Race/ethnicity and socioeconomic status affect the assessment of lipoprotein(a) levels in clinical practice.

Background And Objective: High lipoprotein(a) [Lp(a)] levels are a risk factor for atherosclerotic cardiovascular disease (ASCVD), however Lp(a) ordering in clinical practice is low. This study examines how race/ethnicity and socioeconomic status influence Lp(a) ordering.

Methods: This is a single center, retrospective study (2/1/2020-6/30/2023) using electronic medical records of adults with at least one personal ICD-10 diagnosis of ASCVD, aortic valve stenosis, resistant hypercholesterolemia (low-density lipoprotein cholesterol >160 mg/dL on statin therapy), and family history of ASCVD or high Lp(a).

Small apolipoprotein(a) isoforms may predict primary patency following peripheral arterial revascularization.

Background: High lipoprotein (a) [Lp(a)] is associated with adverse limb events in patients undergoing lower extremity revascularization. Lp(a) levels are genetically pre-determined, with gene encoding for two apolipoprotein (a) [apo(a)] isoforms. Isoform size variations are driven by the number of kringle IV type 2 (KIV-2) repeats.

Race/ethnicity and socioeconomic status affect the assessment of lipoprotein(a) levels in clinical practice.

Background And Objective: High Lp(a) levels are a risk factor for ASCVD, however Lp(a) ordering in clinical practice is low. This study examines how race/ethnicity and socioeconomic status influence Lp(a) ordering.

Methods: This is a single center, retrospective study (2/1/2020-6/30/2023) using electronic medical records of adults with at least one ICD-10 diagnosis of ASCVD or resistant hyperlipidemia (LDL-C >160 mg/dL on statin therapy).

Small apolipoprotein(a) isoforms may predict primary patency following peripheral arterial revascularization.

Background: High lipoprotein (a) [Lp(a)] is associated with adverse limb events in patients undergoing lower extremity revascularization. Lp(a) levels are genetically pre-determined, with gene encoding for two apolipoprotein (a) [apo(a)] isoforms. Isoform size variations are driven by the number of kringle IV type 2 (KIV-2) repeats.

Supporting evidence for lipoprotein(a) measurements in clinical practice.

High levels of lipoprotein(a) [Lp(a)] are causal for development of atherosclerotic cardiovascular disease and highly regulated by genetics. Levels are higher in Blacks compared to Whites, and in women compared to men. Lp(a)'s main protein components are apolipoprotein (apo) (a) and apoB100, the latter being the main component of Low-Density Lipoprotein (LDL) particles.

Endovenous microfoam ablation of below knee superficial truncal veins is safe and effective in patients with prior saphenous treatment across a wide range of CEAP classes.

Objective: Patients requiring thermal or chemical ablation of below knee (BK) truncal veins often have their proximal saphenous veins treated initially and comprise a study population with multilevel, refractory chronic venous insufficiency. The study objective was to assess the outcomes after microfoam ablation of BK truncal and tributary veins in patients with a history of proximal great saphenous vein (GSV) ablation or stripping.

Methods: A retrospective review of a prospectively maintained database was performed.

Effects of mipomersen, an apolipoprotein B100 antisense, on lipoprotein (a) metabolism in healthy subjects.

Elevated lipoprotein (a) [Lp(a)] levels increase the risk for CVD. Novel treatments that decrease LDL cholesterol (LDL-C) have also shown promise for reducing Lp(a) levels. Mipomersen, an antisense oligonucleotide that inhibits apoB synthesis, is approved for the treatment of homozygous familial hypercholesterolemia.

Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans.

Background: Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB). Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism. In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.