Inflammation, Atherosclerosis, and Coronary Artery Disease

doi:10.1056/NEJMra043430

Volume 352:1685-1695		April 21, 2005		Number 16

Inflammation, Atherosclerosis, and Coronary Artery Disease

Göran K. Hansson, M.D., Ph.D.

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Recent research has shown that inflammation plays a key rolein coronary artery disease (CAD) and other manifestations ofatherosclerosis. Immune cells dominate early atheroscleroticlesions, their effector molecules accelerate progression ofthe lesions, and activation of inflammation can elicit acutecoronary syndromes. This review highlights the role of inflammationin the pathogenesis of atherosclerotic CAD. It will recountthe evidence that atherosclerosis, the main cause of CAD, isan inflammatory disease in which immune mechanisms interactwith metabolic risk factors to initiate, propagate, and activatelesions in the arterial tree.

A decade ago, the treatment of hypercholesterolemia and hypertension. . . [Full Text of this Article]

Main Features of Atherosclerotic Lesions

Evolution of the Rupture-Prone Atherosclerotic Plaque

Gene-Targeted Mouse Models

Lipoprotein Retention and Activation of Immune Cells

Role of Endothelial Activation, Adhesion Molecules, and Chemokines

Macrophages in the Developing Plaque

T-Cell Activation and Vascular Inflammation

Antiinflammatory Factors and Disease Activity

Cross-Talk between Inflammation and Metabolism

Infections and CAD

Acute Coronary Syndromes

Mechanisms of Plaque Rupture

Systemic Indicators of Inflammation

Inflammatory Markers and the Risk of CAD

Therapeutic Opportunities

Source Information

From the Karolinska Institute, Center for Molecular Medicine, Department of Medicine, Karolinska University Hospital, Stockholm.

Address reprint requests to Dr. Hansson at the Center for Molecular Medicine, L8:03, Karolinska University Hospital, SE-17176 Stockholm, Sweden, or at goran.hansson@cmm.ki.se.

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Inflammation, Atherosclerosis, and Coronary Artery Disease
García de Tena J., Kriszbacher I., Koppán M., Bódis J., Hansson G. K.
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N Engl J Med 2005; 353:429-430, Jul 28, 2005. Correspondence

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