my first impression is: platelet microparticles. There is no data about it but in my opinion they can participate in platelet (and other cell) aggregation because of their specific proaggregation and procoagulation activity. They are conveyors of adhesion molecules, activation factors etc.
SPS is mainly reported as an arterial thrombophilic risk factor. But there are a few reports on venous thromboembolism associated to this platelet dysfunction. it's common to involve platelets in arterial thrombosis and clotting factors in venous thrombo embolic events but we know that for some patients, aspirin may prevent venous thrombosis then platelets may be obviously also involved.
We have seen some cases of venous thromboembolism in patients with SPS. Some of them suffered from VTE and also from arterial thrombosis, in some of them recurrent VTE occurred despite of warfarin therapy and no recurrence was observed after switching to aspirin.
I could not find satisfactory experimental proof relating sticky platelet syndrome and deep vein thrombosis. Theoretically hyper-coagulable platelets have possibility to interact with venous endothelia and occlude vascular lumen. It would be interesting to devise a computational model predicting possible interaction between mutated GP VI and collagen followed by validating the predictions in platelet-platelet interaction and platelet-endothelial interaction.
Discrepancy in genetic studies as well as laboratory geterogeneity of SPS might suggest multifactorial genetic as know in some other hemostatic disorders such as some types of von Willebrand disease,where various mutations of the same or even other genetic loci can result in the similar phenotype.