Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Case Study
  • Published:

Antiphospholipid antibodies from a patient with primary antiphospholipid syndrome enhance experimental atherosclerosis

Nature Reviews Cardiology volume 6, pages 215–218 (2009)Cite this article

Abstract

Background A 35-year-old man with primary antiphospholipid syndrome and no risk factors for atherosclerosis presented with postinfarction angina.

Investigations Coronary angiography, intravascular ultrasonography, injection of apolipoprotein–E-knockout mice with patient's IgG.

Diagnosis Myocardial infarction caused by a newly occluded proximal left circumflex artery. The left anterior descending artery exhibited a recanalized thrombus throughout the vessel.

Management The patient was managed by intensive angicoagulation including aspirin, clopidogrel, and enoxaparin for 2 months. After follow-up coronary angiography, he was switched to warfarin with a target International Normalized Ratio of 3.5–4.0.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Coronary angiographic studies from a patient with primary antiphospholipid syndrome.
Figure 2: Atherosclerotic lesion size and plaque phenotype in apolipoprotein-E-knockout mice injected with IgG from either a patient with antiphospholipid syndrome or healthy control individual.
Figure 3: Representative atherosclerotic lesions in the aortic sinuses of apolipoprotein-E-knockout mice injected with IgG from a patient with antiphospholipid syndrome or a healthy control individual.

References

  1. Wilson WA et al. (1999) International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an International Workshop. Arthritis Rheum 42: 1309–1311

    Article  CAS  Google Scholar 

  2. Hansson GK (2005) Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 352: 1685–1695

    Article  CAS  Google Scholar 

  3. George J et al. (2001) Accelerated atheroma, antiphospholipid antibodies, and the antiphospholipid syndrome. Rheum Dis Clin North Am 27: 603–610

    Article  CAS  Google Scholar 

  4. Brey RL et al. (2001) β2-Glycoprotein 1-dependent anticardiolipin antibodies and risk of ischemic stroke and myocardial infarction: The Honolulu heart program. Stroke 32: 1701–1706

    Article  CAS  Google Scholar 

  5. Vaarala O et al. (1995) Anti-cardiolipin antibodies and risk of myocardial infarction in a prospective cohort of middle-aged men. Circulation 91: 23–27

    Article  CAS  Google Scholar 

  6. George J et al. (1998) Induction of early atherosclerosis in LDL-receptor–deficient mice immunized with β2-glycoprotein I. Circulation 98: 1108–1115

    Article  CAS  Google Scholar 

  7. Afek A et al. (1999) Enhancement of atherosclerosis in β2-glycoprotein I-immunized apolipoprotein E-deficient mice. Pathobiology 67: 19–25

    Article  CAS  Google Scholar 

  8. George J et al. (2000) Adoptive transfer of β2-glycoprotein I–reactive lymphocytes enhances early atherosclerosis in LDL receptor-deficient mice. Circulation 102: 1822–1827

    Article  CAS  Google Scholar 

  9. Palinski W et al. (1995) Immunization of low density lipoprotein (LDL) receptor-deficient rabbits with homologous malondialdehyde-modified LDL reduces atherogenesis. Proc Natl Acad Sci USA 92: 821–825

    Article  CAS  Google Scholar 

  10. George J et al. (1999) Immunolocalization of β2-glycoprotein I (apolipoprotein H) to human atherosclerotic plaques: potential implications for lesion progression. Circulation 99: 2227–2230

    Article  CAS  Google Scholar 

  11. Plump AS et al. (1992) Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells. Cell 71: 343–353

    Article  CAS  Google Scholar 

  12. Paigen B et al. (1987) Quantitative assessment of atherosclerotic lesions in mice. Atherosclerosis 68: 231–240

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. G Keren is Chairman and J George is a Professor at the Department of Cardiology, A Adler is a Resident, A Afek and Y Levy are both Senior Lecturers, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.,

    Arnon Adler, Arnon Afek, Yair Levy, Gad Keren & Jacob George

Authors
  1. Arnon Adler
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Arnon Afek
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Yair Levy
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Gad Keren
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Jacob George
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Jacob George.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Adler, A., Afek, A., Levy, Y. et al. Antiphospholipid antibodies from a patient with primary antiphospholipid syndrome enhance experimental atherosclerosis. Nat Rev Cardiol 6, 215–218 (2009). https://doi.org/10.1038/ncpcardio1436

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/ncpcardio1436

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing