Post by partimefriend on Dec 24, 2019 9:13:39 GMT -5
Very Good Read 
Stronger’ Evidence That High Lp(a) Concentrations Cause CVD
www.tctmd.com/news/stronger-evidence-high-lpa-concentrations-cause-cvd
“In the poststatin and postgenomic era, finding much needed therapeutic targets for residual cardiovascular risk can be compared to a gold-digging expedition,” Arsenault concludes. “Like a map to the location of the gold, several genome-wide association studies and mendelian randomization studies are consistently pointing us in the direction of Lp(a). It is time to coordinate our efforts to dig where the map told us, to see once and for all, if we will find the golden target of residual cardiovascular risk that we are hoping for and to give hope to high-risk patients with elevated Lp(a) levels.”
The clinical relevance is that for people . . . with very marked elevations of Lp(a), it looks like that the antisense [oligonucleotides] would be beneficial, and even if you knocked the levels down 80% or 90%, you wouldn't actually get into the low levels where you might have some increased risk for diabetes,” Christie Ballantyne, MD (Baylor College of Medicine, Houston, TX), who was not involved in the study, told TCTMD.
Disclosures
Gudbjartsson and Stefansson are employees of deCODE genetics, which is owned by the pharmaceutical company Amgen, which is currently developing Lp(a) lowering drugs aimed at decreasing coronary artery disease risk.
Arsenault reports receiving support by a junior scholar award from the Fonds de recherche du Québec: Santé and the Canadian Institutes of Health Research; receiving research funding from Pfizer, Merck, and Ionis Pharmaceuticals; and serving as a consultant to Pfizer and Novartis.
Ballantyne reports serving as a consultant to Amgen and as an investigator for both Amgen and Novartis trials in the Lp(a) space.
Stronger’ Evidence That High Lp(a) Concentrations Cause CVD
www.tctmd.com/news/stronger-evidence-high-lpa-concentrations-cause-cvd
“In the poststatin and postgenomic era, finding much needed therapeutic targets for residual cardiovascular risk can be compared to a gold-digging expedition,” Arsenault concludes. “Like a map to the location of the gold, several genome-wide association studies and mendelian randomization studies are consistently pointing us in the direction of Lp(a). It is time to coordinate our efforts to dig where the map told us, to see once and for all, if we will find the golden target of residual cardiovascular risk that we are hoping for and to give hope to high-risk patients with elevated Lp(a) levels.”
The clinical relevance is that for people . . . with very marked elevations of Lp(a), it looks like that the antisense [oligonucleotides] would be beneficial, and even if you knocked the levels down 80% or 90%, you wouldn't actually get into the low levels where you might have some increased risk for diabetes,” Christie Ballantyne, MD (Baylor College of Medicine, Houston, TX), who was not involved in the study, told TCTMD.
Disclosures
Gudbjartsson and Stefansson are employees of deCODE genetics, which is owned by the pharmaceutical company Amgen, which is currently developing Lp(a) lowering drugs aimed at decreasing coronary artery disease risk.
Arsenault reports receiving support by a junior scholar award from the Fonds de recherche du Québec: Santé and the Canadian Institutes of Health Research; receiving research funding from Pfizer, Merck, and Ionis Pharmaceuticals; and serving as a consultant to Pfizer and Novartis.
Ballantyne reports serving as a consultant to Amgen and as an investigator for both Amgen and Novartis trials in the Lp(a) space.