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Review article
peer-reviewed

Atherothrombosis is a Thrombotic, not Inflammatory Disease



Abstract

The authors hypothesize that thrombosis causes both the complications of atherosclerosis as well as the underlying lesion, the atherosclerotic plaque, which develops from the organization of mural thrombi. These form in areas of slow blood flow, which develop because of flow separation created by changing vascular geometry and elevated blood viscosity. Many phenomena typically ascribed to inflammation or “chronic oxidative stress”, such as the development of fatty streaks, “endothelial dysfunction,” “vulnerable plaques,” and the association of mild elevations of C-reactive protein and cytokines with atherothrombosis are better explained by hemorheologic and hemodynamic abnormalities, particularly elevated blood viscosity. Elevated blood viscosity decreases the perfusion of skeletal muscle, leading to myocyte expression of the myokine IL-6, decreased glucose uptake, insulin resistance, hyperglycemia, and metabolic syndrome. The hyperfibrinogenemia and hypergammaglobulinemia present in true inflammatory diseases foster atherothrombosis by increasing blood viscosity.



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Review article
peer-reviewed

Atherothrombosis is a Thrombotic, not Inflammatory Disease


Author Information

Gregory Sloop Corresponding Author

N/A, Independent Researcher

Joseph J. Weidman

N/A, Independent Researcher

John A. St. Cyr

Research and Development, Jacqmar, Inc.


Ethics Statement and Conflict of Interest Disclosures

Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Acknowledgements

Thanks to K.C. Hayes, D.V.M., Ph.D., for helpful discussions.


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Review article
peer-reviewed

Atherothrombosis is a Thrombotic, not Inflammatory Disease

Gregory Sloop">Gregory Sloop , Joseph J. Weidman">Joseph J. Weidman, John A. St. Cyr">John A. St. Cyr

  • Author Information
    Gregory Sloop Corresponding Author

    N/A, Independent Researcher

    Joseph J. Weidman

    N/A, Independent Researcher

    John A. St. Cyr

    Research and Development, Jacqmar, Inc.


    Ethics Statement and Conflict of Interest Disclosures

    Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

    Acknowledgements

    Thanks to K.C. Hayes, D.V.M., Ph.D., for helpful discussions.


    Article Information

    Published: December 05, 2017

    DOI

    10.7759/cureus.1909

    Cite this article as:

    Sloop G, Weidman J J, St. cyr J A (December 05, 2017) Atherothrombosis is a Thrombotic, not Inflammatory Disease. Cureus 9(12): e1909. doi:10.7759/cureus.1909

    Publication history

    Received by Cureus: October 17, 2017
    Peer review began: November 01, 2017
    Peer review concluded: December 01, 2017
    Published: December 05, 2017

    Copyright

    © Copyright 2017
    Sloop et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 3.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

    License

    This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The authors hypothesize that thrombosis causes both the complications of atherosclerosis as well as the underlying lesion, the atherosclerotic plaque, which develops from the organization of mural thrombi. These form in areas of slow blood flow, which develop because of flow separation created by changing vascular geometry and elevated blood viscosity. Many phenomena typically ascribed to inflammation or “chronic oxidative stress”, such as the development of fatty streaks, “endothelial dysfunction,” “vulnerable plaques,” and the association of mild elevations of C-reactive protein and cytokines with atherothrombosis are better explained by hemorheologic and hemodynamic abnormalities, particularly elevated blood viscosity. Elevated blood viscosity decreases the perfusion of skeletal muscle, leading to myocyte expression of the myokine IL-6, decreased glucose uptake, insulin resistance, hyperglycemia, and metabolic syndrome. The hyperfibrinogenemia and hypergammaglobulinemia present in true inflammatory diseases foster atherothrombosis by increasing blood viscosity.



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Gregory Sloop, M.D.

N/A, Independent Researcher

For correspondence:
bigdaddypathologist@gmail.com

Joseph J. Weidman, Pharm.D.

N/A, Independent Researcher

John A. St. Cyr, M.D., Ph.D., Researcher

Research and Development, Jacqmar, Inc.

Gregory Sloop, M.D.

N/A, Independent Researcher

For correspondence:
bigdaddypathologist@gmail.com

Joseph J. Weidman, Pharm.D.

N/A, Independent Researcher

John A. St. Cyr, M.D., Ph.D., Researcher

Research and Development, Jacqmar, Inc.