Summary
Clinical manifestations of atherosclerosis are the consequences of atherosclerotic
plaque rupture that triggers thrombus formation. Tissue factor (TF) is a key element
in the initiation of the coagulation cascade and is crucial in thrombus formation
following plaque disruption. TF activity is highly dependent on the presence of phosphatidylserine
(PS), an anionic phospholipid that is redistributed on the cell surface during apoptotic
death conferring a potent procoagulant activity to the apoptotic cell. Apoptosis occurs
in the human atherosclerotic plaque and shed membrane apoptotic microparticles rich
in PS are produced in considerable amounts within the lipid core. These microparticles
carry almost all TF activity and are responsible for the procoagulant activity of
the plaque. Moreover, luminal endothelial cell apoptosis might be responsible for
thrombus formation on eroded plaques without rupture. Apoptosis might also play a
major role in blood thrombogenicity via circulating procoagulant microparticles that
are found at high levels in patients with acute coronary syndromes.
Key words
Atherosclerosis - plaque stability - apoptosis - tissue factor - phosphatidylserine