Introduction
Thrombosis is commonly associated with arterial injury. Clinically, this is seen with
all interventional procedures designed to treat coronary artery stenosis, such as
percutaneous transluminal coronary angioplasty (PTCA),1 directional coronary, 1 atherectomy (DCA)2 and coronary artery stenting.3 Acute thrombosis occasionally results in total occlusion of the vessel lumen. However,
more typical is the deposition of smaller nonocclusive mural thrombi.
Thrombosis is also a common feature of many animal models of arterial injury.4-8 These models have provided considerable information about the molecular events associated
with injury-induced thrombus formation. Platelet adherence to the injured arterial
wall occurs within minutes in all models of arterial injury. In some models, platelet
deposition is followed by fibrin deposition, a consequence of activation of the coagulation
cascade. The presence and extent of fibrin deposition varies with the degree of injury
(superficial or deep), the type of vessel (carotid, femoral, aorta, or coronary),
the state of the vessel prior to injury (normal, cholesterol fed, previously injured),
and the species. In the pig carotid balloon injury model, endothelial denudation in
the absence of medial injury is associated with platelet deposition but no fibrin
generation. More severe injury, defined by the presence of a medial tear, results
in marked platelet accumulation and fibrin generation, even in the presence of high
doses of heparin.4,9 Unlike the porcine model, balloon injury to normal rodent arteries is associated
with rapid platelet deposition but does not result in significant fibrin deposition,
even in the presence of medial injury.5-8
In contrast to that found using normal arteries, fibrin deposition is seen when previously
injured rabbit arteries, possessing a neointima, are subjected to a second injury.5,7,8,10 As determined by scanning and transmission electron microscopy, abundant fibrin formation
is detected within 30 minutes of the reinjury. Platelet deposition is also more dense
after the second injury and associated with fibrin-platelet microthrombi. We have
recently found a similar difference between single and double injury in rat aorta
and carotid arteries. These studies suggest that, in contrast to the deposition of
platelets, which accompanies any injury to the arterial wall, the deposition of fibrin
and the formation of large thrombi are more dependent on the type of injury produced
and may be regulated by specific processes occurring in the arterial wall.
