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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