if a stent Is implanted into a narrowed part of a vein the question Is if there will be blond coagulation preferable? Is it dependent on the blood system of the individual? What are the duration times for coagulation?
I am not sure whether or not I understand your question correctly?
However, if you put wire into a vessel, you will always get clotting along the wire (=stent). You can imagine blood vessels as very smooth pipes, the innermost part of the vessel wall being called endothel. This cell layer could be compared to teflon in a pan. As long as your teflon stays unscratched, you will not burn stuff to the pan. However, if you cut meat in your pan using a steel knife, you will hurt or even destroy your teflon layer.
In a blood vessel, either injury or arteriosklerosis could be viewed as the knife destroying your teflon, the endothelial cells, and this will lead to coagulation at the site of injury. Now, if you plant iron wire across this endothelial cell layer, you will surely get coagulation at the stent, as long as you do not impair thrombocytic function.
There will surely be inter- and intraindividual differences in time of clot formation, however, if you do not give inhibitors of thrombocytic aggregation like ASS or clopidogrel (or else...) as soon as or better prior to stent implantation, those times will be rather short (a couple of minutes, maybe? Wouldn´t want to try).
Dear Peter Eyerer, naturally, if a stent or another artificial implant been introduced into vein or arteria vessel, the conditions of blood flow are changed in hemodynamic and hemocompatibility sense. As Julian Strobel said, the surface of metallic wire is not equivalent to endothelium one. When we have been developed of artificial heart valve (AHV), the problem of coagulation and hemolysis was partially solved by means of optimisation of blood flow and surface modification of AHV leaflets, namely, by PTFE (teflon) coating. This seemed typical for all vital organisms, but individual peculiarities of blood and vessels are playing important role. All the best, Serge
Stents are generally coated to prevent thrombus formation and re-stenosis, but even this is not 100% effective.
One cause for restenosis is endothelial proliferation. Intravascular radiation has been tried but never causght on, one reason being the development of drug (anti-inlammatory immunosuppressive and antiproliferative) eluting stents which kill of proliferating cell. At present, use of drug eluting stents combined with anticlotting drugs is considered best.
Yes, mentioned above biophysical and biochemical methods of implant surface modification are seemed an effective enough. To prevent thrombus formation, new attempts of formation of bioactive coatings with mosaic surface structure have been undertaken lately. Also, some references (not very new) may be useful:
Tanzi M.C., Petrini P., Fare S. Advanced polyurethanes for blood contacting applications containing prime as “smart” heparin-adsorbing moieties // Journal of Biomechanics. – 2001. – Vol. 34. – P. 51-66.
Rasche, H. Haemostasis and thrombosis: an overview / H. Rasche // European Heart Journal Supplements. – 2001. – Vol. 3. – P. 3–7.
Bluestein D., Li Y.M., Krukenkamp I.B. Free emboli formation in the wake of bi-leaflet mechanical heart valves and the effects of implantation techniques // J. Biomechanics.– 2002.– Vol. 35, P. 1533-1540.