This study evaluated the independent and joint associations of elevated Lp(a) and family history of CHD with incident ASCVD and CHD events among asymptomatic subjects.
Elevated Lp(a) levels were associated with greater risk of MACE in optimally treated patients with high-risk vascular disease when hsCRP levels ≥2 mg/L, but not in those with hsCRP levels <2 mg/L.
Nick Nurmohamed explains what Lp(a) is and how correction of LDL-c for Lp(a) reduces genetic testing for FH.
This phase 2 study with alirocumab decreased LDL-c levels and was generally well tolerated in pediatric HeFH patients. Two dosing regimens were selected for further investigation in a phase 3 trial.
Prof. Jukema explains the main principles for LDL-c-lowering therapy as described in the 2019 ESC/EAS guidelines and discusses results from several trials that investigated the effect of Lp(a) on CV outcomes.
Elevated Lp(a) contributes to pro-inflammatory gene expression of monocytes in both healthy subjects and CVD patients. Potent Lp(a)-lowering reduced the pro-inflammatory state of circulating monocytes.
Genetically determined elevated Lp(a) levels were inversely associated with high parental life span and health span (chronic disease–free survival), and higher measured Lp(a) levels were associated with all-cause and CV mortality.
Progression rate of aortic stenosis is predicted by high levels of ApoCIII-Lp(a) complexes in combination with high levels of Lp(a) or oxidized phospholipids.
Which lipids/lipoproteins, besides LDL-c, play a role in determining CV risk and can help targeting therapy in those with residual lipid risk?
Prof. Landmesser shows data that form the rationale behind new guideline recommendations, among which the lower LDL-c target for patients at very high risk.
Erin Bohula explains which determinants of residual CV risk we nowadays know and presents study results on how to target these.
Prof. Steg presents data of the ODYSSEY Outcomes trial in specific subgroups of ACS patients that benefit most from alirocumab therapy, and discusses the effect of this PCSK9 inhibitor by baseline Lp(a) levels.