SummaryThrombotic disorders are the most common cause of death in the United States. About two million individuals die each year from an arterial or venous thrombosis or related disorders. About 80% to 90% of all cases of thrombosis can now be defined with respect to cause. Of these, over 50% occur in patients who harbor a congenital or acquired blood coagulation protein or platelet defect which caused the thrombotic event. It is obviously of major importance to define those individuals harboring such a defect as this allows: 1) appropriate antithrombotic therapy to decrease risks of recurrence; 2) determination of the length of time the patient must remain on therapy for secondary prevention; and 3) allow for testing of family members of those harboring a blood coagulation protein or platelet defect which is hereditary (about 50% of all coagulation and platelet defects mentioned above). Aside from mortality, significant additional morbidity occurs from both arterial or venous thrombotic events, including, but not limited to paralysis (non-fatal thrombotic stroke), cardiac disability (repeated coronary events), loss of vision (retinal vascular thrombosis), fetal waste syndrome (placental vascular thrombosis), stasis ulcers and other manifestations of post-phlebitic syndrome, etc.
Tmem16F forms a Ca2+-Activated Cation Channel Required for Lipid Scrambling in Platelets during Blood Coagulation