From my understanding, when the endothelial lining of arteries is damaged, atheroma is formed at the site of the damaged area. If the atheromas is ruptured, thromboplastin contained in atheroma is released into blood stream thus thrombus is formed after atheroma gets ruptured - this phenomenon is known as atherothrombosis. As a result, atheroma is characterised by its thrombogenic activity.
My question is, how come atheroma contains thromboplastin thus when it is damaged, thrombosis occurs? What was the source of this thromboplastin? Was it in the bloodstream? If thromboplastin was always present in the blood in which it entered into the atheroma during the formation of atheroma, why don't thrombosis occurs at the start when endothelial lining of the artery is damaged (without the need for an atheroma to rupture)?
I've read a couple papers and watched some videos on this topic. I've put one of my research below for reference to back up 'my understanding'.