of treatment goals, i.e., lowering the bad cholesterol and raising the good. Triglycerides are a fourth type of lipid routinely found in the blood stream. They are important sources for energy, but high levels are associated with the metabolic syndrome and its increased risk for cardiovascular disease and type 2 diabetes mellitus.


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