ReviewCurrent atherosclerosis reports2019
Looking at Lp(a) and Related Cardiovascular Risk: from Scientific Evidence and Clinical Practice.
Review in Current atherosclerosis reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Pooled it
- Could the Hemodynamic Progression of Aortic Valve Stenosis be Slowed Pharmacologically? The Unsolved Dilemma.Reviews in cardiovascular medicine · 2025Article
- Mineral composition and ratios in aortic valves, serum, and epicardial fat among patients with aortic stenosis undergoing aortic valve replacement.Scientific reports · 2025Article
- Application and Analysis of Random Forest and Support Vector Classification in Risk Prediction of Childhood Obesity and Hyperuricemia.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Unraveling the Enigma of Moderate Aortic Stenosis: Challenges and Future Prospects.Journal of clinical medicine · 2024Review
- Lipoprotein(a) and thromboembolism: current state of knowledge and unsolved issues.Archives of medical science : AMS · 2024Article
- Relationship between carotid atherosclerosis and lipoprotein (a) in patients with acute ischemic stroke.Frontiers in neurology · 2024Article
- Lipoprotein(a): Cardiovascular Disease, Aortic Stenosis and New Therapeutic Option.International journal of molecular sciences · 2022Review
- Non-Lipid Effects of PCSK9 Monoclonal Antibodies on Vessel Wall.Journal of clinical medicine · 2022Review
- Assessment of Associations Between Serum Lipoprotein (a) Levels and Atherosclerotic Vascular Diseases in Hungarian Patients With Familial Hypercholesterolemia Using Data Mining and Machine Learning.Frontiers in genetics · 2022Article
- Lipoprotein(a)-The Crossroads of Atherosclerosis, Atherothrombosis and Inflammation.Biomolecules · 2021Review
- Lipids and Lipoproteins in Health and Disease: Focus on Targeting Atherosclerosis.Biomedicines · 2021Review
- Review
- Role of Increased Lipoprotein (a) in Retinal Vein Occlusion: A Systematic Review and Meta-analysis.TH open : companion journal to thrombosis and haemostasis · 2021Review
- A brief overview of currently used atherosclerosis treatment approaches targeting lipid metabolism alterations.American journal of cardiovascular disease · 2020Review
- Increased cardiovascular risk associated with hyperlipoproteinemia (a) and the challenges of current and future therapeutic possibilities.Anatolian journal of cardiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewA considerable body of data from genetic and epidemiological studies strongly support a causal relationship between high lipoprotein(a) [Lp(a)] levels, and the development of atherosclerosis and cardiovascular disease. This relationship is continuous, unrelated to Lp(a) threshold, and independent of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels. Unfortunately, the mechanism(s) through which Lp(a) promotes atherosclerosis are not clarified yet. Suggested hypotheses include: an increased Lp(a)-associated cholesterol entrapment in the arterial intima followed by inflammatory cell recruitment, abnormal upload of proinflammatory oxidized phospholipids, impaired fibrinolysis by inhibition of plasminogen activation, and enhanced coagulation, through inhibition of the tissue factor pathway inhibitor. This review is aimed at summarizing the available evidence on the topic. RECENT
findingsThere are two clinical forms, isolated hyperlipidemia(a) [HyperLp(a)] with acceptable LDL-C levels (< 70 mg/dL), and combined elevation of Lp(a) and LDL-C in plasma. To date, no drugs that selectively decrease Lp(a) are available. Some novel lipid-lowering drugs can lower Lp(a) levels, but to a limited extent, as their main effect is aimed at decreasing LDL-C levels. Significant Lp(a) lowering effects were obtained with nicotinic acid at high doses. However, adverse effects apart, nicotinic acid is no longer prescribed and available in Europe for clinical use, after European Agency of Medicines (EMA) ban. The only effective therapeutic option for now is Lipoprotein Apheresis (LA), albeit with some limitations. Lastly, it is to be acknowledged that the body of evidence confirming that reducing plasma isolated elevation of Lp(a) brings cardiovascular benefit is still insufficient. However, the growing bulk of clinical, genetic, mechanistic, and epidemiological available evidence strongly suggests that Lp(a) is likely to be the smoking gun.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.