After this operative procedure is performed how come the 'new' arterial surface doesn't form thrombi (or does it)? Shouldn't the exposed non-endothelial surface be highly thromogenic?
I link some studies concerning survival and long term outcomes which clearly prove the benefits od intervention and prove that thrombi formation isn't a rule, but which is in disagreement with the standard thaught mechanism of vascular thrombi formation (exposed subendothelium being highly thrombogenic).
Looking forward to hear some answers, thoughts and ideas from experienced people.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561447/
http://www.ncbi.nlm.nih.gov/pubmed/10753280