William E. Feeman Jr, MD

I agree wholeheartedly with Dr. Wahawisan et al (Statin therapy: When to think twice. J Fam Pract. 2013;62:726-730,732) that one shouldn’t use medications to ameliorate dyslipidemia unless those medications have been proven to stabilize or regress plaque and/or improve atherothrombotic disease (ATD) outcomes. However, I believe the article deserves further comment.

I have a fairly large (about 250 patients) lipid clinic that I established in 1974; approximately 20% of my patients are taking statin-fenofibrate therapy. I use statin-fibrate (fenofibrate, never gemfibrozil1) in patients with both low high-density lipoprotein and high triglycerides, although I usually do so after starting statins. When the lipid goal is achieved, fibrates can induce plaque stabilization/regression.²

I rarely use niacin because of the associated itching and flushing, and because no stand-alone trials have shown a positive effect of niacin on ATD events. The Coronary Drug Project failed to find immediate effects of niacin, but there seemed to be a survival benefit 15 years after the trial ended.³ I use fish oil (but not krill oil, since there have been no population studies) combined with low-dose aspirin for these agents’ antiplatelet and vasodilatory effects. The dosages I use are docosahexaenoic acid plus eicosapentaenoic acid 1 g/d and aspirin 81 mg/d.

I stopped using ezetimibe when the SEAS trial⁴ found an increase in total cancers and fatal cancers in the simvastatin-ezetimibe cohort as compared with the simvastatin cohort.

Finally, one must be careful about the new American Heart Association/American College of Cardiology guidelines, which relied solely on randomized controlled trials (RCTs) that studied high-risk patients, many of whom already had ATD. It is not clear that the results of those RCTs are applicable to the general population. I suggest treating patients in the at-risk (for ATD) population and to treat them to low-density lipoprotein levels that are associated with maximum plaque stabilization/regression⁵ or alternately so that their risk factors are in line with those of the low-risk population.

William E. Feeman Jr, MD
Bowling Green, Ohio

I agree wholeheartedly with Dr. Wahawisan et al (Statin therapy: When to think twice. J Fam Pract. 2013;62:726-730,732) that one shouldn’t use medications to ameliorate dyslipidemia unless those medications have been proven to stabilize or regress plaque and/or improve atherothrombotic disease (ATD) outcomes. However, I believe the article deserves further comment.

I have a fairly large (about 250 patients) lipid clinic that I established in 1974; approximately 20% of my patients are taking statin-fenofibrate therapy. I use statin-fibrate (fenofibrate, never gemfibrozil1) in patients with both low high-density lipoprotein and high triglycerides, although I usually do so after starting statins. When the lipid goal is achieved, fibrates can induce plaque stabilization/regression.²

I rarely use niacin because of the associated itching and flushing, and because no stand-alone trials have shown a positive effect of niacin on ATD events. The Coronary Drug Project failed to find immediate effects of niacin, but there seemed to be a survival benefit 15 years after the trial ended.³ I use fish oil (but not krill oil, since there have been no population studies) combined with low-dose aspirin for these agents’ antiplatelet and vasodilatory effects. The dosages I use are docosahexaenoic acid plus eicosapentaenoic acid 1 g/d and aspirin 81 mg/d.

I stopped using ezetimibe when the SEAS trial⁴ found an increase in total cancers and fatal cancers in the simvastatin-ezetimibe cohort as compared with the simvastatin cohort.

Finally, one must be careful about the new American Heart Association/American College of Cardiology guidelines, which relied solely on randomized controlled trials (RCTs) that studied high-risk patients, many of whom already had ATD. It is not clear that the results of those RCTs are applicable to the general population. I suggest treating patients in the at-risk (for ATD) population and to treat them to low-density lipoprotein levels that are associated with maximum plaque stabilization/regression⁵ or alternately so that their risk factors are in line with those of the low-risk population.

William E. Feeman Jr, MD
Bowling Green, Ohio

I agree wholeheartedly with Dr. Wahawisan et al (Statin therapy: When to think twice. J Fam Pract. 2013;62:726-730,732) that one shouldn’t use medications to ameliorate dyslipidemia unless those medications have been proven to stabilize or regress plaque and/or improve atherothrombotic disease (ATD) outcomes. However, I believe the article deserves further comment.

I have a fairly large (about 250 patients) lipid clinic that I established in 1974; approximately 20% of my patients are taking statin-fenofibrate therapy. I use statin-fibrate (fenofibrate, never gemfibrozil1) in patients with both low high-density lipoprotein and high triglycerides, although I usually do so after starting statins. When the lipid goal is achieved, fibrates can induce plaque stabilization/regression.²

I rarely use niacin because of the associated itching and flushing, and because no stand-alone trials have shown a positive effect of niacin on ATD events. The Coronary Drug Project failed to find immediate effects of niacin, but there seemed to be a survival benefit 15 years after the trial ended.³ I use fish oil (but not krill oil, since there have been no population studies) combined with low-dose aspirin for these agents’ antiplatelet and vasodilatory effects. The dosages I use are docosahexaenoic acid plus eicosapentaenoic acid 1 g/d and aspirin 81 mg/d.

I stopped using ezetimibe when the SEAS trial⁴ found an increase in total cancers and fatal cancers in the simvastatin-ezetimibe cohort as compared with the simvastatin cohort.

Finally, one must be careful about the new American Heart Association/American College of Cardiology guidelines, which relied solely on randomized controlled trials (RCTs) that studied high-risk patients, many of whom already had ATD. It is not clear that the results of those RCTs are applicable to the general population. I suggest treating patients in the at-risk (for ATD) population and to treat them to low-density lipoprotein levels that are associated with maximum plaque stabilization/regression⁵ or alternately so that their risk factors are in line with those of the low-risk population.

William E. Feeman Jr, MD
Bowling Green, Ohio