Summary
Atherothrombosis defines the occurrence of thrombosis on athero-sclerotic lesions.
Atherosclerosis is the most prevalent disease of our time and its thrombotic complications
are responsible for an exceedingly high number of deaths 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 syndromes. A thrombus is usually found secondary to atherosclerotic
plaque disruption. Mural thrombosis, also at the site of plaque rupture, is an important
mechanism in the progression of atherosclerosis even when symptoms are absent. Because
atherosclerosis is a silent and asymptomatic disease until complications arise with
thrombosis producing clinical symptoms, it is necessary to have models that reproduce
the human disease in its early stages. Unfortunately, not all the experimental models
of vascular disease have human resemblance and validity. Knowledge of the disease
process and of what an experimental animal model can offer is a milestone for a successful
investigation. Experimental models of vascular disease have enhanced our understanding
of the pathophysiological processes leading to vascular obstruction in both spontaneous
and accelerated atherosclerosis and thrombosis. Animal models have provided insight
into the role of platelets, lipids, renin-angiotensin system (RAS), cytokines and
growth factors in the evolution and progression of atherosclerosis and have suggested
potential therapeutic interventions. Significant advances in our understanding of
the vascular biology and pathology of atherosclerosis and thrombosis, and of the interactions
of blood cells, lipids and proteins with the vascular wall, have allowed us to formulate
new experimental hypotheses and to test therapeutic strategies, either pharmacological
or surgical.
Key words
Atherosclerosis - thrombosis - animal models - risk factors - platelets
