It's all about the stasis in this case, not the endothelial damage; the random, erratic contractions of myocytes in the atrium leads to areas of blood stasis rather than a coordinated contraction. Think deep venous thrombosis. If blood sits for a long period of time, spontaneous activation of thrombin may eventually occur, leading to the cascade.
There's a slight distinction between the stasis-based clots and endothelial-damaged ones: Stasis is more clotting factor+fibrin-dependant, and endothelial damage is more platelet-dependant. I've really only heard this be of any importance in explaining why they give aspirin+warfarin/heparin in anterior MI's. These MI's have the greatest risk for mural thrombi, which are mixed clots of platelets and fibrin - the weak muscle causes stasis, and the infarction is endothelial damage. Therefore, the aspirin is a platelet block for endothelial damage, then warfarin/heparin on top of it is for the stasis.
(I'm not trying to be a gunner here with my answers, you just keep posting right when I happen to be checking the forum hahaha)
