Arterial thrombotic disease is one of the most common causes of morbidity a
nd mortality in the Western world. In contrast to venous thrombosis, arteri
al thrombosis is initiated by platelet activation at sites of vascular wall
damage, the latter often related to atheromatous change. Thus, environment
al and hereditary conditions that promote vascular damage set the stage for
subsequent thrombotic complications. There is a growing body of work that
suggests that these thrombotic events may be accelerated by genetic risk fa
ctors that promote coagulation or enhance platelet reactivity. In this revi
ew, the possible role of platelet membrane receptor polymorphisms as risk f
actors for acute thrombotic events such as myocardial infarction and stroke
will be reviewed.