Lipoprotein(a) and PCSK9 Utilization



Howard Weintraub, MD: I’m going to chime in with 1 point. I have a question for you as well. We have found so many cases in which individuals were running around with LDL [low-density lipoprotein] in the 60s, 70s, and 80s mg/dL on statins and ezetimibe and were progressing. In many cases when we drew an LP(a) [lipoprotein (a)], which was often not even thought about, we would find the culprit. The data from ODYSSEY OUTCOMES, with what Vera Bittner wrote, and the data out of Brigham and Women’s Hospital on FOURIER both seem to show that those with the highest LDL and the highest LP(a) got the greatest value out of the use of the PCSK9 monoclonal antibody. Vera’s analysis, as you correctly point out, was very suggestive that there was independent impact from lowering LP(a). It was not just the fact that LDL went down, and that was really what powered the benefit.

What you just pointed out is very important. For the PCSK9-reluctant individual physician, 1 of the best ways to consider the appropriateness is to go after the subgroups that you just discussed. Those are namely individuals with multivessel disease, recent MIs [myocardial infarctions], bad PVD [peripheral vascular disease], diabetes, and high LP(a). We’re not talking about never-heard-of situations. We are talking about a large segment of the population of patients with high-risk cardiovascular disease. If a doctor is not quite certain about whether the work that he or she has to do to get a PCSK9 inhibitor is going to pay off, let them be initially focused on the groups that they already have the data about, except for LP(a). Consider them the people who get it.

Transcript Edited for Clarity

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