Platelets have evolved an intricate array of overlapping mechanisms to respond effectively to vessel damage by forming a clot to minimize blood loss. Unfortunately, these same responses may also be triggered by atherosclerotic lesions in diseased arteries. Vessels can become occluded when platelets form a thrombus at the site of a ruptured plaque, causing myocardial infarction (MI) or ischemic stroke, depending on where the thrombus forms or where a resulting embolus becomes lodged.
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