![]() They were first used to identify genetic variants associated with specific diseases.Because statins work well in most people, but there’s a huge inter-individual variability in terms of LDL lowering associated with statins.At that time they were also wondering if there were any genetic variants that could explain statin response.Published in the Journal of the American College of Cardiology, Oxidation-Specific Biomarkers, Lipoprotein(a), and Risk of Fatal and Nonfatal Coronary Events.This was the first paper he published on Lp(a) in those years.And it turned out that of a huge list of 18 biomarkers that they had measured in thousands of individuals, Lp(a) was actually the strongest of them that was predicting residual cardiovascular risk.They had just measured a whole panel of emerging biomarkers that could be associated with cardiovascular events like CRP, NT-proBNP, inflammatory markers, other biomarkers of insulin sensitivity, and Lp(a).They were working on a bunch of sub analyses for that trial.This is one of the first trials that showed that if you reduce low density lipoprotein (LDL) levels by increasing the statin dose, you’ll get an incremental benefit in cardiovascular outcomes. ![]() John was working on the treating-to-new-targets trial, the TnT trial.During that time he was a postdoc in Amsterdam working with John Kastelein.Genetic association studies have resurrected the field of Lp(a).Studies of biomarkers associated with cardiovascular events point to Lp(a) Such as myocardial infarction (MIs) and stroke and so on.Not that many people talked about Lp(a) because there had been so many negative studies on Lp(a) and the risk of cardiovascular disease.Did work in the field of lipids, looking at LDL particle size, triglycerides, APOB, etc., on cardiovascular outcomes.He trained at Laval University in Quebec City from 2006-2009.Benoît got involved in Lp(a) research during his postdoc years.Δ How Benoît came to study Lp(a)-a new marker for cardiovascular risk Antisense oligonucleotides-a potential new therapeutic for Lp(a) and.Peter’s approach to managing patients with high Lp(a), and Benoît’s personal approach to managing his risk.The variability in PCSK9 inhibitors’ ability to lower Lp(a) and why we need more research on individuals with high levels of Lp(a).The biology of PCSK9 protein, familial hypercholesterolemia, and the case for inhibiting PCSK9.Diseases most associated with high Lp(a). ![]()
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