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Lipoprotein(a) and Cardiovascular Diseases
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Lipoprotein(a) and Cardiovascular Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 December 2024 | Viewed by 8920

Special Issue Editor

Dr. Christina E. Kostara

E-Mail Website
Guest Editor
Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Interests: metabolism; lipid metabolism; metabolic diseases; atherosclerosis; lipoproteins; lipids; cholesterol; lipid analysis; lipid biochemistry; NMR spectroscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Lipoprotein(a) [Lp(a)] that is composed of a low-density lipoprotein (LDL)–like moiety bound covalently to apolipoprotein(a), has been associated with the development of atherothrombotic disorders including cardiovascular and calcified aortic valve disease. Over the last decades, epidemiological and clinical research have focused on the proatherogenic, proinflammatory and prothrombotic potential of Lp(a), nevertheless the pathophysiological mechanisms underlying the causal relationship between Lp(a) and atherothrombotic diseases remain incompletely understood. In addition, the elucidation of the molecular, cellular and metabolic pathways of Lp(a), that are critical points of Lp(a) metabolic route still remains poorly understood. Thus, the aim of this Special Issue is to gather submissions (original articles, reviews, or short communications) from clinical, translational, and basic research focused on this topic and, therefore, bring to the forefront new insights into pathophysiological aspects of atherothrombotic potential of Lp(a).

Dr. Christina E. Kostara
Guest Editor

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Keywords

  • lipoprotein(a)
  • cardiovascular risk
  • atherothrombotic traits
  • prevention
  • treatment

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Published Papers (3 papers)

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Research

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7 pages, 477 KiB  
Communication
Changes in Lipoprotein(a) Levels in People after ST Elevation Myocardial Infarction—The STEMI-Lipids Study
by Caren Sourij, Faisal Aziz, Sarah Krappinger, Andreas Praschk, Thomas Metzner, Harald Kojzar, Andreas Zirlik, Tatjana Stojakovic, Dieter Pätzold, Dirk von Lewinski, Robert Zweiker, Hubert Scharnagl and Harald Sourij
Int. J. Mol. Sci. 2023, 24(21), 15531; https://doi.org/10.3390/ijms242115531 - 24 Oct 2023
Cited by 1 | Viewed by 1755
Abstract
Lipoprotein(a) (Lp(a)) is considered an independent risk factor for cardiovascular diseases. The plasma concentration of Lp(a) is largely genetically determined but varies over a wide range within the population. This study investigated changes in Lp(a) levels after an acute myocardial infarction. Patients who [...] Read more.
Lipoprotein(a) (Lp(a)) is considered an independent risk factor for cardiovascular diseases. The plasma concentration of Lp(a) is largely genetically determined but varies over a wide range within the population. This study investigated changes in Lp(a) levels after an acute myocardial infarction. Patients who underwent coronary angiography due to an ST elevation myocardial infarction were enrolled (n = 86), and Lp(a) levels were measured immediately after the intervention, one day, two days, and at a post-discharge follow-up visit at 3 to 6 months after the acute myocardial infarction. Median Lp(a) levels increased from a median of 7.9 mg/dL (3.8–37.1) at hospital admission to 8.4 mg/dL (3.9–35.4) on the following day, then to 9.3 mg/dL (3.7–39.1) on day two (p < 0.001), and to 11.2 mg/dL (4.4–59.6) at the post-discharge follow-up (p < 0.001). Lp(a) levels were the lowest during the acute myocardial infarction and started to increase significantly immediately thereafter, with the highest levels at the post-discharge follow-up. The moderate but significant increase in Lp(a) in people with acute myocardial infarction appears to be clinically relevant on an individual basis, especially when specific Lp(a) cut-off levels are supposed to determine the initiation of future treatment. Hence, a repeated measurement of Lp(a) after myocardial infarction should be performed. Full article
(This article belongs to the Special Issue Lipoprotein(a) and Cardiovascular Diseases)
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Review

