I would say that for DVT, that platelet messaging via TXa2 would play a larger part in the full clot formation.
Fibrin would be more important in the initiation of the clot formation, followed by the platelets releasing TXa2 which increases coagulation, increasing the clot size. By taking warfarin, this prevents several steps in the clotting cascade before fibrin is even involved in the cascade.
As for this thread, the combination of being on cycle w/o any estrogen controlling measures combined w/ the OP's travel habits was a clot waiting to happen. Non-medical interventions that the OP can do to help avoid a DVT is wearing compression stockings while traveling, also while seated for extended periods of time is to do calf raises to help keep the blood flowing and not becoming stagnant. The calf is nick-named " the heart of the leg" because of its "pumping" action during contraction to return blood to the heart. The calf is surrounded by a thick viscera membrane which doesnt stretch very easily and during extended periods of inactivity, the relaxed state of the muscle allows the blood to become stagnant which increases the chance of clot formation.
As for a future cycle, using an AI would most def help keep the DVT from occuring again, since estrogen is a known pro-coagulation hormone. The use of Tamox is currently debated on its effects on the clotting cycle, there are studies out there ( granted not for use during an AAS cycle) stating that tamox is pro-coagulation, and studies stating that it is anti-coag. Therefore, I am uncertain on how tamoxifen would affect the formation of a DVT.
If you do start an aspirin regimen, be sure to discuss this w/ ur doc; it may affect the dosages of warfarin.
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