Dr. LaFleur is a research assistant professor in the University of Utah College of Pharmacy Pharmacotherapy Outcomes Research Center within the Department of Pharmacotherapy.
The leading cause of death in the United States—coronary artery disease (CAD)—is also one of the most preventable.1,2 Eating a healthy diet, exercising, and avoiding tobacco smoke exposure can improve many CAD risk factors: obesity, physical inactivity, elevated triglycerides, low high-density lipoprotein cholesterol, and metabolic syndrome.3 Largely because of our failure to implement these preventive measures, more than half of us eventually will have one of the most treatable causes and predictors of CAD—hyperlipidemia.4 Fortunately, modern pharmaceutical science has equipped us with a toolkit to help our patients stave off CAD; it includes lipid-lowering medications and effective goal-setting.
Specific goals are more likely to improve performance than vague goals.5 Every patient should know his or her specific goal for low-density lipoprotein cholesterol (LDL-C) (Table 1).3,6,7 LDL-C is the primary treatment target in hyperlipidemia.
Self-efficacy—the belief that one has the power to produce the desired effect— is an important performance modifier.8 Self-efficacy requires having the "right" tools (medications) and the "right" information (how to use them and what to expect). Statins capable of a 30% to 40% LDL-C reduction are first-line therapy, regardless of the patient's initial distance from goal (Table 2).3 Answers to frequently asked patient questions include the following:
Patients may be concerned about the risk of muscle toxicity due to reports cited in the lay press.9,10 Tell patients that muscle toxicity depends on plasma drug concentrations with all statins.11 As doses increase, so does the risk.
All the statins except pravastatin are metabolized by liver enzymes; drugs that inhibit these enzymes increase the risk of muscle toxicity.11 Experts believed that this caused the increased rate of muscle toxicity with fibrate/statin combinations. We now know, however, that the interaction is specific to gemfibrozil's inhibition of statin glucuronidation, which does not happen with fenofibrate.11
3. Patients may have read about the Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression trial in the news.12 This study showed that ezetimibe in combination with a statin did not reduce coronary artery plaques, compared with a statin alone. Ezetimibe still can help patients reach their LDL-C goal in combination with a statin, however.
Feedback enhances performance.5 Encourage your patients to seek a followup fasting lipid panel every 6 weeks after beginning treatment until they reach goal.13 Inform your patients that every 1% reduction in LDL-C reduces their risk of having a major CAD event by 1%.3
For more information about CAD risk factors, visit the National Heart, Lung, and Blood Institute's Web site at www.nhlbi.nih.gov/health/index.htm.
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