Evidence indicates that the following factors are concerned with atherogenesis: Blood
flow, thrombosis, endothelial injury, lipid and protein accumulation in the intima.
The initiating mechanism is unknown. Several investigators have observed thrombus
formation on structurally normal intima. The changes in the intima starting the process
may, however, be biochemical rather than structural, HS is a weak heparin-like anticoagulant
attached to the external endothelial cell surface. HS may be liberated by a platelet
endoglycosidase, and may be inactivated by platelet factor 4 or beta-lipo-proteins.
Assuming platelet damage because of the flow pattern, platelet aggregation and release
reaction may result in inactivation of endothelial bound HS, thus favouring local
thromboeia. High levels of beta-lipo-proteins in the circulating blood may add to
this effect. Released platelet substances may increase vascular permeability counting
for the plasma components found in atherosclerotic lesions. Exogeneous heparin binds
to the intima, probably by substituting HS at the endothelial cell surface. Long term
heparin prophylaxis may hypothetically prevent or retard advancing atherosclerosis.
Heparin fractions, possibly with less side effects, could be of value.
