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Mendelian randomization analysis does not support a causal influence between lipoprotein(A) and immune-mediated inflammatory diseases.

Sci Rep

January 2025

State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China.

Observational studies have reported an association between lipoprotein(a) (Lp(a)) and immune-mediated inflammatory diseases (IMIDs). This study used Mendelian Randomization (MR) and multivariable MR (MVMR) to explore the causal relationship between lipoprotein(a) [Lp(a)] and immune-mediated inflammatory diseases (IMIDs). We performed a bidirectional two-sample mendelian randomization analyses based on genome-wide association study (GWAS) summary statistics of Lp(a) and nine IMIDs, specifically celiac disease (CeD), Crohn's disease (CD), ulcerative colitis (UC), inflammatory bowel disease (IBD), multiple sclerosis (MS), psoriasis (Pso), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes (T1D), and summary-level data for lipid traits.

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Background: Lipoprotein(a) [Lp(a)] has been independently associated with increased cardiovascular risk.

Objectives: The authors examined the effect of monoclonal antibody proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9is) on plasma Lp(a) levels across multiple trials.

Methods: Studies were retrieved comparing the effect of PCSK9i vs placebo on Lp(a) levels.

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Molecular Therapeutics in Development to Treat Hyperlipoproteinemia.

Mol Diagn Ther

January 2025

Department of Medicine and Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, 4288A-1151 Richmond Street North, London, ON, N6A 5B7, Canada.

Clinical endpoints caused by hyperlipoproteinemia include atherosclerotic cardiovascular disease and acute pancreatitis. Emerging lipid-lowering therapies targeting proprotein convertase subtilisin/kexin 9 (PCSK9), lipoprotein(a), apolipoprotein C-III, and angiopoietin-like protein 3 represent promising advances in the management of patients with hyperlipoproteinemia. These therapies offer novel approaches for lowering pathogenic lipid and lipoprotein species, particularly in patients with serious perturbations who are not adequately controlled with conventional treatments or who are unable to tolerate them.

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Background: Thrombolysis in Myocardial Infarction (TIMI) risk score in patients with ST-segment elevation myocardial infarction (STEMI) is associated with major adverse cardiovascular events (MACE). This study aimed to develop a prediction model based on the TIMI risk score for MACE in STEMI patients after percutaneous coronary intervention (PCI).

Methods: We conducted a retrospective data analysis on 290 acute STEMI patients admitted to the Affiliated Hospital of Yangzhou University from January 2022 to June 2023 and met the inclusion criteria.

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Statins-Their Effect on Lipoprotein(a) Levels.

Rev Cardiovasc Med

January 2025

Department of Clinical and Experimental Pharmacology, Faculty of Medicine, Medical University of Warsaw, 02-097 Warsaw, Poland.

Lipoprotein(a) (Lp(a)) serum concentration plays a crucial role as a risk factor in cardiovascular diseases and is gaining more and more attention. Patients with elevated lipoprotein(a) levels are often prescribed statins as they also have high concentrations of low-density lipoprotein cholesterol (LDL-C). Statins are drugs that successfully decrease LDL-C, but their effectiveness in Lp(a) levels reduction is uncertain.

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