CardioSource WorldNews July 2015 | Page 35

Sponsored content This material was developed with Sanofi and Regeneron I think this person has familial hypercholesterolemia?” Does that knowledge trigger you to alter your treatment or screening strategy? Dr. Foody: Well, we have to stay vigilant, and, in some respects, the success of statins has unfortunately eliminated the need to look at this. We have to recognize that when individuals are on a maximally tolerated dose of statin—and I use “tolerated” because we all know that statins may not be without side effects—and their numbers are still above 130 or 160 mg/dL, it may be a good signal to start looking for presence of familial hypercholesterolemia. The maximal intensive dose of statins should reduce LDL by about 50%. You could argue that, if someone’s LDL was above 100 mg/dL on maximal-intensity statins, they probably, in fact, started in a range that would signal that they had either heterozygous or homozygous familial hypercholesterolemia. Dr. Bhatt: As we have seen from epidemiologic and clinical studies, poorly controlled LDL is linked with persistent cardiovascular risk. There has also been some confusion about lowering LDL in recent years, but I think it is good to prescribe statins to at-risk patients. That is probably one of the most important steps in ensuring that patients have the best outcomes: being on a statin versus not being on a statin for patients at appropriate levels of cardiovascular risk. The second step, then, is making sure that a patient’s LDL levels are actually reduced. There are two methods for this: the patient’s adherence to therapy (because, obviously, if they are not adherent to therapy, their LDL levels are not going to be reduced by the statin) and making sure that the patient has the correct intensity and dose of statin. There is a subset of patients who continue to have poorly controlled LDL despite treatment with current standard of care. Dr. Foody: Absolutely, Deepak—that is a critical point that should be emphasized. The power of the genetic findings, Mendelian randomization, and—as you mentioned—the lack of similar findings with HDL, have really further bolstered an approach focusing on LDL cholesterol. To your point, there has been significant misunderstanding about the guidelines because they were interpreted as throwing out cholesterol targets. I tend to take a more moderate view: yes, they focused on evidence-based intensity and dosing of statins, but the trials also required that patients met certain endpoints for LDL cholesterol. The guidelines have been very clear to emphasize that LDL remains an i