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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'.

Rupture of the fibrous cap will typically release all the semiliquid material from the central portion of the atheroma. Because this material contains thromboplastin, it will trigger blood clotting, and a thrombus will develop at the site of intimal ulceration.

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Tissue factor is present in subendothelial tissue and leukocytes - in this case this would be within the atheroma since the atheroma consists of damaged endothelium.

Tissue factor's presence in the subendotheilum in general implies that whenever the endothelium is damaged, tissue factor is released which promotes clotting at that site. Clotting starts after an atheroma ruptures because up until that point all the tissue factor is encased within the atheroma, protected from direct contact with the bloodstream - there is still no superficial injury to the endothelium to expose the underlying tissue factor that would signal the clotting cascade to begin. Therefore, clotting only starts after the atheroma ruptures and all the tissue factor stored within the atheroma is released into the blood vessel.

It is worth noting here that in homeostasis without any injury, the coagulation cascade and fibrinolytic pathways (the clot-lysis or pathways) are both active, but they balance out each other's effects. Disruption of this balance due to pathology, injury, or other insult causes an imbalance between the two pathways which the body seeks to rectify. The imbalance is what leads to clot lysis (in the case of wound healing - after the wound has healed) and clot formation (in the case of a new injury).

Sources:

  1. https://www.ahajournals.org/doi/full/10.1161/01.CIR.94.6.1226

  2. https://www.ahajournals.org/doi/full/10.1161/01.CIR.96.2.396

  3. https://ascpt.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1752-8062.2011.00351.x

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