Atherothrombosis defines the occurrence of thrombosis on atherosclerotic le
sions. Atherosclerosis is the most prevalent disease of our time and its th
rombotic complications are responsible for an exceedingly high number of de
aths and disabilities. Over the past few years, experimental investigation
and clinical and pathologic observations have led to a better understanding
of how a thrombus forms and also of its incidence in acute ischemic syndro
mes. A thrombus is usually found secondary to atherosclerotic plaque disrup
tion. Mural thrombosis, also at the site of plaque rupture, is an important
mechanism in the progression of atherosclerosis even when symptoms are abs
ent. Because atherosclerosis is a silent and asymptomatic disease until com
plications arise with thrombosis producing clinical symptoms, it is necessa
ry to have models that reproduce the human disease in its early stages. Unf
ortunately, not all the experimental models of vascular disease have human
resemblance and validity. Knowledge of the disease process and of what an e
xperimental animal model can offer is a milestone for a successful investig
ation. Experimental models of vascular disease have enhanced our understand
ing of the pathophysiological processes leading to vascular obstruction in
both spontaneous and accelerated atherosclerosis and thrombosis. Animal mod
els have provided insight into the role of platelets, lipids, renin-angiote
nsin system (RAS), cytokines and growth factors in the evolution and progre
ssion of atherosclerosis and have suggested potential therapeutic intervent
ions. Significant advances in our understanding of the vascular biology and
pathology of atherosclerosis and thrombosis, and of the interactions of bl
ood cells, lipids and proteins with the vascular wall, have allowed us to f
ormulate new experimental hypotheses and to test therapeutic strategies, ei
ther pharmacological or surgical.