4 Key Pieces of Research Released in November

This November the American Heart Association held their annual conference in Chicago. Over 10,000 clinicians and researchers in attendance. Sessions focused on the latest insights and below we’ve listed the key takeaways from the research presented.

1. Family Heart Foundation Presents Lp(a) Findings from the Family Heart Database

Family Heart Foundation Vice President of Research, Diane MacDougall, presented a poster entitled, “Lipoprotein(a) and Risk of Cardiovascular Disease Events: An analysis of a large US national database.” This is one of the largest studies looking at lipoprotein(a), also known as Lp(a). The study included 393,000 Americans.

The result: The findings indicated that higher Lp(a) consistently predicted an increased risk of cardiovascular events in both individuals with and without existing cardiovascular disease.

What this means: These findings continue to show the importance of screening for Lp(a) to give people the knowledge and options for care to prevent a cardiovascular event.

2. The ALPACAR-360 Trial Shows Zerlasiran Lowers Lp(a) by Over 90%

The ALPACAR-360 trial examined the use of zerlasiran, a small interfering RNA (siRNA) therapy targeting Lp(a), in 178 people with cardiovascular disease and levels of Lp(a) greater than or equal to 125 nmol/L. Three different doses of zerlasiran were studied.

The result: All doses of zerlasiran reduced Lp(a) levels by more than 80% in individuals with ASCVD.

What this means: As Dr. Curtis Rambaran, chief medical officer at Silence Therapeutics puts it, “The Phase 2 data show zerlasiran has the potential to provide long term reductions in Lp(a) with infrequent dosing. We look forward to progressing zerlasiran into Phase 3 as a potentially promising new treatment for patients with high Lp(a).”

3. The KRAKEN Trial Looked at An Oral Lp(a) Treatment

The KRAKEN trial involved giving muvalaplin to patients with Lp(a) levels of 175 nol/L or greater with established cardiovascular disease, diabetes, or familial hypercholesterolemia (FH). This medication works by preventing lipoprotein(a) from forming in the body. Individuals were randomized to placebo or one of three doses of muvalaplin for a duration of 12 weeks – 10 mg/day, 60 mg/day, or 240 mg/day

The result: Muvalaplin reduced Lp(a) levels by 40-70% depending on the dose, and no safety or tolerability concerns were observed at any dosage.

Results were reported using 2 different assays. Muvalaplin was associated with placebo-adjusted reductions in Lp(a) of 47.6% (95% CI, 35.1% to 57.7%), 81.7% (95% CI, 78.1%-84.6%), and 85.8% (95% CI, 83.1% to 88.0%) for the 10 mg/d, 60 mg/d, and 240 mg/d dosages, respectively, using the intact Lp(a) assay.

What this means: Dr Stephen Nicholls, director of the Victorian Heart Institute in Melbounre, Australia said, “Most medications being developed to lower Lp(a) are injectable. Muvalaplin is the first oral agent being developed to lower Lp(a) levels and acts by disrupting formation of the Lp(a) particle.”

4. The BROOKLYN Trial Shows Obicetrapib Significantly Reduced LDL Cholesterol

The Phase III results of New Amsterdam’s BROOKLYN study examine the use of the oral drug obicetrapib in 354 individuals with HeFH whose LDL is not fully controlled with maximally tolerated lipid-lowering therapy.

The result: Obicetrapib reduced LDL-C by 41.5% at day 365 and reduced Lp(a) by 54.3%.

What this means: The efficacy of this drug is a hopeful sign for those with FH who cannot bring their LDL to the Safe Zone with existing medication. It may also be an important addition for those with both FH and elevated Lp(a).