Evidence map›Paper›PMID 32710255›Full record

ReviewCurrent atherosclerosis reports2020

Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis.

Patrick M Moriarty, Lauryn K Gorby, Erik S Stroes, John P Kastelein, Michael Davidson, Sotirios Tsimikas

Open access · bronzeAbstract readReview
In one paragraph

Review in Current atherosclerosis reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
1.4field-weighted citation impact, top 10% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
  2. Article
  3. Journal of the American Heart Association · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Lipoprotein(a) and cardiovascular disease.The Biochemical journal · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Lipoprotein(a): Levels and Reference Intervals Among People in Saudi Arabia.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Patrick M MoriartyDivision of Clinical Pharmacology, University of Kansas Medical Center, Kansas City, KS, USA. pmoriart@kumc.edu.
Lauryn K GorbyDivision of Clinical Pharmacology, University of Kansas Medical Center, Kansas City, KS, USA.
Erik S StroesDepartment of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands.
John P KasteleinDepartment of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands.
Michael DavidsonLipid Clinic, The University of Chicago Pritzker School of Medicine, Chicago, IL, USA.
Sotirios TsimikasDivision of Cardiovascular Medicine, University of California San Diego, La Jolla, CA, USA. stsimikas@ucsd.edu.
Amsterdam UMC Location University of Amsterdam · NLUniversity of Kansas Medical Center · USUniversity of California San Diego · USUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe COVID-19 pandemic has infected over > 11 million as of today people worldwide and is associated with significant cardiovascular manifestations, particularly in subjects with preexisting comorbidities and cardiovascular risk factors. Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications. RECENT

findingsThe Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase-type increase in Lp(a) levels following a cytokine storm from COVID-19. Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. We propose studies to test the hypothesis that Lp(a) may contribute to cardiovascular complications of COVID-19.

Indexed as

Acute-Phase ProteinsAnticoagulantsApolipoprotein E4AtherosclerosisBetacoronavirusBiomarkersBiomedical ResearchBlood Component RemovalCoronavirus InfectionsCOVID-19GenotypeHumansInflammationInterleukin-6Interleukin-6 InhibitorsLipoprotein(a)Acute-Phase ProteinsAnticoagulantsApolipoprotein E4BiomarkersInterleukin-6Interleukin-6 InhibitorsLipoprotein(a)COVID-19FibrinolysisInflammationLipoprotein(a)Thrombosis

Identifiers

PMID32710255
PMCPMC7381416
OpenAlexW3043957329

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.