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Atherothrombosis

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PanVascular Medicine

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Abstract

Atherothrombotic cardiovascular disease (CVD) is the leading cause of death and disability not only in affluent countries but globally and, as such, has a large economic and public health impact. The serious and potentially lethal consequences of atherosclerosis such as acute coronary syndromes (unstable angina, acute myocardial infarction, and many cases of sudden death) and ischemic stroke are usually caused by acute thrombosis superimposed on a chronic atherosclerotic plaque with a disrupted or eroded surface in what can consequently be termed atherothrombosis. Because of these pathophysiologic considerations, factors that determine the vulnerability of plaques to disruption or superficial erosion, as well as factors that determine the likelihood of subsequent thrombosis, are key determinants of the ability to prevent the lethal manifestations of atherosclerosis. Tremendous efforts in the past decade have culminated in a deeper understanding of the mechanisms that lead to plaque formation, plaque rupture, plaque erosion, artery lumen stenosis, and atherothrombosis. While many questions remain unanswered, this expanded awareness has resulted in a paradigmatic shift in certain aspects relating to the pathophysiology of atherothrombosis, opening the door to novel therapeutic opportunities.

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Abbreviations

Atherothrombosis:

Atherosclerosis with superimposed thrombosis.

Calcified nodule:

A heavily calcified plaque with loss and/or dysfunction of endothelial cells over a calcified nodule, resulting in loss of fibrous cap and therefore making the plaque at high risk/vulnerable. This is the least common of the three types of potential high-risk/vulnerable plaques.

High-risk plaque:

Vulnerable plaque, a plaque that is at increased risk of thrombosis and rapid stenosis progression.

Plaque erosion:

A plaque with loss and/or dysfunction of the luminal endothelial cells leading to thrombosis. There is usually no additional defect or gap in the plaque, which is often rich in smooth muscle cells and proteoglycans.

Plaque rupture:

A plaque with deep injury and a defect or gap in the overlying fibrous cap that had previously separated the lipid-rich atheromatous core from the flowing blood, thereby exposing the thrombogenic core of the plaque. This is the most common cause of thrombosis.

Thrombosed plaque:

A plaque with an overlying thrombus extending into the lumen of the vessel. The thrombus may be occlusive or nonocclusive.

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Authors and Affiliations

  1. Centro Nacional de Investigaciones Cardiovasculares, CNIC, Madrid, Spain

    Jose M. Castellano & Valentin Fuster

  2. The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA

    Jose M. Castellano & Valentin Fuster

  3. The Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, One Gustave Levy Place, 1030, New York, NY, 10029, USA

    Jason C. Kovacic

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  1. Jose M. Castellano
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  2. Jason C. Kovacic
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  3. Valentin Fuster
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Correspondence to Jose M. Castellano .

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Editors and Affiliations

  1. Division of Cardiovascular Disease Department of Internal Medicine, Health Care Center Bitterfeld, Bitterfeld-Wolfen, Germany

    Peter Lanzer

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Castellano, J.M., Kovacic, J.C., Fuster, V. (2015). Atherothrombosis. In: Lanzer, P. (eds) PanVascular Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-37078-6_19

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