2020.01.02 07:44
2020.01.02 07:47
2020.01.02 08:08
Many people never heard of Lp(a).
Most doctors including cardiologists do not order or include Lp(a)
in the lipid panel screening although the elevated Lp(a) is a known risk
for CVD and one in five has elevated Lp(a) over 30mg% chiefly because
there is no drug or effective therapy for this genetically transmitted CVD risk.
Statins and PCSK9 do not lower Lp(a).
Now for the first time in history we found an agent, antisense, oligonucleotide,
that effectively brings it down in its phase II trial.
This is certainly an exciting news.
We finally found a way conquering the last barrier to reach the goal, i.e.
discovering all the weapons to conquer or prevent atherosclerosis.
2020.01.02 13:14
2020.01.03 01:37
Candidates for Lp(a) screening include 1) premature or family history premature CVD; 2) FH or other genetic lipidemia; 3) recurrent cardiovascular events or rapidly progressive CVD; 4) genetic defects of hemostasis, homocysteine metabolism, as well as diabetes mellitus or autoimmune diseases; 5) ≥ 10% 10-year risk of fatal and/or nonfatal CHD; 6) inadequate LDL-C responses to statin.
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Lipoprotein(a) Reduction in Persons with Cardiovascular Disease
List of authors.
Abstract
BACKGROUND
Lipoprotein(a) levels are genetically determined and, when elevated, are a risk factor for cardiovascular disease and aortic stenosis. There are no approved pharmacologic therapies to lower lipoprotein(a) levels.
METHODS
We conducted a randomized, double-blind, placebo-controlled, dose-ranging trial involving 286 patients with established cardiovascular disease and screening lipoprotein(a) levels of at least 60 mg per deciliter (150 nmol per liter). Patients received the hepatocyte-directed antisense oligonucleotide AKCEA-APO(a)-LRx, referred to here as APO(a)-LRx (20, 40, or 60 mg every 4 weeks; 20 mg every 2 weeks; or 20 mg every week), or saline placebo subcutaneously for 6 to 12 months. The lipoprotein(a) level was measured with an isoform-independent assay. The primary end point was the percent change in lipoprotein(a) level from baseline to month 6 of exposure (week 25 in the groups that received monthly doses and week 27 in the groups that received more frequent doses).
RESULTS
The median baseline lipoprotein(a) levels in the six groups ranged from 204.5 to 246.6 nmol per liter. Administration of APO(a)-LRx resulted in dose-dependent decreases in lipoprotein(a) levels, with mean percent decreases of 35% at a dose of 20 mg every 4 weeks, 56% at 40 mg every 4 weeks, 58% at 20 mg every 2 weeks, 72% at 60 mg every 4 weeks, and 80% at 20 mg every week, as compared with 6% with placebo (P values for the comparison with placebo ranged from 0.003 to <0.001). There were no significant differences between any APO(a)-LRx dose and placebo with respect to platelet counts, liver and renal measures, or influenza-like symptoms. The most common adverse events were injection-site reactions.
CONCLUSIONS
APO(a)-LRx reduced lipoprotein(a) levels in a dose-dependent manner in patients who had elevated lipoprotein(a) levels and established cardiovascular disease. (Funded by Akcea Therapeutics; ClinicalTrials.gov number b.)