Influence of Pelacarsen on Patients After Myocardial Infarction With High Lp(a) Values (PEMILA)

Sponsor
University Medical Centre Ljubljana
Study ID
NCT04993664
Status
Withdrawn

Conditions

  • Acute Coronary Syndrome
  • Genetic Polymorphisms
  • Inflammation
  • Lipoproteinemia

Eligibility Criteria

Sex
ALL
Age
18 Years - 65 Years
Healthy Volunteers
Not accepted

Interventions

  • Pelacarsen (TQJ230) — DRUG
    The first group will receive pelacarsen. Blood samples from all patients will be drawn for laboratory measurements and genetics determination. Ultrasound measurement of endothelium-dependent dilatation of the brachial artery and beta stiffness of carotid arteries will be measured.
  • Placebo — DRUG
    The second group will receive placebo. Blood samples from all patients will be drawn for laboratory measurements and genetics determination. Ultrasound measurement of endothelium-dependent dilatation of the brachial artery and beta stiffness of carotid arteries will be measured.

Study Details

The aim of study is to examine the relationship between lipid subfractions, inflammation and structural-functional properties of the arterial wall in patients after myocardial infarction with high lipoprotein (a) (Lp (a)) levels, to study genetic polymorphisms that determine lipid subfractions concentration on the functional and morphological properties of the arterial vascular wall in patients after myocardial infarction with high Lp (a) levels, to study the effect of pelacarsen on lipid subfractions, inflammation and structural-functional properties of arterial wall in patients after myocardial infarction with high Lp (a) levels and to study the influence of NOS-3 gene expression on the functional and morphological properties of the arterial vascular wall in the same patients. Impaired blood fat metabolism and chronic inflammation represent possible causes of atherosclerosis. Lp (a) is an independent risk factor for cardiovascular disease and a prognostic predictor in patients after myocardial infarction. Despite recommended screening for elevated Lp (a), there is no specific drug treatment approved to reduce cardiovascular risk through lowering Lp (a). Besides subtilisin-kexin convertase type 9 (PCSK9) inhibitors, antisense oligonucleotides (ASOs) are currently only therapeutic agents that significantly reduce serum Lp (a) concentration. Pelacarsen by using an ASO directed against the messenger ribonucleic acid (mRNA) of apolipoprotein (a), reduces the production of apolipoprotein (a) in the liver and thus, the level of Lp (a). However, there are no data on the relationship between Lp (a) values and polymorphisms for Lp (a), indicators of inflammation and impaired arterial function, and response to treatment with pelacarsen in patients after myocardial infarction with extremely high Lp (a) levels.

Key Dates

Start date
Oct 1, 2021
Status verified
Dec 2021
Primary completion
Jun 30, 2022
Completion
Oct 1, 2022

Study Design

Enrollment
0 participants (actual)
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT

Arms

  • Experimental: Pelacarsen group (TQJ230)
    The first group will receive 80 mg of pelacarsen every month subcutaneously for 6 months.
  • Placebo Comparator: Placebo group
    The first group will receive 80 mg of placebo every month subcutaneously for 6 months.

Primary Outcome Measure

Ultrasound functional and morphological properties of the arterial wall and Lp (a) concentration [ Time Frame: Baseline ]

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