Links between inflammation and thrombogenicity in atherosclerosis

J. F. Viles-Gonzalez, Valentin Fuster, Juan J. Badimon

Research output: Contribution to journalReview articlepeer-review

59 Scopus citations


Plaque disruption and subsequent thrombus formation play a critical role in the clinical manifestations of atherothrombosis. Vulnerable lesions are characterized by the existence of core rich in lipid, macrophages and tissue factor (TF). Plaque disruption facilitates the interaction between flowing blood with the inner components (TF) of disrupted atherosclerotic lesions triggering the coagulation cascade. TF, thrombin, platelets, fibrin and inflammatory cells are involved in this process of acute thrombus formation. This pathologic process is significantly accelerated by several "cardiovascular risk factors" such as diabetes, smoking, dyslipemia, etc. We will review on the role of TF, plaque cell apoptosis and blood thrombogenicity acting as a thread of inflammatory and prothrombotic mediators. We will also review the role of activated platelets as source for pro-inflammatory cytokines and enunciation of thrombotic process. Overall, we will try to emphasize the most recent understanding of the concepts involved in the interaction between inflammation and coagulation within the setting of atherothrombotic disease.

Original languageEnglish (US)
Pages (from-to)489-499
Number of pages11
JournalCurrent Molecular Medicine
Issue number5
StatePublished - Aug 2006
Externally publishedYes


  • Apoptosis
  • Atherosclerosis
  • Atherothrombosis
  • High-risk patient
  • High-risk plaque
  • Inflammation
  • Plaque
  • Platelet
  • Thrombin
  • Thrombosis
  • Tissue factor
  • Vulnerable blood
  • Vulnerable plaque

ASJC Scopus subject areas

  • Biochemistry


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