Arterial vs venous clots

Arterial clots

Arteries are thick blood vessels with fast flowing blood. Blood clots in arteries are typically triggered by underlying arteriosclerosis (roughening of the artery wall). Blood platelets get stuck to the roughened blood vessel wall and form a clot. Thus, the medication of choice in trying to prevent thrombosis in arteries are medications that act against platelets. The following medications are anti-platelet drugs:

• Aspirin (= ASA)
• Plavix (= Clopidogrel)
• Ticlid (= Ticlopidine)
• Aggrenox (= aspirin plus dipyridamole)

By interfering with platelet function, these drugs increase the patient's risk of bleeding, even though to a lesser degree than coumadin. The INR is not influenced by these drugs and vitamin K intake does not influence their effect.

Venous clots

Veins are thin blood vessels with slow flowing blood. Blood clots that form in veins (DVT, pulmonary embolism) are mainly made up of clotting proteins; platelets do not play a big role in venous clots. Warfarin is an effective anticoagulant by preventing the production of clotting factors in the liver, increasing the INR. It is therefore the drug of choice in venous thrombosis. Anti-platelet drugs do not play much of a role in preventing venous clots.

Occasionally, clots in arteries originate from one of the two left heart chambers and travel from there with the blood stream to the brain, the retina, or the extremities. This typically happens in atrial fibrillation. Such a clot is an arterial embolism that resembles the type of clots seen in veins i.e. they have little platelet participation. They are therefore best treated with warfarin, not with anti-platelet drugs, even though they are clots in arteries.

References:

• Thrombophilia Support page