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16 pages, 2033 KiB  
Review
Lp(a) in the Pathogenesis of Aortic Stenosis and Approach to Therapy with Antisense Oligonucleotides or Short Interfering RNA
by Assunta Di Costanzo, Ciro Indolfi, Anna Franzone, Giovanni Esposito and Carmen Anna Maria Spaccarotella
Int. J. Mol. Sci. 2023, 24(19), 14939; https://doi.org/10.3390/ijms241914939 - 6 Oct 2023
Cited by 5 | Viewed by 2638
Abstract
To date, no medical therapy can slow the progression of aortic stenosis. Fibrocalcific stenosis is the most frequent form in the general population and affects about 6% of the elderly population. Over the years, diagnosis has evolved thanks to echocardiography and computed tomography [...] Read more.
To date, no medical therapy can slow the progression of aortic stenosis. Fibrocalcific stenosis is the most frequent form in the general population and affects about 6% of the elderly population. Over the years, diagnosis has evolved thanks to echocardiography and computed tomography assessments. The application of artificial intelligence to electrocardiography could further implement early diagnosis. Patients with severe aortic stenosis, especially symptomatic patients, have valve repair as their only therapeutic option by surgical or percutaneous technique (TAVI). The discovery that the pathogenetic mechanism of aortic stenosis is similar to the atherosclerosis process has made it possible to evaluate the hypothesis of medical therapy for aortic stenosis. Several drugs have been tested to reduce low-density lipoprotein (LDL) and lipoprotein(a) (Lp(a)) levels, inflammation, and calcification. The Proprotein Convertase Subtilisin/Kexin type 9 inhibitors (PCSK9-i) could decrease the progression of aortic stenosis and the requirement for valve implantation. Great interest is related to circulating Lp(a) levels as causally linked to degenerative aortic stenosis. New therapies with ASO (antisense oligonucleotides) and siRNA (small interfering RNA) are currently being tested. Olpasiran and pelacarsen reduce circulating Lp(a) levels by 85–90%. Phase 3 studies are underway to evaluate the effect of these drugs on cardiovascular events (cardiovascular death, non-fatal myocardial injury, and non-fatal stroke) in patients with elevated Lp(a) and CVD (cardiovascular diseases). For instance, if a reduction in Lp(a) levels is associated with aortic stenosis prevention or progression, further prospective clinical trials are warranted to confirm this observation in this high-risk population. Full article
(This article belongs to the Special Issue Lipoprotein(a) and Cardiovascular Diseases)
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24 pages, 425 KiB  
Review
Novel Pharmacological Therapies for the Management of Hyperlipoproteinemia(a)
by Constantine E. Kosmas, Maria D. Bousvarou, Evangelia J. Papakonstantinou, Donatos Tsamoulis, Andreas Koulopoulos, Rogers Echavarria Uceta, Eliscer Guzman and Loukianos S. Rallidis
Int. J. Mol. Sci. 2023, 24(17), 13622; https://doi.org/10.3390/ijms241713622 - 3 Sep 2023
Cited by 9 | Viewed by 3609
Abstract
Lipoprotein(a) [Lp(a)] is a well-established risk factor for cardiovascular disease, predisposing to major cardiovascular events, including coronary heart disease, stroke, aortic valve calcification and abdominal aortic aneurysm. Lp(a) is differentiated from other lipoprotein molecules through apolipoprotein(a), which possesses atherogenic and antithrombolytic properties attributed [...] Read more.
Lipoprotein(a) [Lp(a)] is a well-established risk factor for cardiovascular disease, predisposing to major cardiovascular events, including coronary heart disease, stroke, aortic valve calcification and abdominal aortic aneurysm. Lp(a) is differentiated from other lipoprotein molecules through apolipoprotein(a), which possesses atherogenic and antithrombolytic properties attributed to its structure. Lp(a) levels are mostly genetically predetermined and influenced by the size of LPA gene variants, with smaller isoforms resulting in a greater synthesis rate of apo(a) and, ultimately, elevated Lp(a) levels. As a result, serum Lp(a) levels may highly vary from extremely low to extremely high. Hyperlipoproteinemia(a) is defined as Lp(a) levels > 30 mg/dL in the US and >50 mg/dL in Europe. Because of its association with CVD, Lp(a) levels should be measured at least once a lifetime in adults. The ultimate goal is to identify individuals with increased risk of CVD and intervene accordingly. Traditional pharmacological interventions like niacin, statins, ezetimibe, aspirin, PCSK-9 inhibitors, mipomersen, estrogens and CETP inhibitors have not yet yielded satisfactory results. The mean Lp(a) reduction, if any, is barely 50% for all agents, with statins increasing Lp(a) levels, whereas a reduction of 80–90% appears to be required to achieve a significant decrease in major cardiovascular events. Novel RNA-interfering agents that specifically target hepatocytes are aimed in this direction. Pelacarsen is an antisense oligonucleotide, while olpasiran, LY3819469 and SLN360 are small interfering RNAs, all conjugated with a N-acetylgalactosamine molecule. Their ultimate objective is to genetically silence LPA, reduce apo(a) production and lower serum Lp(a) levels. Evidence thus so far demonstrates that monthly subcutaneous administration of a single dose yields optimal results with persisting substantial reductions in Lp(a) levels, potentially enhancing CVD risk reduction. The Lp(a) reduction achieved with novel RNA agents may exceed 95%. The results of ongoing and future clinical trials are eagerly anticipated, and it is hoped that guidelines for the tailored management of Lp(a) levels with these novel agents may not be far off. Full article
(This article belongs to the Special Issue Lipoprotein(a) and Cardiovascular Diseases)
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