Inflammatory pathways in atherosclerosis and acute coronary syndromes

Am J Cardiol. 2001 Oct 18;88(8A):10K-15K. doi: 10.1016/s0002-9149(01)01924-5.


Evidence from a broad range of studies demonstrates that atherosclerosis is a chronic disease that, from its origins to its ultimate complications, involves inflammatory cells (T cells, monocytes, macrophages), inflammatory proteins (cytokines, chemokines), and inflammatory responses from vascular cells (endothelial cell expression of adhesion molecules). Investigators have identified a variety of proteins whose levels might predict cardiovascular risk. Of these candidates, C-reactive protein, tumor necrosis factor-alpha, and interleukin-6 have been most widely studied. There is also the prospect of inflammation as a therapeutic target, with investigators currently debating to what extent the decrease in cardiovascular risk seen with statins, angiotensin-converting enzyme inhibitors, and peroxisome proliferator-activated receptor ligands derives from changes in inflammatory parameters. These advances in basic and clinical science have placed us on a threshold of a new era in cardiovascular medicine.

Publication types

  • Review

MeSH terms

  • Angina, Unstable / physiopathology*
  • C-Reactive Protein / physiology
  • Coronary Artery Disease / drug therapy
  • Coronary Artery Disease / physiopathology*
  • DNA-Binding Proteins / therapeutic use
  • Humans
  • Inflammation / physiopathology
  • Interleukin-6 / physiology
  • Myocardial Infarction / physiopathology*
  • Receptors, Cytoplasmic and Nuclear / therapeutic use
  • Syndrome
  • Transcription Factors / therapeutic use
  • Tumor Necrosis Factor-alpha / physiology


  • DNA-Binding Proteins
  • Interleukin-6
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • C-Reactive Protein