1. Acute coronary syndromes: biology
Dr Valentin Fuster, MD, Zahi A Fayad, PhD, Juan J Badimon, PhD 
The Lancet 
Volume 353, Pages s5-s9 (June 1999)
DOI: /S (99)
Copyright © 1999 Elsevier Ltd Terms and Conditions

2. Figure 1
Phases and lesion morphology of progression of coronary atherosclerosis according to gross pathological and clinical findings
Modified with permission from Fuster and colleagues.7
The Lancet  , s5-s9DOI: ( /S (99) )
Copyright © 1999 Elsevier Ltd Terms and Conditions

3. Figure 2
Plaque vulnerability, disruption, and thrombosis: anatomical changes leading to ACS and subsequent plaque remodelling
An element of vasoconstriction is usually present. Modified with permission from Theroux and Fuster.34
The Lancet  , s5-s9DOI: ( /S (99) )
Copyright © 1999 Elsevier Ltd Terms and Conditions

4. Figure 3
Effects of rTFPi on thrombogenicity of disrupted lipid-rich human atherosclerotic plaques: control (A) and rTFPI-treated(B)
Fibrinogen deposition is shown as green, platelet deposistion as red, and their co-localisation as orange. Note the significant antithrombotic effect of rTFPI on deposition of platelet and fibrin(ogen)deposition. With permission from Badimon and colleagues.23
The Lancet  , s5-s9DOI: ( /S (99) )
Copyright © 1999 Elsevier Ltd Terms and Conditions

5. Figure 4
In-vivo cross-sectional imaging of human thoracic aorta with MRI(A) and tansoesophageal echo(B)
Observe presence of a lipid-rich core indicated by the arrow in MRI view.
The Lancet  , s5-s9DOI: ( /S (99) )
Copyright © 1999 Elsevier Ltd Terms and Conditions

6. Figure 5
In-vivo MRI cross-sectional imaging of the lumen(left) and wall (right) of patient with plaque in left anterior descending coronary artery
LAD=left anterior descending coronary artery; GCV=great cardiac vein; RV=right ventricle; LV=left ventricle.
The Lancet  , s5-s9DOI: ( /S (99) )
Copyright © 1999 Elsevier Ltd Terms and Conditions