Microparticles may be responsible for the exacerbated pro-coagulant status. I would suggest you to follow papers with author Leroyer A.S. As an example, see Canault M, Leroyer A.S. et al Am J Pathol 2007: extract: "human plaque MPs carry catalytically active TACE/ADAM17 and significantly enhance the cell surface processing of the TACE/ADAM17 substrates TNF, TNFR-1, and endothelial protein C receptor, suggesting that TACE/ADAM17(+) MPs could regulate the inflammatory balance in the culprit lesion."

Exactly .. but TF alone may not do that much. It needs to be exposed on (activated) cell membranes or their cell-derived microparticles (e.g. from activated monocytes/macrophages/foam as well as sub-endotjelial cells that are in the ruptured plaque) which can go out of the plaque even more easily than their (bigger and somehow adherent) cells of origin., see Leroyer AS et al, 2008 Journal of Internal Medicine 263; 528–537. By chance, some of them may also be anti-coagulant/pro-fibrinolytic in essence, see Lacroix R, et al. Revisited role of microparticles in arterial and venous thrombosis. J Thromb Haemost 2013; 11 (Suppl. 1): 24–35.

Altered blood matrix (the surrounding of F12 or PK) triggers intrinsic coagulation.

Although I am a very great fan of the contact activation system, I am personally not completely convinced that FXII and intrinsic coagulation are strongly involved in human atherosclerotic thrombosis patients. Certainly, interesting data has been generated in knockout/antisense oligo treated mouse models. However, human epidemiology in this area is much less clear. I would put my 'money' on VWF/platelets for flow disturbances/collagen exposure and the TF pathway + MPs for clotting.

Also to note related to the question: an important role for monocytes/macrophages. A paper that shed light on the potential involvement of both TF and TFPI in carotid plaques and a potential value of their relative expression levels on circulating blood monocytes as surrogate markers for thrombotic risk. Basaravaj et al (2012) Circulating monocytes mirror the imbalance in TF and TFPI expression in carotid atherosclerotic plaques with lipid-rich and calcified morphology. Thromb Res 129 (4):e134-41. Interesting discussion and list of references to read.

Extract from discussion": Our findings may suggest that an imbalance between TF and TFPI in circulation monocytes may occur prior to extravasation of monocytes into atherosclerotic plaques or reflect the prothrombotic milieu of lipid-rich plaques prone

to rupture." .."monocytes in circulation may reflect the prothrombotic phenotype of plaque-residing macrophages, a major source of TF within the plaques."

I agree with Jeffrey and Philippe in that when it comes to triggering thrombus generation, Tissue Factor is one (yet perhaps not the only) major player; however, when it comes to thrombus growth / propagation, many other factors may and do kick in.

I agree with Jeffrey Weitz.